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Would you describe Overweight, to me Aarogya

Overweight

Being overweight or fat is having more body fat than is optimally healthy. Being overweight is especially common where food supplies are plentiful and lifestyles are sedentary. As of 2003, excess weight reached epidemic proportions globally, with more than 1 billion adults being either overweight or obese. In 2013, this increased to more than 2 billion. Increases have been observed across all age groups. A healthy body requires a minimum amount of fat for proper functioning of the hormonal, reproductive, and immune systems, as thermal insulation, as shock absorption for sensitive areas, and as energy for future use; however, the accumulation of too much storage fat can impair movement, flexibility, and alter the appearance of the body. Classification The degree to which a person is overweight is generally described by the body mass index (BMI). Overweight is defined as a BMI of 25 or more, thus it includes pre-obesity defined as a BMI between 25 and 29.9 and obesity as defined by a BMI of 30 or more. Pre-obese and overweight however are often used interchangeably, thus giving overweight a common definition of a BMI of between 25 and 29.9. There are, however, several other common ways to measure the amount of adiposity or fat present in an individuals body. Body mass indexThe body mass index (BMI) is a measure of a persons weight taking into account their height. It is given by the following formula: BMI equals a persons weight (mass) in kilograms divided by the square of the persons height in metres. The units therefore are kg/m2 but BMI measures are typically used and written without units.BMI provides a significantly more accurate representation of body fat content than simply measuring a persons weight. It is only moderately correlated with both body fat percentage and body fat mass (R2 of 0.68). It does not take into account certain factors such as pregnancy or bodybuilding; however, the BMI is an accurate reflection of fat percentage in the majority of the adult population.Body volume indexThe body volume index (BVI) was devised in 2000 as a computer, rather than manual, measurement of the human body for obesity and an alternative to the BMIBVI uses 3D software to create an accurate image of a person so BVI can differentiate between people with the same BMI rating, but who have a different shape and different weight distribution. BVI measures where a persons weight and the fat are located on the body, rather than total weight or total fat content and places emphasis on the weight carried around the abdomen, commonly known as central obesity. There has been an acceptance in recent years that abdominal fat and weight around the abdomen constitute a greater health risk.Simple weighingA persons weight is measured and compared to an estimated ideal weight. This is the easiest and most common method, but by far the least accurate, as it only measures one quantity (weight) and often does not take into account many factors such as height, body type, and relative amount of muscle mass.Skinfold calipers or "pinch test"The skin at several specific points on the body is pinched and the thickness of the resulting fold is measured. This measures the thickness of the layers of fat located under the skin, from which a general measurement of total amount of fat in the body is calculated. This method can be reasonably accurate for many people, but it assumes particular fat distribution patterns over the body—which may not apply to all individuals, and does not account for fat deposits not directly under the skin. Also, as the measurement and analysis generally involves a high degree of practice and interpretation, an accurate result requires that a professional perform it. It cannot generally be done by patients themselves.Bioelectrical impedance analysisA small electric current is passed through the body to measure its electrical resistance. As fat and muscle conduct electricity differently, this method can provide a direct measurement of the body fat percentage, in relation to muscle mass. In the past, this technique could only be performed reliably by trained professionals with specialized equipment, but it is now possible to buy home testing kits that let people do this themselves with a minimum of training. Despite the improved simplicity of this process over the years, however, a number of factors can affect the results, including hydration and body temperature, so it still needs some care when taking the test to ensure that the results are accurate.Hydrostatic weighingConsidered one of the more accurate methods of measuring body fat, this technique involves complete submersion of a person in water, with special equipment to measure the persons weight while submerged. This weight is then compared with "dry weight" as recorded outside the water to determine overall body density. As fat is less dense than muscle, careful application of this technique can provide a reasonably close estimate of fat content in the body. This technique does, however, require expensive specialized equipment and trained professionals to administer it properly.Dual-energy X-ray absorptiometry (DEXA)Originally developed to measure bone density, DEXA imaging is also used to precisely determine body fat content by using the density of various body tissues to identify which portions of the body are fat. This test is generally considered very accurate, but requires a great deal of expensive medical equipment and trained professionals to perform.The most common method for discussing this subject and the one used primarily by researchers and advisory institutions is BMI. Definitions of what is considered overweight vary by ethnicity. The current definition proposed by the US National Institutes of Health (NIH) and the World Health Organization (WHO) designates whites, Hispanics and blacks with a BMI of 25 or more as overweight. For Asians, overweight is a BMI between 23 and 29.9 and obesity for all groups is a BMI of 30 or more. BMI, however, does not account extremes of muscle mass, some rare genetic factors, the very young, and a few other individual variations. Thus it is possible for an individuals with a BMI of less than 25 to have excess body fat, while others may have a BMI that is significantly higher without falling into this category. Some of the above methods for determining body fat are more accurate than BMI but are less convenient to measure. If an individual is overweight and has excess body fat it can create or lead to health risks. Reports are surfacing, however, that being mildly overweight to slightly obese – BMI being between 24 and 31.9 – may be actually beneficial and that people with a BMI between 24 and 31.9 could actually live longer than normal weight or underweight persons. Health effects While some negative health outcomes associated with obesity are accepted within the medical community, the health implications of the overweight category are more controversial. A 2016 review estimated that the risk of death increases by seven percent among overweight people with a BMI of 25 to 27.5 and 20 percent among overweight people with a BMI of 27.5 to 30. Katherine Flegal et al., however, found that the mortality rate for individuals who are classified as overweight (BMI 25 to 29.9) may actually be lower than for those with an "ideal" weight (BMI 18.5 to 24.9), noting that many studies show that the lowest mortality rate is at a BMI close to 25. The specific conclusions appear to depend on what other factors are controlled for, and Flegal has accordingly alleged that the findings from the 2016 review are driven by bias toward preconceived opinions.Being overweight has been identified as a risk factor for cancer, and Walter Willett predicts that being overweight will overtake smoking as the primary cause of cancer in developed countries as cases of smoking-related cancer dwindle. Being overweight also increases the risk of oligospermia and azoospermia in men.Psychological well-being is also at risk in the overweight individual due to social discrimination. Being overweight has been shown not to increase mortality in older people: in a study of 70 to 75-year old Australians, mortality was lowest for "overweight" individuals (BMI 25 to 29.9), while a study of Koreans found that, among those initially aged 65 or more, an increase in BMI to above 25 was not associated with increased risk of death. Causes Being overweight is generally caused by the intake of more calories (by eating) than are expended by the body (by exercise and everyday activity). Factors that may contribute to this imbalance include: Alcoholism Eating disorders (such as binge eating) Genetic predisposition Hormonal imbalances (e.g. hypothyroidism) Insufficient or poor-quality sleep Limited physical exercise and a sedentary lifestyle Poor nutrition Metabolic disorders, which could be caused by repeated attempts to lose weight by weight cycling Overeating Psychotropic medication (e.g. olanzapine) Smoking cessation and other stimulant withdrawal StressPeople who have insulin dependent diabetes and chronically overdose insulin may gain weight, while people who already are overweight may develop insulin tolerance, and in the long run develop type II diabetes. Treatment The usual treatments for overweight individuals is diet and physical exercise. Dietitians generally recommend eating several balanced meals dispersed through the day, with a combination of progressive, primarily aerobic, physical exercise. In fact, some research found benefits from physical activity, diet and behaviour changes on BMI in children from 12 to 17 years old.Considering that most of the treatment strategies are directed to change lifestyle-related behaviours of individuals (namely in dietary and physical activity), the transtheoretical model (TTM) has been used as a framework to design weight management interventions. A systematic review assessed the effectiveness of dietary and physical activity interventions based on the TTM in producing sustainable (one year or longer) weight loss in overweight and obese adults. The included studies did not allow to produce conclusive evidence about the impact of the use of this model combined with these interventions on sustainable weight loss. Nevertheless, very low quality scientific evidence suggests that this approach may lead to improvements in physical activity and dietary habits, namely increased in both exercise duration and frequency, and fruits and vegetables consumption, along with reduced dietary fat intake. Epidemiology The World Health Organization (WHO) estimated that nearly 2 billion adults worldwide, aged 18 years and older, were overweight in 2016.According to the National Health and Nutrition Examination Survey (NHANES), an estimated 71.6% of the United States adult population aged 20 and over is considered either overweight or obese, and this percentage has increased over the last four decades. See also Body image Canadian Obesity Network Fat acceptance movement Physical attractiveness References External links Obesity Epidemic: U.S. Temporal Trends 1985–2004 at the Wayback Machine (archived December 8, 2006) Ranking of Most Overweight Countries in the World 2005 at the Wayback Machine (archived June 29, 2007) World Health Organization fact sheet on obesity and overweight

Give me a short description about Pedophilia , Aarogya

Pedophilia

Pedophilia (alternatively spelt paedophilia) is a psychiatric disorder in which an adult or older adolescent experiences a primary or exclusive sexual attraction to prepubescent children. Although girls typically begin the process of puberty at age 10 or 11, and boys at age 11 or 12, criteria for pedophilia extend the cut-off point for prepubescence to age 13. A person must be at least 16 years old, and at least five years older than the prepubescent child, for the attraction to be diagnosed as pedophilia.Pedophilia is termed pedophilic disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and the International Classification of Diseases (ICD-11). The DSM-5 defines it as a paraphilia involving intense and recurrent sexual urges towards and fantasies about prepubescent children that have either been acted upon or which cause the person with the attraction distress or interpersonal difficulty. The ICD-11 defines it as a "sustained, focused, and intense pattern of sexual arousal—as manifested by persistent sexual thoughts, fantasies, urges, or behaviours—involving pre-pubertal children."In popular usage, the word pedophilia is often applied to any sexual interest in children or the act of child sexual abuse, including any sexual interest in minors below the local age of consent, regardless of their level of physical or mental development. This use conflates the sexual attraction to prepubescent children with the act of child sexual abuse and fails to distinguish between attraction to prepubescent and pubescent or post-pubescent minors. Researchers recommend that these imprecise uses be avoided, because although some people who commit child sexual abuse are pedophiles, child sexual abuse offenders are not pedophiles unless they have a primary or exclusive sexual interest in prepubescent children, and some pedophiles do not molest children.Pedophilia was first formally recognized and named in the late 19th century. A significant amount of research in the area has taken place since the 1980s. Although mostly documented in men, there are also women who exhibit the disorder, and researchers assume available estimates underrepresent the true number of female pedophiles. No cure for pedophilia has been developed, but there are therapies that can reduce the incidence of a person committing child sexual abuse. The exact causes of pedophilia have not been conclusively established. Some studies of pedophilia in child sex offenders have correlated it with various neurological abnormalities and psychological pathologies. In the United States, following Kansas v. Hendricks in 1997, sex offenders who are diagnosed with certain mental disorders, particularly pedophilia, can be subject to indefinite involuntary commitment. Definitions The word pedophilia comes from the Greek παῖς, παιδός (paîs, paidós), meaning "child", and φιλία (philía), "friendly love" or "friendship". Pedophilia is used for individuals with a primary or exclusive sexual interest in prepubescent children aged 13 or younger. Infantophilia is a sub-type of pedophilia; it is used to refer to a sexual preference for children under the age of 5 (especially infants and toddlers). This is sometimes referred to as nepiophilia (from the Greek: νήπιος (népios) meaning "infant" or "child," which in turn derives from "ne-" and "epos" meaning "not speaking"), though this term is rarely used in academic sources. Hebephilia is defined as individuals with a primary or exclusive sexual interest in 11- to 14-year-old pubescents. The DSM-5 does not list hebephilia among the diagnoses. While evidence suggests that hebephilia is separate from pedophilia, the ICD-10 includes early pubertal age (an aspect of hebephilia) in its pedophilia definition, covering the physical development overlap between the two philias. In addition to hebephilia, some clinicians have proposed other categories that are somewhat or completely distinguished from pedophilia; these include pedohebephilia (a combination of pedophilia and hebephilia) and ephebophilia (though ephebophilia is not considered pathological). Signs and symptoms Development Pedophilia emerges before or during puberty, and is stable over time. It is self-discovered, not chosen. For these reasons, pedophilia has been described as a disorder of sexual preference, phenomenologically similar to a heterosexual or homosexual orientation. These observations, however, do not exclude pedophilia from being classified as a mental disorder since pedophilic acts cause harm, and mental health professionals can sometimes help pedophiles to refrain from harming children.In response to misinterpretations that the American Psychiatric Association considers pedophilia a sexual orientation because of wording in its printed DSM-5 manual, which distinguishes between paraphilia and what it calls "paraphilic disorder", subsequently forming a division of "pedophilia" and "pedophilic disorder", the association commented: "[S]exual orientation is not a term used in the diagnostic criteria for pedophilic disorder and its use in the DSM-5 text discussion is an error and should read sexual interest." They added, "In fact, APA considers pedophilic disorder a paraphilia, not a sexual orientation. This error will be corrected in the electronic version of DSM-5 and the next printing of the manual." They said they strongly support efforts to criminally prosecute those who sexually abuse and exploit children and adolescents, and "also support continued efforts to develop treatments for those with pedophilic disorder with the goal of preventing future acts of abuse." Comorbidity and personality traits Studies of pedophilia in child sex offenders often report that it co-occurs with other psychopathologies, such as low self-esteem, depression, anxiety, and personality problems. It is not clear whether these are features of the disorder itself, artifacts of sampling bias, or consequences of being identified as a sex offender. One review of the literature concluded that research on personality correlates and psychopathology in pedophiles is rarely methodologically correct, in part owing to confusion between pedophiles and child sex offenders, as well as the difficulty of obtaining a representative, community sample of pedophiles. Seto (2004) points out that pedophiles who are available from a clinical setting are likely there because of distress over their sexual preference or pressure from others. This increases the likelihood that they will show psychological problems. Similarly, pedophiles recruited from a correctional setting have been convicted of a crime, making it more likely that they will show anti-social characteristics.Impaired self-concept and interpersonal functioning were reported in a sample of child sex offenders who met the diagnostic criteria for pedophilia by Cohen et al. (2002), which the authors suggested could contribute to motivation for pedophilic acts. The pedophilic offenders in the study had elevated psychopathy and cognitive distortions compared to healthy community controls. This was interpreted as underlying their failure to inhibit their criminal behavior. Studies in 2009 and 2012 found that non-pedophilic child sex offenders exhibited psychopathy, but pedophiles did not.Wilson and Cox (1983) studied the characteristics of a group of pedophile club members. The most marked differences between pedophiles and controls were on the introversion scale, with pedophiles showing elevated shyness, sensitivity and depression. The pedophiles scored higher on neuroticism and psychoticism, but not enough to be considered pathological as a group. The authors caution that "there is a difficulty in untangling cause and effect. We cannot tell whether paedophiles gravitate towards children because, being highly introverted, they find the company of children less threatening than that of adults, or whether the social withdrawal implied by their introversion is a result of the isolation engendered by their preference i.e., awareness of the social [dis]approbation and hostility that it evokes" (p. 324). In a non-clinical survey, 46% of pedophiles reported that they had seriously considered suicide for reasons related to their sexual interest, 32% planned to carry it out, and 13% had already attempted it.A review of qualitative research studies published between 1982 and 2001 concluded that child sexual abusers use cognitive distortions to meet personal needs, justifying abuse by making excuses, redefining their actions as love and mutuality, and exploiting the power imbalance inherent in all adult–child relationships. Other cognitive distortions include the idea of "children as sexual beings", uncontrollability of sexual behavior, and "sexual entitlement-bias". Child pornography Consumption of child pornography is a more reliable indicator of pedophilia than molesting a child, although some non-pedophiles also view child pornography. Child pornography may be used for a variety of purposes, ranging from private sexual gratification or trading with other collectors, to preparing children for sexual abuse as part of the child grooming process.Pedophilic viewers of child pornography are often obsessive about collecting, organizing, categorizing, and labeling their child pornography collection according to age, gender, sex act and fantasy. According to FBI agent Ken Lanning, "collecting" pornography does not mean that they merely view pornography, but that they save it, and "it comes to define, fuel, and validate their most cherished sexual fantasies". Lanning states that the collection is the single best indicator of what the offender wants to do, but not necessarily of what has been or will be done. Researchers Taylor and Quayle reported that pedophilic collectors of child pornography are often involved in anonymous internet communities dedicated to extending their collections. Causes Although what causes pedophilia is not yet known, researchers began reporting a series of findings linking pedophilia with brain structure and function, beginning in 2002. Testing individuals from a variety of referral sources inside and outside the criminal justice system as well as controls, these studies found associations between pedophilia and lower IQs, poorer scores on memory tests, greater rates of non-right-handedness, greater rates of school grade failure over and above the IQ differences, being below average height, greater probability of having had childhood head injuries resulting in unconsciousness, and several differences in MRI-detected brain structures.Such studies suggest that there are one or more neurological characteristics present at birth that cause or increase the likelihood of being pedophilic. Some studies have found that pedophiles are less cognitively impaired than non-pedophilic child molesters. A 2011 study reported that pedophilic child molesters had deficits in response inhibition, but no deficits in memory or cognitive flexibility. Evidence of familial transmittability "suggests, but does not prove that genetic factors are responsible" for the development of pedophilia. A 2015 study indicated that pedophilic offenders have a normal IQ.Another study, using structural MRI, indicated that male pedophiles have a lower volume of white matter than a control group. Functional magnetic resonance imaging (fMRI) has indicated that child molesters diagnosed with pedophilia have reduced activation of the hypothalamus as compared with non-pedophilic persons when viewing sexually arousing pictures of adults. A 2008 functional neuroimaging study notes that central processing of sexual stimuli in heterosexual "paedophile forensic inpatients" may be altered by a disturbance in the prefrontal networks, which "may be associated with stimulus-controlled behaviours, such as sexual compulsive behaviours". The findings may also suggest "a dysfunction at the cognitive stage of sexual arousal processing".Blanchard, Cantor, and Robichaud (2006) reviewed the research that attempted to identify hormonal aspects of pedophiles. They concluded that there is some evidence that pedophilic men have less testosterone than controls, but that the research is of poor quality and that it is difficult to draw any firm conclusion from it. While not causes of pedophilia themselves, childhood abuse by adults or comorbid psychiatric illnesses—such as personality disorders and substance abuse—are risk factors for acting on pedophilic urges. Blanchard, Cantor, and Robichaud addressed comorbid psychiatric illnesses that, "The theoretical implications are not so clear. Do particular genes or noxious factors in the prenatal environment predispose a male to develop both affective disorders and pedophilia, or do the frustration, danger, and isolation engendered by unacceptable sexual desires—or their occasional furtive satisfaction—lead to anxiety and despair?" They indicated that, because they previously found mothers of pedophiles to be more likely to have undergone psychiatric treatment, the genetic possibility is more likely.A study analyzing the sexual fantasies of 200 heterosexual men by using the Wilson Sex Fantasy Questionnaire exam determined that males with a pronounced degree of paraphilic interest (including pedophilia) had a greater number of older brothers, a high 2D:4D digit ratio (which would indicate low prenatal androgen exposure), and an elevated probability of being left-handed, suggesting that disturbed hemispheric brain lateralization may play a role in deviant attractions. Diagnosis DSM and ICD-11 The Diagnostic and Statistical Manual of Mental Disorders 5th edition (DSM-5) has a significantly larger diagnostic features section for pedophilia than the previous DSM version, the DSM-IV-TR, and states, "The diagnostic criteria for pedophilic disorder are intended to apply both to individuals who freely disclose this paraphilia and to individuals who deny any sexual attraction to prepubertal children (generally age 13 years or younger), despite substantial objective evidence to the contrary." Like the DSM-IV-TR, the manual outlines specific criteria for use in the diagnosis of this disorder. These include the presence of sexually arousing fantasies, behaviors or urges that involve some kind of sexual activity with a prepubescent child (with the diagnostic criteria for the disorder extending the cut-off point for prepubescence to age 13) for six months or more, or that the subject has acted on these urges or is distressed as a result of having these feelings. The criteria also indicate that the subject should be 16 or older and that the child or children they fantasize about are at least five years younger than them, though ongoing sexual relationships between a 12- to 13-year-old and a late adolescent are advised to be excluded. A diagnosis is further specified by the sex of the children the person is attracted to, if the impulses or acts are limited to incest, and if the attraction is "exclusive" or "nonexclusive".The ICD-10 defines pedophilia as "a sexual preference for children, boys or girls or both, usually of prepubertal or early pubertal age". Like the DSM, this systems criteria require that the person be at least 16 years of age or older before being diagnosed as a pedophile. The person must also have a persistent or predominant sexual preference for prepubescent children at least five years younger than them. The ICD-11 defines pedophilic disorder as a "sustained, focused, and intense pattern of sexual arousal—as manifested by persistent sexual thoughts, fantasies, urges, or behaviours—involving pre-pubertal children." It also states that for a diagnosis of pedophilic disorder, "the individual must have acted on these thoughts, fantasies or urges or be markedly distressed by them. This diagnosis does not apply to sexual behaviours among pre- or post-pubertal children with peers who are close in age."Several terms have been used to distinguish "true pedophiles" from non-pedophilic and non-exclusive offenders, or to distinguish among types of offenders on a continuum according to strength and exclusivity of pedophilic interest, and motivation for the offense (see child sexual offender types). Exclusive pedophiles are sometimes referred to as true pedophiles. They are sexually attracted to prepubescent children, and only prepubescent children. Showing no erotic interest in adults, they can only become sexually aroused while fantasizing about or being in the presence of prepubescent children, or both. Non-exclusive offenders—or "non-exclusive pedophiles"—may at times be referred to as non-pedophilic offenders, but the two terms are not always synonymous. Non-exclusive offenders are sexually attracted to both children and adults, and can be sexually aroused by both, though a sexual preference for one over the other in this case may also exist. If the attraction is a sexual preference for prepubescent children, such offenders are considered pedophiles in the same vein as exclusive offenders.Neither the DSM nor the ICD-11 diagnostic criteria require actual sexual activity with a prepubescent youth. The diagnosis can therefore be made based on the presence of fantasies or sexual urges even if they have never been acted upon. On the other hand, a person who acts upon these urges yet experiences no distress about their fantasies or urges can also qualify for the diagnosis. Acting on sexual urges is not limited to overt sex acts for purposes of this diagnosis, and can sometimes include indecent exposure, voyeuristic or frotteuristic behaviors, or masturbating to child pornography. Often, these behaviors need to be considered in-context with an element of clinical judgment before a diagnosis is made. Likewise, when the patient is in late adolescence, the age difference is not specified in hard numbers and instead requires careful consideration of the situation.Ego-dystonic sexual orientation (66 .1 F 66 .1) includes people who acknowledge that they have a sexual preference for prepubertal children, but wish to change it due to the associated psychological or behavioral problems (or both). Debate regarding criteria There was discussion on the DSM-IV-TR being overinclusive and underinclusive. Its criterion A concerns sexual fantasies or sexual urges regarding prepubescent children, and its criterion B concerns acting on those urges or the urges causing marked distress or interpersonal difficulty. Several researchers discussed whether or not a "contented pedophile"—an individual who fantasizes about having sex with a child and masturbates to these fantasies, but does not commit child sexual abuse, and who does not feel subjectively distressed afterward—met the DSM-IV-TR criteria for pedophilia since this person did not meet criterion B. Criticism also concerned someone who met criterion B, but did not meet criterion A. A large-scale survey about usage of different classification systems showed that the DSM classification is only rarely used. As an explanation, it was suggested that the underinclusiveness, as well as a lack of validity, reliability and clarity might have led to the rejection of the DSM classification.Ray Blanchard, an American-Canadian sexologist known for his research studies on pedophilia, addressed (in his literature review for the DSM-5) the objections to the overinclusiveness and under underinclusiveness of the DSM-IV-TR, and proposed a general solution applicable to all paraphilias. This meant namely a distinction between paraphilia and paraphilic disorder. The latter term is proposed to identify the diagnosable mental disorder which meets Criterion A and B, whereas an individual who does not meet Criterion B can be ascertained but not diagnosed as having a paraphilia. Blanchard and a number of his colleagues also proposed that hebephilia become a diagnosable mental disorder under the DSM-5 to resolve the physical development overlap between pedophilia and hebephilia by combining the categories under pedophilic disorder, but with specifiers on which age range (or both) is the primary interest. The proposal for hebephilia was rejected by the American Psychiatric Association, but the distinction between paraphilia and paraphilic disorder was implemented.The American Psychiatric Association stated that "[i]n the case of pedophilic disorder, the notable detail is what wasnt revised in the new manual. Although proposals were discussed throughout the DSM-5 development process, diagnostic criteria ultimately remained the same as in DSM-IV TR" and that "[o]nly the disorder name will be changed from pedophilia to pedophilic disorder to maintain consistency with the chapters other listings." If hebephilia had been accepted as a DSM-5 diagnosable disorder, it would have been similar to the ICD-10 definition of pedophilia that already includes early pubescents, and would have raised the minimum age required for a person to be able to be diagnosed with pedophilia from 16 years to 18 years (with the individual needing to be at least 5 years older than the minor).ODonohue, however, suggests that the diagnostic criteria for pedophilia be simplified to the attraction to children alone if ascertained by self-report, laboratory findings, or past behavior. He states that any sexual attraction to children is pathological and that distress is irrelevant, noting "this sexual attraction has the potential to cause significant harm to others and is also not in the best interests of the individual." Also arguing for behavioral criteria in defining pedophilia, Howard E. Barbaree and Michael C. Seto disagreed with the American Psychiatric Associations approach in 1997 and instead recommended the use of actions as the sole criterion for the diagnosis of pedophilia, as a means of taxonomic simplification. Treatment General There is no evidence that pedophilia can be cured. Instead, most therapies focus on helping pedophiles refrain from acting on their desires. Some therapies do attempt to cure pedophilia, but there are no studies showing that they result in a long-term change in sexual preference. Michael Seto suggests that attempts to cure pedophilia in adulthood are unlikely to succeed because its development is influenced by prenatal factors. Pedophilia appears to be difficult to alter but pedophiles can be helped to control their behavior, and future research could develop a method of prevention.There are several common limitations to studies of treatment effectiveness. Most categorize their participants by behavior rather than erotic age preference, which makes it difficult to know the specific treatment outcome for pedophiles. Many do not select their treatment and control groups randomly. Offenders who refuse or quit treatment are at higher risk of offending, so excluding them from the treated group, while not excluding those who would have refused or quit from the control group, can bias the treated group in favor of those with lower recidivism. The effectiveness of treatment for non-offending pedophiles has not been studied. Cognitive behavioral therapy Cognitive behavioral therapy (CBT) aims to reduce attitudes, beliefs, and behaviors that may increase the likelihood of sexual offenses against children. Its content varies widely between therapists, but a typical program might involve training in self-control, social competence and empathy, and use cognitive restructuring to change views on sex with children. The most common form of this therapy is relapse prevention, where the patient is taught to identify and respond to potentially risky situations based on principles used for treating addictions.The evidence for cognitive behavioral therapy is mixed. A 2012 Cochrane Review of randomized trials found that CBT had no effect on risk of reoffending for contact sex offenders. Meta-analyses in 2002 and 2005, which included both randomized and non-randomized studies, concluded that CBT reduced recidivism. There is debate over whether non-randomized studies should be considered informative. More research is needed. Behavioral interventions Behavioral treatments target sexual arousal to children, using satiation and aversion techniques to suppress sexual arousal to children and covert sensitization (or masturbatory reconditioning) to increase sexual arousal to adults. Behavioral treatments appear to have an effect on sexual arousal patterns during phallometric testing, but it is not known whether the effect represents changes in sexual interests or changes in the ability to control genital arousal during testing, nor whether the effect persists in the long term. For sex offenders with mental disabilities, applied behavior analysis has been used. Sex drive reduction Pharmacological interventions are used to lower the sex drive in general, which can ease the management of pedophilic feelings, but does not change sexual preference. Antiandrogens work by interfering with the activity of testosterone. Cyproterone acetate (Androcur) and medroxyprogesterone acetate (Depo-Provera) are the most commonly used. The efficacy of antiandrogens has some support, but few high-quality studies exist. Cyproterone acetate has the strongest evidence for reducing sexual arousal, while findings on medroxyprogesterone acetate have been mixed.Gonadotropin-releasing hormone analogues such as leuprorelin (Lupron), which last longer and have fewer side-effects, are also used to reduce libido, as are selective serotonin reuptake inhibitors. The evidence for these alternatives is more limited and mostly based on open trials and case studies. All of these treatments, commonly referred to as "chemical castration", are often used in conjunction with cognitive behavioral therapy. According to the Association for the Treatment of Sexual Abusers, when treating child molesters, "anti-androgen treatment should be coupled with appropriate monitoring and counseling within a comprehensive treatment plan." These drugs may have side-effects, such as weight gain, breast development, liver damage and osteoporosis.Historically, surgical castration was used to lower sex drive by reducing testosterone. The emergence of pharmacological methods of adjusting testosterone has made it largely obsolete, because they are similarly effective and less invasive. It is still occasionally performed in Germany, the Czech Republic, Switzerland, and a few U.S. states. Non-randomized studies have reported that surgical castration reduces recidivism in contact sex offenders. The Association for the Treatment of Sexual Abusers opposes surgical castration and the Council of Europe works to bring the practice to an end in Eastern European countries where it is still applied through the courts. Epidemiology Pedophilia and child molestation The prevalence of pedophilia in the general population is not known, but is estimated to be lower than 5% among adult men. Less is known about the prevalence of pedophilia in women, but there are case reports of women with strong sexual fantasies and urges towards children. Male perpetrators account for the vast majority of sexual crimes committed against children. Among convicted offenders, 0.4% to 4% are female, and one literature review estimates that the ratio of male-to-female child molesters is 10 to 1. The true number of female child molesters may be underrepresented by available estimates, for reasons including a "societal tendency to dismiss the negative impact of sexual relationships between young boys and adult women, as well as womens greater access to very young children who cannot report their abuse", among other explanations.The term pedophile is commonly used by the public to describe all child sexual abuse offenders. This usage is considered problematic by researchers, because many child molesters do not have a strong sexual interest in prepubescent children, and are consequently not pedophiles. There are motives for child sexual abuse that are unrelated to pedophilia, such as stress, marital problems, the unavailability of an adult partner, general anti-social tendencies, high sex drive or alcohol use. As child sexual abuse is not automatically an indicator that its perpetrator is a pedophile, offenders can be separated into two types: pedophilic and non-pedophilic (or preferential and situational). Estimates for the rate of pedophilia in detected child molesters generally range between 25% and 50%. A 2006 study found that 35% of its sample of child molesters were pedophilic. Pedophilia appears to be less common in incest offenders, especially fathers and step-fathers. According to a U.S. study on 2429 adult male sex offenders who were categorized as "pedophiles", only 7% identified themselves as exclusive; indicating that many or most child sexual abusers may fall into the non-exclusive category.Some pedophiles do not molest children. Little is known about this population because most studies of pedophilia use criminal or clinical samples, which may not be representative of pedophiles in general. Researcher Michael Seto suggests that pedophiles who commit child sexual abuse do so because of other anti-social traits in addition to their sexual attraction. He states that pedophiles who are "reflective, sensitive to the feelings of others, averse to risk, abstain from alcohol or drug use, and endorse attitudes and beliefs supportive of norms and the laws" may be unlikely to abuse children. A 2015 study indicates that pedophiles who molested children are neurologically distinct from non-offending pedophiles. The pedophilic molesters had neurological deficits suggestive of disruptions in inhibitory regions of the brain, while non-offending pedophiles had no such deficits.According to Abel, Mittleman, and Becker (1985) and Ward et al. (1995), there are generally large distinctions between the characteristics of pedophilic and non-pedophilic molesters. They state that non-pedophilic offenders tend to offend at times of stress; have a later onset of offending; and have fewer, often familial, victims, while pedophilic offenders often start offending at an early age; often have a larger number of victims who are frequently extrafamilial; are more inwardly driven to offend; and have values or beliefs that strongly support an offense lifestyle. One study found that pedophilic molesters had a median of 1.3 victims for those with girl victims and 4.4 for those with boy victims. Child molesters, pedophilic or not, employ a variety of methods to gain sexual access to children. Some groom their victims into compliance with attention and gifts, while others use threats, alcohol or drugs, or physical force. History Pedophilia is believed to have occurred in humans throughout history, but was not formally named, defined or studied until the late 19th century. The term paedophilia erotica was coined in an 1886 article by the Viennese psychiatrist Richard von Krafft-Ebing but does not enter the authors Psychopathia Sexualis until the 10th German edition. A number of authors anticipated Krafft-Ebings diagnostic gesture. In Psychopathia Sexualis, the term appears in a section titled "Violation of Individuals Under the Age of Fourteen", which focuses on the forensic psychiatry aspect of child sexual offenders in general. Krafft-Ebing describes several typologies of offender, dividing them into psychopathological and non-psychopathological origins, and hypothesizes several apparent causal factors that may lead to the sexual abuse of children.Krafft-Ebing mentioned paedophilia erotica in a typology of "psycho-sexual perversion". He wrote that he had only encountered it four times in his career and gave brief descriptions of each case, listing three common traits: The individual is tainted [by heredity] (hereditär belastete) The subjects primary attraction is to children, rather than adults. The acts committed by the subject are typically not intercourse, but rather involve inappropriate touching or manipulating the child into performing an act on the subject.He mentions several cases of pedophilia among adult women (provided by another physician), and also considered the abuse of boys by homosexual men to be extremely rare. Further clarifying this point, he indicated that cases of adult men who have some medical or neurological disorder and abuse a male child are not true pedophilia and that, in his observation, victims of such men tended to be older and pubescent. He also lists pseudopaedophilia as a related condition wherein "individuals who have lost libido for the adult through masturbation and subsequently turn to children for the gratification of their sexual appetite" and claimed this is much more common.Austrian neurologist Sigmund Freud briefly wrote about the topic in his 1905 book Three Essays on the Theory of Sexuality in a section titled The Sexually immature and Animals as Sexual objects. He wrote that exclusive pedophilia was rare and only occasionally were prepubescent children exclusive objects. He wrote that they usually were the subject of desire when a weak person "makes use of such substitutes" or when an uncontrollable instinct which will not allow delay seeks immediate gratification and cannot find a more appropriate object.In 1908, Swiss neuroanatomist and psychiatrist Auguste Forel wrote of the phenomenon, proposing that it be referred to it as "Pederosis", the "Sexual Appetite for Children". Similar to Krafft-Ebings work, Forel made the distinction between incidental sexual abuse by persons with dementia and other organic brain conditions, and the truly preferential and sometimes exclusive sexual desire for children. However, he disagreed with Krafft-Ebing in that he felt the condition of the latter was largely ingrained and unchangeable.The term pedophilia became the generally accepted term for the condition and saw widespread adoption in the early 20th century, appearing in many popular medical dictionaries such as the 5th Edition of Stedmans in 1918. In 1952, it was included in the first edition of the Diagnostic and Statistical Manual of Mental Disorders. This edition and the subsequent DSM-II listed the disorder as one subtype of the classification "Sexual Deviation", but no diagnostic criteria were provided. The DSM-III, published in 1980, contained a full description of the disorder and provided a set of guidelines for diagnosis. The revision in 1987, the DSM-III-R, kept the description largely the same, but updated and expanded the diagnostic criteria. Law and forensic psychology Definitions Pedophilia is not a legal term, and having a sexual attraction to children is not illegal. In law enforcement circles, the term pedophile is sometimes used informally to refer to any person who commits one or more sexually-based crimes that relate to legally underage victims. These crimes may include child sexual abuse, statutory rape, offenses involving child pornography, child grooming, stalking, and indecent exposure. One unit of the United Kingdoms Child Abuse Investigation Command is known as the "Paedophile Unit" and specializes in online investigations and enforcement work. Some forensic science texts, such as Holmes (2008), use the term to refer to offenders who target child victims, even when such children are not the primary sexual interest of the offender. FBI agent Kenneth Lanning, however, makes a point of distinguishing between pedophiles and child molesters. Civil and legal commitment In the United States, following Kansas v. Hendricks, sex offenders who have certain mental disorders, including pedophilia, can be subject to indefinite civil commitment under various state laws (generically called SVP laws) and the federal Adam Walsh Child Protection and Safety Act of 2006. Similar legislation exists in Canada.In Kansas v. Hendricks, the US Supreme Court upheld as constitutional a Kansas law, the Sexually Violent Predator Act, under which Hendricks, a pedophile, was found to have a "mental abnormality" defined as a "congenital or acquired condition affecting the emotional or volitional capacity which predisposes the person to commit sexually violent offenses to the degree that such person is a menace to the health and safety of others", which allowed the State to confine Hendricks indefinitely irrespective of whether the State provided any treatment to him. In United States v. Comstock, this type of indefinite confinement was upheld for someone previously convicted on child pornography charges; this time a federal law was involved—the Adam Walsh Child Protection and Safety Act. The Walsh Act does not require a conviction on a sex offense charge, but only that the person be a federal prisoner, and one who "has engaged or attempted to engage in sexually violent conduct or child molestation and who is sexually dangerous to others", and who "would have serious difficulty in refraining from sexually violent conduct or child molestation if released".In the US, offenders with pedophilia are more likely to be recommended for civil commitment than non-pedophilic offenders. About half of committed offenders have a diagnosis of pedophilia. Psychiatrist Michael First writes that, since not all people with a paraphilia have difficulty controlling their behavior, the evaluating clinician must present additional evidence of volitional impairment instead of recommending commitment based on pedophilia alone. Society and culture General Pedophilia is one of the most stigmatized mental disorders. One study reported high levels of anger, fear and social rejection towards pedophiles who have not committed a crime. The authors suggested such attitudes could negatively impact child sexual abuse prevention by reducing pedophiles mental stability and discouraging them from seeking help. According to sociologists Melanie-Angela Neuilly and Kristen Zgoba, social concern over pedophilia intensified greatly in the 1990s, coinciding with several sensational sex crimes (but a general decline in child sexual abuse rates). They found that the word pedophile appeared only rarely in The New York Times and Le Monde before 1996, with zero mentions in 1991.Social attitudes towards child sexual abuse are extremely negative, with some surveys ranking it as morally worse than murder. Early research showed that there was a great deal of misunderstanding and unrealistic perceptions in the general public about child sexual abuse and pedophiles. However, a 2004 study concluded that the public was well-informed on some aspects of these subjects. Misuse of medical terminology The words pedophile and pedophilia are commonly used informally to describe an adults sexual interest in pubescent or post-pubescent persons under the age of consent. The terms hebephilia or ephebophilia may be more accurate in these cases.Another common usage of pedophilia is to refer to the act of sexual abuse itself, rather than the medical meaning, which is a preference for prepubescents on the part of the older individual (see above for an explanation of the distinction). There are also situations where the terms are misused to refer to relationships where the younger person is an adult of legal age, but is either considered too young in comparison to their older partner, or the older partner occupies a position of authority over them. Researchers state that the above uses of the term pedophilia are imprecise or suggest that they are best avoided. The Mayo Clinic states that pedophilia "is not a criminal or legal term". Pedophile advocacy groups From the late 1950s to early 1990s, several pedophile membership organizations advocated age of consent reform to lower or abolish age of consent laws, as well as for the acceptance of pedophilia as a sexual orientation rather than a psychological disorder, and for the legalization of child pornography. The efforts of pedophile advocacy groups did not gain mainstream acceptance, and today those few groups that have not dissolved have only minimal membership and have ceased their activities other than through a few websites. In contrast to these organizations, members of the support group Virtuous Pedophiles believe that child sexual abuse is wrong and seek to raise awareness that some pedophiles do not offend; this is generally not considered pedophile advocacy, as the Virtuous Pedophiles organization does not approve of the legalization of child pornography and does not support age of consent reform. Anti-pedophile activism Anti-pedophile activism encompasses opposition against pedophiles, against pedophile advocacy groups, and against other phenomena that are seen as related to pedophilia, such as child pornography and child sexual abuse. Much of the direct action classified as anti-pedophile involves demonstrations against sex offenders, against pedophiles advocating for the legalization of sexual activity between adults and children, and against Internet users who solicit sex from minors.High-profile media attention to pedophilia has led to incidents of moral panic, particularly following reports of pedophilia associated with Satanic ritual abuse and day care sex abuse. Instances of vigilantism have also been reported in response to public attention on convicted or suspected child sex offenders. In 2000, following a media campaign of "naming and shaming" suspected pedophiles in the UK, hundreds of residents took to the streets in protest against suspected pedophiles, eventually escalating to violent conduct requiring police intervention. See also Age disparity in sexual relationships Age of consent Child marriage Child sexuality Circles of Support and Accountability Gerontophilia List of paraphilias Pedobear Prevention Project Dunkelfeld Trafficking of children References Further reading Gladwell, Malcolm. "In Plain View." ("Jerry Sandusky and the Mind of a Pedophile") The New Yorker. September 24, 2012. Philby, Charlotte. "Female sexual abuse: The untold story of societys last taboo." The Independent. Saturday August 8, 2009. Bleyer, Jennifer. "How Can We Stop Pedophiles? Stop treating them like monsters." Slate. Monday September 24, 2012. Fong, Diana. Editor: Nancy Isenson. "If Im attracted to children, I must be a monster." Die Welt. May 29, 2013. External links Understanding MRI research on pedophilia Archived 2011-05-26 at the Wayback Machine Indictment from Operation Delego (PDF) (Archive) Virtuous Pedophiles, online support for non-offending pedophiles working to remain offence-free. HelpWantedPrevention.org, an online self-help course from Johns Hopkins University for managing attraction to children

Hey Aarogya, explain a scenario commonly referred as Schizoaffective disorder

Schizoaffective disorder

Schizoaffective disorder (SZA, SZD or SAD) is a mental disorder characterized by abnormal thought processes and an unstable mood. This diagnosis is made when the person has symptoms of both schizophrenia (usually psychosis) and a mood disorder: either bipolar disorder or depression. The main criterion for a diagnosis of schizoaffective disorder is the presence of psychotic symptoms for at least two weeks without any mood symptoms present. Schizoaffective disorder can often be misdiagnosed when the correct diagnosis may be psychotic depression, bipolar I disorder, schizophreniform disorder, or schizophrenia. It is imperative for providers to accurately diagnose patients, as treatment and prognosis differ greatly for most of these diagnoses.There are three forms of schizoaffective disorder: bipolar (or manic) type (marked by symptoms of schizophrenia and mania), depressive type (marked by symptoms of schizophrenia and depression), and mixed type (marked by symptoms of schizophrenia, depression, and mania). Common symptoms of the disorder include hallucinations, delusions, and disorganized speech and thinking. Auditory hallucinations, or "hearing voices", are most common. The onset of symptoms usually begins in adolescence or young adulthood. On a ranking scale of symptom progression of mental health issues relating to the schizophrenic spectrum, schizoaffective disorder falls between mood disorders and schizophrenia in regards to severity, with other disorders included on the ranking as well depending on symptoms. Schizoaffective disorder and other disorders on the schizophrenic spectrum are evaluated as a psychotic disorder in the DSM-V, so the line between psychotic or not psychotic begins at a mood disorder, as being considered not psychotic, and schizoaffective disorder along with other disorders of the schizophrenia spectrum, as being considered psychotic.Genetics (researched in the field of genomics); problems with neural circuits; chronic early, and chronic or short-term current environmental stress appear to be important causal factors. No single isolated organic cause has been found, but extensive evidence exists for abnormalities in the metabolism of tetrahydrobiopterin (BH4), dopamine, and glutamic acid in people with schizophrenia, psychotic mood disorders, and schizoaffective disorder. People with schizoaffective disorder are likely to have co-occurring conditions, including anxiety disorders and substance use disorders. While a diagnosis of schizoaffective disorder is rare in the general population, it is considered a common diagnosis among psychiatric disorders. Though schizoaffective disorder and schizophrenia are often thought of as mood disorders, DSM-V criteria classifies them as psychotic disorders. Diagnosis of schizoaffective disorder is based on DSM-V criteria as well as the presence of various symptoms such as mania, depression, and schizophrenia. The mainstay of current treatment is antipsychotic medication combined with mood stabilizer medication or antidepressant medication, or both. There is growing concern by some researchers that antidepressants may increase psychosis, mania, and long-term mood episode cycling in the disorder. When there is risk to self or others, usually early in treatment, hospitalization may be necessary. Psychiatric rehabilitation, psychotherapy, and vocational rehabilitation are very important for recovery of higher psychosocial function. As a group, people with schizoaffective disorder that were diagnosed using DSM-IV and ICD-10 criteria (which have since been updated) have a better outcome, but have variable individual psychosocial functional outcomes compared to people with mood disorders, from worse to the same. Outcomes for people with DSM-5 diagnosed schizoaffective disorder depend on data from prospective cohort studies, which have not been completed yet. The DSM-5 diagnosis was updated because DSM-IV criteria resulted in overuse of the diagnosis; that is, DSM-IV criteria led to many patients being misdiagnosed with the disorder. DSM-IV prevalence estimates were less than one percent of the population, in the range of 0.5–0.8 percent; newer DSM-5 prevalence estimates are not yet available. Signs and symptoms Schizoaffective disorder is defined by mood disorder-free psychosis in the context of a long-term psychotic and mood disorder. Psychosis must meet criterion A for schizophrenia which may include delusions, hallucinations, disorganized thinking and speech or behavior and negative symptoms. Both delusions and hallucinations are classic symptoms of psychosis. Delusions are false beliefs which are strongly held despite evidence to the contrary. Beliefs should not be considered delusional if they are in keeping with cultural beliefs. Delusional beliefs may or may not reflect mood symptoms (for example, someone experiencing depression may or may not experience delusions of guilt). Hallucinations are disturbances in perception involving any of the five senses, although auditory hallucinations (or "hearing voices") are the most common. Negative symptoms include alogia (lack of speech), blunted affect (reduced intensity of outward emotional expression), avolition (lack of motivation), and anhedonia (inability to experience pleasure). Negative symptoms can be more lasting and more debilitating than positive symptoms of psychosis. Mood symptoms are of mania, hypomania, mixed episode, or depression, and tend to be episodic rather than continuous. A mixed episode represents a combination of symptoms of mania and depression at the same time. Symptoms of mania include elevated or irritable mood, grandiosity (inflated self-esteem), agitation, risk-taking behavior, decreased need for sleep, poor concentration, rapid speech, and racing thoughts. Symptoms of depression include low mood, apathy, changes in appetite or weight, disturbances in sleep, changes in motor activity, fatigue, guilt or feelings of worthlessness, and suicidal thinking. DSM-5 states that if a patient only experiences psychotic symptoms during a mood episode, their diagnosis is Mood Disorder with Psychotic Features and not Schizophrenia or Schizoaffective Disorder. If the patient experiences psychotic symptoms without mood symptoms for longer than a two-week period, their diagnosis is either Schizophrenia or Schizoaffective Disorder. If mood disorder episodes are present for the majority and residual course of the illness and up until the diagnosis, the patient can be diagnosed with Schizoaffective Disorder. Causes A combination of genetic and environmental factors are believed to play a role in the development of schizoaffective disorder. Genetic studies do not support the view that schizophrenia, psychotic mood disorders and schizoaffective disorder are distinct etiological entities, but rather the evidence suggests the existence of common inherited vulnerability that increases the risks for all these syndromes. Some susceptibility pathways may be specific for schizophrenia, others for bipolar disorder, and yet other mechanisms and genes may confer risk for mixed schizophrenic and affective [or mood disorder] psychoses, but there is no support from genetics for the view that these are distinct disorders with distinct etiologies and pathogenesis. Laboratory studies of putative endophenotypes, brain imaging studies, and post mortem studies shed little additional light on the validity of the schizoaffective disorder diagnosis, as most studies combine subjects with different chronic psychoses in comparison to healthy subjects. Viewed broadly then, biological and environmental factors interact with a persons genes in ways which may increase or decrease the risk for developing schizoaffective disorder; exactly how this happens (the biological mechanism) is not yet known. Schizophrenia spectrum disorders, of which schizoaffective disorder is a part, have been increasingly linked to advanced paternal age at the time of conception, a known cause of genetic mutations. The physiology of people diagnosed with schizoaffective disorder appears to be similar, but not identical, to that of those diagnosed with schizophrenia and bipolar disorder; however, human neurophysiological function in normal brain and mental disorder syndromes is not fully understood.While there are various medications and treatment options for those with schizoaffective disorder, this disorder can affect a person for their entire lifespan. In some cases, this disorder can affect a persons ability to have a fulfilling social life and they may also have trouble forming bonds or relationships with others. Schizoaffective disorder is also more likely to occur in women and begins at a young age. Substance use disorder A clear causal connection between substance use and psychotic spectrum disorders, including schizoaffective disorder, has been difficult to prove. In the specific case of cannabis (marijuana), however, evidence supports a link between earlier onset of psychotic illness and cannabis use. The more often cannabis is used, particularly in early adolescence, the more likely a person is to develop a psychotic illness, with frequent use being correlated with double the risk of psychosis and schizoaffective disorder. A 2009 Yale review stated that in individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. While cannabis use is accepted as a contributory cause of schizoaffective disorder by many, it remains controversial, since not all young people who use cannabis later develop psychosis, but those who do use cannabis have an increased odds ratio of about 3. Certain drugs can imitate symptoms of schizophrenia (which is known to have similar symptoms to schizoaffective disorder). This is important to note when including that substance-induced psychosis should be ruled out when diagnosing patients so that patients are not misdiagnosed. Mechanisms Though the pathophysiology of schizoaffective disorder remains unclear, studies suggest that dopamine, norepinephrine, and serotonin may be factors in the development of the disorder.White matter and Grey Matter reductions in the right lentiform nucleus, left superior temporal gyrus, and right precuneus, and other areas in the brain are also characteristic of schizoaffective disorder. Deformities in white matter have also been found to worsen with time in individuals with schizoaffective disorder. Due to its role in emotional regulation, researchers believe that the hippocampus is also involved in the progression of schizoaffective disorder. Specifically, psychotic disorders (such as schizoaffective disorder) have been associated with lower hippocampal volumes. Moreover, deformities in the medial and thalamic regions of the brain have been implicated as contributing factors to the disorder as well. Diagnosis Psychosis as a symptom of a psychiatric disorder is first and foremost a diagnosis of exclusion. So a new-onset episode of psychosis cannot be considered to be a symptom of a psychiatric disorder until other relevant and known medical causes of psychosis are excluded, or ruled out. Many clinicians improperly perform, or entirely miss this step, introducing avoidable diagnostic error and misdiagnosis.An initial assessment includes a comprehensive history and physical examination. Although no biological laboratory tests exist which confirm schizoaffective disorder, biological tests should be performed to exclude psychosis associated with or caused by substance use, medications, toxins or poisons, surgical complications, or other medical illnesses. Since non-medical mental health practitioners are not trained to exclude medical causes of psychosis, people experiencing psychosis should be referred to an emergency department or hospital. Delirium should be ruled out, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, indicating other underlying factors which includes medical illnesses. Excluding medical illnesses associated with psychosis is performed by using blood tests to measure: Thyroid-stimulating hormone to exclude hypo- or hyperthyroidism, Basic electrolytes and serum calcium to rule out a metabolic disturbance, Full blood count including ESR to rule out a systemic infection or chronic disease, and Serology to exclude syphilis or HIV infection.Other investigations which may be performed include: EEG to exclude epilepsy, and an MRI or CT scan of the head to exclude brain lesions.Blood tests are not usually repeated for relapse in people with an established diagnosis of schizoaffective disorder, unless there is a specific medical indication. These may include serum BSL if olanzapine has previously been prescribed, thyroid function if lithium has previously been taken to rule out hypothyroidism, liver function tests if chlorpromazine has been prescribed, CPK levels to exclude neuroleptic malignant syndrome, and a urinalysis and serum toxicology screening if substance use is suspected. Assessment and treatment may be done on an outpatient basis; admission to an inpatient facility is considered if there is a risk to self or others. Because psychosis may be precipitated or exacerbated by common classes of psychiatric medications, such as antidepressants, ADHD stimulant medications, and sleep medications, prescribed medication-induced psychosis should be ruled out, particularly for first-episode psychosis. This is an essential step to reduce diagnostic error and to evaluate potential medication sources of further patient harm. Regarding prescribed medication sources of patient harm, Yale School of Medicine Professor of Psychiatry Malcolm B. Bowers, Jr, MD wrote: Illicit drugs arent the only ones that precipitate psychosis or mania—prescribed drugs can too, and in particular, some psychiatric drugs. We investigated this and found that about 1 in 12 psychotic or manic patients in an inpatient psychiatric facility are there due to antidepressant-induced psychosis or mania. Thats unfortunate for the field [of psychiatry] and disastrous for some of our patients. It is important to be understood here. I want to call attention to the fact that some persons with a family history of even the subtler forms of bipolar disorder or psychosis are more vulnerable than others to the mania- or psychosis-inducing potential of antidepressants, stimulants and sleeping medications. While Im not making a blanket statement against these medications, I am urging caution in their use. I believe [clinicians] should ask patients and their families whether there is a family history of bipolar disorder or psychosis before prescribing these medications. Most patients and their families dont know the answer when they are first asked, so time should be allowed for the patient to ask family or relatives, between the session when asked by [the clinician] and a follow-up session. This may increase the wait for a medication slightly, but because some patients are vulnerable, this is a necessary step for [the clinician] to take. I believe that psychiatry as a field has not emphasized this point sufficiently. As a result, some patients have been harmed by the very treatments that were supposed to help them; or to the disgrace of psychiatry, harmed and then misdiagnosed. Substance-induced psychosis should also be ruled out. Both substance- and medication-induced psychosis can be excluded to a high level of certainty while the person is psychotic, typically in an emergency department, using both a Broad spectrum urine toxicology screening, and a Full serum toxicology screening (of the blood).Some dietary supplements may also induce psychosis or mania, but cannot be ruled out with laboratory tests. So a psychotic persons family, partner, or friends should be asked whether he or she is currently taking any dietary supplements.Common mistakes made when diagnosing psychotic patients include: Not properly excluding delirium, Missing a toxic psychosis by not screening for substances and medications, Not appreciating medical abnormalities (e.g., vital signs), Not obtaining a medical history and family history, Indiscriminate screening without an organizing framework, Not asking family or others about dietary supplements, Premature diagnostic closure, and Not revisiting or questioning the initial diagnostic impression of primary psychiatric disorder.Schizoaffective disorder can only be diagnosed among those who have undergone a clinical evaluation with a psychiatrist. The criterion includes mental and physical symptoms such as, hallucinations or delusions, and depressive episodes. There are also links to bad hygiene and a troubled social life for those with schizoaffective disorder. Research has failed to conclusively demonstrate a positive relationship between schizoaffective disorder and substance abuse. There are several theorized causations for the onset of Schizoaffective disorder, including, genetics, general brain function, like chemistry, and structure, and stress.Only after these relevant and known causes of psychosis have been ruled out can a psychiatric differential diagnosis be made. A mental health clinician will incorporate family history, observation of a psychotic persons behavior while the person is experiencing active symptoms, to begin a psychiatric differential diagnosis. Diagnosis also includes self-reported experiences, as well as behavioral abnormalities reported by family members, friends, or significant others. Mistakes in this stage include: Not screening for dissociative disorders. Dissociative identity disorder and psychotic symptoms in schizoaffective disorder have considerable overlap, yet a different overall treatment approach. DSM-5 criteria The most widely used criteria for diagnosing schizoaffective disorder are from the American Psychiatric Associations Diagnostic and Statistical Manual of Mental Disorders-5.The DSM-IV schizoaffective disorder definition was plagued by problems of being inconsistently (or unreliably) used on patients; when the diagnosis is made, it does not stay with most patients over time, and it has questionable diagnostic validity (that is, it does not describe a distinct disorder, nor predict any particular outcome). These problems have been slightly reduced (or "modestly improved") in the DSM-5 according to Carpenter.When psychotic symptoms are confined to an episode of mania or depression (with or without mixed features), the diagnosis is that of a “psychotic” mood disorder, namely either psychotic bipolar disorder or psychotic major depression. Only when psychotic states persist in a sustained fashion for two weeks or longer without concurrent affective symptoms is the diagnosis schizoaffective disorder, schizophreniform disorder or schizophrenia.The second cardinal guideline in the DSM-5 diagnosis of schizoaffective disorder is one of timeframe. DSM-5 requires two episodes of psychosis (whereas DSM-IV needed only one) to qualify for the schizoaffective disorder diagnosis. As such, it is no longer an "episode diagnosis." The new schizoaffective framework looks at the time from "the [first episode of] psychosis up to the current episode [of psychosis], rather than only defining a single episode with [co-occurring] psychotic and mood syndromes." Specifically, one of the episodes of psychosis must last a minimum of two weeks without mood disorder symptoms, but the person may be mildly to moderately depressed while psychotic. The other period of psychosis "requires the overlap of mood [disorder] symptoms with psychotic symptoms to be conspicuous" and last for a greater portion of the disorder.These two changes are intended by the DSM-5 workgroup to accomplish two goals: Increase the diagnosis consistency (or reliability) when it is used; Significantly decrease the overall use of the schizoaffective disorder diagnosis.If the schizoaffective diagnosis is used less often, other diagnoses (like psychotic mood disorders and schizophrenia) are likely to be used more often; but this is hypothetical until real-world data arrive. Validity problems with the diagnosis remain and await further work in the fields of psychiatric genetics, neuroimaging, and cognitive science that includes the overlapping fields of cognitive, affective, and social neuroscience, which may change the way schizoaffective disorder is conceptualized and defined in future versions of the DSM and ICD. Comorbidities Schizoaffective disorder shares a high level of comorbidity with other psychiatric disorders, specifically anxiety disorders, depression, and bipolar disorder. Individuals with schizoaffective disorder are also often diagnosed with substance abuse disorder, usually relating to tobacco, marijuana, or alcohol. Health care providers indicate the importance of assessing for co-occurring substance use disorders, as multiple diagnoses not only potentially increase negative symptomology, but may also adversely affect the treatment of schizoaffective disorder. Types One of three types of schizoaffective disorder may be noted in a diagnosis based on the mood component of the disorder: Bipolar type, when the disturbance includes manic episodes, hypomania, or mixed episodes—major depressive episodes also typically occur; Depressive type, when the disturbance includes major depressive episodes exclusively—that is, without manic, hypomanic, or mixed episodes. Mixed type, when the disturbance includes both manic and depressive symptoms, but psychotic symptoms exist separately from bipolar disorder. Problems with DSM-IV schizoaffective disorder The American Psychiatric Associations DSM-IV criteria for schizoaffective disorder persisted for 19 years (1994–2013). Clinicians adequately trained in diagnosis used the schizoaffective diagnosis too often, largely because the criteria were poorly defined, ambiguous, and hard to use (or poorly operationalized). Poorly trained clinicians used the diagnosis without making necessary exclusions of common causes of psychosis, including some prescribed psychiatric medications. Specialty books written by experts on schizoaffective disorder have existed for over eight years before DSM-5 describing the overuse of the diagnosis.Carpenter and the DSM-5 schizoaffective disorders workgroup analyzed data made available to them in 2009, and reported in May 2013 that: a recent review of psychotic disorders from large private insurance and Medicare databases in the U.S. found that the diagnosis of DSM-IV schizoaffective disorder was used for about a third of cases with non-affective psychotic disorders. Hence, this unreliable and poorly defined diagnosis is clearly overused. As stated above, the DSM-IV schizoaffective disorder diagnosis is very inconsistently used or unreliable. A diagnosis is unreliable when several different mental health professionals observing the same individual make different diagnoses excessively. Even when a structured DSM-IV diagnostic interview and best estimate procedures were made by experts in the field that included information from family informants and prior clinical records, reliability was still poor for the DSM-IV schizoaffective diagnosis.The DSM-IV schizoaffective diagnosis is not stable over time either. An initial diagnosis of schizoaffective disorder during time spent at a psychiatric inpatient facility was stable at 6-month and 24-month follow ups for only 36% of patients. By comparison, diagnostic stability was 92% for schizophrenia, 83% for bipolar disorder and 74% for major depression. Most patients diagnosed with DSM-IV schizoaffective disorder are later diagnosed with a different disorder, and that disorder is more stable over time than the DSM-IV schizoaffective disorder diagnosis.In April 2009, Carpenter and the DSM-5 schizoaffective disorder workgroup reported that they were "developing new criteria for schizoaffective disorder to improve reliability and face validity," and were "determining whether the dimensional assessment of mood [would] justify a recommendation to drop schizoaffective disorder as a diagnostic category." Speaking to an audience at the May 2009 annual conference of the American Psychiatric Association, Carpenter said: We had hoped to get rid of schizoaffective [disorder] as a diagnostic category [in the DSM-5] because we dont think its [a] valid [scientific entity] and we dont think its reliable. On the other hand, we think its absolutely indispensable to clinical practice. A major reason why DSM-IV schizoaffective disorder was indispensable to clinical practice is because it offered clinicians a diagnosis for patients with psychosis in the context of mood disorder whose clinical picture, at the time diagnosed, appeared different from DSM-IV "schizophrenia" or "mood disorder with psychotic features". But DSM-IV schizoaffective disorder carries an unnecessarily worse prognosis than a "mood disorder with psychotic features" diagnosis, because long-term data revealed that a significant proportion of DSM-IV schizoaffective disorder patients had 15-year outcomes indistinguishable from patients with mood disorders with or without psychotic features, even though the clinical picture at the time of first diagnosis looked different from both schizophrenia and mood disorders.These problems with the DSM-IV schizoaffective disorder definition result in most people the diagnosis is used on being misdiagnosed; furthermore, outcome studies done 10 years after the diagnosis was released showed that the group of patients defined by the DSM-IV and ICD-10 schizoaffective diagnosis had significantly better outcomes than predicted, so the diagnosis carries a misleading and unnecessarily poor prognosis. The DSM-IV criteria for schizoaffective disorder will continue to be used on U.S. board examinations in psychiatry through the end of 2014; established practitioners may continue to use the problematic DSM-IV definition much further into the future also. DSM-5 research directions The new schizoaffective disorder criteria continue to have questionable diagnostic validity. Questionable diagnostic validity does not doubt that people with symptoms of psychosis and mood disorder need treatment—psychosis and mood disorder must be treated. Instead, questionable diagnostic validity means there are unresolved problems with the way the DSM-5 categorizes and defines schizoaffective disorder. A core concept in modern psychiatry since DSM-III was released in 1980, is the categorical separation of mood disorders from schizophrenia, known as the Kraepelinian dichotomy. Emil Kraepelin introduced the idea that schizophrenia was separate from mood disorders after observing patients with symptoms of psychosis and mood disorder, over a century ago, in 1898. This was a time before genetics were known and before any treatments existed for mental illness. The Kraepelinian dichotomy was not used for DSM-I and DSM-II because both manuals were influenced by the dominant psychodynamic psychiatry of the time, but the designers of DSM-III wanted to use more scientific and biological definitions. Consequently, they looked to psychiatrys history and decided to use the Kraepelinian dichotomy as a foundation for the classification system. The Kraepelinian dichotomy continues to be used in DSM-5 despite having been challenged by data from modern psychiatric genetics for over eight years, and there is now evidence of a significant overlap in the genetics of schizophrenia and bipolar disorder. According to this genetic evidence, the Kraepelinian categorical separation of mood disorders from schizophrenia at the foundation of the current classification and diagnostic system is a mistaken false dichotomy.The dichotomy at the foundation of the current system forms the basis for a convoluted schizoaffective disorder definition in DSM-IV that resulted in excessive misdiagnosis. Real life schizoaffective disorder patients have significant and enduring symptoms that bridge what are incorrectly assumed to be categorically separate disorders, schizophrenia and bipolar disorder. People with psychotic depression, bipolar disorder with a history of psychosis, and schizophrenia with mood symptoms also have symptoms that bridge psychosis and mood disorders. The categorical diagnostic manuals do not reflect reality in their separation of psychosis (via the schizophrenia diagnosis) from mood disorder, nor do they currently emphasize the actual overlap found in real-life patients. Thus, they are likely to continue to introduce either-or conceptual and diagnostic error, by way of confirmation bias into clinicians mindsets, hindering accurate assessment and treatment.The new definition continues the lack of parsimony of the old definition. Simpler, clearer, and more usable definitions of the diagnosis were supported by certain members of the DSM-5 workgroup (see next paragraph); these were debated but deemed premature, because more "research [is] needed to establish a new classification system of equal or greater validity" to the existing system. Because of DSM-5s continuing problematic categorical foundation, schizoaffective disorders conceptual and diagnostic validity remains doubtful. After enough research is completed and data exists, future diagnostic advances will need to either eliminate and replace, or soften and bridge, the hard categorical separation of mood disorders from schizophrenia; most likely using a spectrum or dimensional approach to diagnosis.More parsimonious definitions than the current one were considered by Carpenter and the DSM-5 workgroup: One option for the DSM-5 would have been to remove the schizoaffective disorder category and to add affective [or mood] symptoms [that is, mania, hypomania, mixed episode, or depression] as a dimension to schizophrenia and schizophreniform disorder or to define a single category for the co-occurrence of psychosis and mood symptoms. This option was extensively debated but ultimately deemed to be premature in the absence of sufficient clinical and theoretical validating data justifying such a … reconceptualization. Additionally, there appeared to be no practical way to introduce affect [or mood] dimensions covering the entire course of illness, that would capture the current concept of periods of psychosis related and unrelated to mood episodes. [N]o valid biomarkers or laboratory measures have emerged to distinguish between affective psychosis [or psychotic mood disorders] and schizophrenia. To the contrary, the idea of a dichotomy between these types of conditions has proven naïve. [T]he admixture of "schizophrenic" and affective [or mood] symptoms is a feature of many, or even most, cases with severe mental illness. Most presenting symptoms of psychosis have little validity in determining diagnosis, prognosis, or treatment response in psychosis. [U]ltimately a more … dimensional approach [to assessment and treatment] will be required. The field of psychiatry has begun to question its assumptions and analyze its data in order to merge closer with evidence-based medicine. The removal of the "episode diagnosis", and the addition of two episodes of psychosis, as qualifications for the DSM-5 schizoaffective diagnosis, may improve the diagnosis consistency over DSM-IV for research purposes, where diagnostic criteria are by necessity followed exactingly. But the new definition remains long, unwieldy, and perhaps still not very useful for community clinicians—with two psychoses, one for two weeks minimum and without mood disorder (but the person can be mildly or moderately depressed) and the other with significant mood disorder and psychosis lasting for most of the time, and with lasting mood symptoms for most of the residual portion of the illness. Community clinicians used the previous definition "for about a third of cases with non-affective psychotic disorders." Non-affective psychotic disorders are, by definition, not schizoaffective disorder. For clinicians to make such sizeable errors of misdiagnosis may imply systemic problems with the schizoaffective disorder diagnosis itself. Already, at least one expert believes the new schizoaffective definition has not gone far enough to solve the previous definitions problems.From a scientific standpoint, modern clinical psychiatry is still a very young, underdeveloped medical specialty because its target organ, the human brain, is not yet well understood. The human brains neural circuits, for example, are just beginning to be mapped by modern neuroscience in the Human Connectome Project and CLARITY. Clinical psychiatry, furthermore, has begun to understand and acknowledge its current limitations—but further steps by the field are required to significantly reduce misdiagnosis and patient harm; this is crucial both for responsible patient care and to retain public trust. Looking forward, a paradigm shift is needed in psychiatric research to address unanswered questions about schizoaffective disorder. The dimensional Research Domain Criteria project currently being developed by the U.S. National Institutes of Mental Health, may be the specific problem solving framework psychiatry needs to develop a more scientifically mature understanding of schizoaffective disorder as well as all other mental disorders. Treatment The primary treatment of schizoaffective disorder is medication, with improved outcomes using combined long-term psychological and social supports. Hospitalization may occur for severe episodes either voluntarily or (if mental health legislation allows it) involuntarily. Long-term hospitalization is uncommon since deinstitutionalization started in the 1950s, although it still occurs. Community support services including drop-in centers, visits by members of a community mental health team, supported employment and support groups are common. Evidence indicates that regular exercise has a positive effect on the physical and mental health of those with schizoaffective disorder.Because of the heterogeneous symptomology associated with schizoaffective disorder, it is common for patients to be misdiagnosed. Many people are either diagnosed with depression, schizophrenia, or bipolar disorder instead of schizoaffective disorder. Because of the broad range of symptoms of Schizoaffective disorder, patients are often misdiagnosed in a clinical setting. In fact, almost 39% of people are misdiagnosed when it comes to psychiatric disorders.While various medications and treatment options exist for those diagnosed with schizoaffective disorder, symptoms may continue to impact a person for their entire lifespan.Schizoaffective disorder can affect a persons ability to experience a fulfilling social life and they may also exhibit difficulty forming bonds or relationships with others. Schizoaffective disorder is more likely to occur in women and symptoms begin manifesting at a young age. Therapy Psychosocial treatments have been found to improve outcomes related to schizoaffective disorder. Supportive psychotherapy and cognitive behavioral therapy are both helpful. Intensive case management (ICM) has been shown to reduce hospitalizations, improve adherence to treatment, and improve social functioning. With ICM, clients are assigned a case manager responsible for coordination of care and assisting clients to access supports to address needs in multiple areas related to well-being, including housing. Psychiatric/psychosocial rehabilitation is often a component of schizoaffective disorder treatment. This rehabilitation method focuses on solving community integration problems such as obtaining and keeping housing and increasing involvement in positive social groups. It also focuses on improving and increasing activities of daily living; increasing daily healthy habits and decreasing unhealthy behaviors, thereby significantly improving quality of life. Psychiatric rehabilitation may also focus on vocational rehabilitation. Evidence suggests that cognition-based approaches may be able to improve work and social functioning.Psychiatric rehabilitation consists of eight main areas: Psychiatric (symptom reduction and management) Health and Medical (maintaining consistency of care) Housing (safe environments) Basic living skills (hygiene, meals [including increasing healthy food intake and reducing processed food intake], safety, planning and chores) Social (relationships, family boundaries, communication and integration of client into the community) Education and vocation (coping skills, motivation and suitable goals chosen by client) Finance (personal budget) Community and legal (resources) Medication Antipsychotic medication is usually required both for acute treatment and the prevention of relapse. There is no single antipsychotic of choice in treating schizoaffective disorder, but atypical antipsychotics may be considered due to their mood-stabilizing abilities. To date, paliperidone (Invega) is the only antipsychotic with FDA approval for the treatment of schizoaffective disorder. Other antipsychotics may be prescribed to further alleviate psychotic symptoms.Though not approved for treatment use by the FDA, research suggests that Clozapine may also be effective in treating schizoaffective disorder, particularly in those resistant to initial medication. Clozapine is an atypical antipsychotic that is recognized as being particularly effective when other antipsychotic agents have failed. When combined with cognitive therapy, Clozapine has been found to decrease positive and negative symptoms of psychosis at a higher rate in schizoaffective individuals. Clozapine has also been associated with a decreased risk of suicide in patients with schizoaffective disorder and a history of suicidality. Despite this, clozapine treatment may be ineffective for some patients, particularly in those that are already drug-resistant.The management of the bipolar type of schizoaffective disorder is similar to the treatment of bipolar disorder, with the goal of preventing mood episodes and cycling. Lithium or anticonvulsant mood stabilizers such as valproic acid, carbamazepine, and lamotrigine are prescribed in combination with an antipsychotic.Antidepressants have also been used to treat schizoaffective disorder. Though they may be useful in treating the depressive subtype of the disorder, research suggests that antidepressants are far less effective in treatment than antipsychotics and mood stabilizers.Some research has supported the efficacy of anxiolytics in treating schizoaffective disorder, though general findings on their effectiveness in treating schizoaffective disorder remain inconclusive. Due to the severe negative outcomes associated with many anti-anxiety drugs, many researchers have cautioned against their long term use in treatment. Electroconvulsive therapy Electroconvulsive therapy (ECT) may be considered for patients with schizoaffective disorder experiencing severe depression or severe psychotic symptoms that have not responded to treatment with antipsychotics. Epidemiology Compared to depression, schizophrenia, and bipolar disorder, schizoaffective disorder is less commonly diagnosed. Schizoaffective disorder is estimated to occur in 0.3 to 0.8 percent of people at some point in their life. 30% of cases occur between the ages of 25 and 35. It is more common in women than men; however, this is because of the high concentration of women in the depressive subcategory, whereas the bipolar subtype has a roughly even gender distribution. Children are less likely to be diagnosed with this disorder, as the onset presents itself in adolescence or young adulthood. History The term schizoaffective psychosis was introduced by the American psychiatrist Jacob Kasanin in 1933 to describe an episodic psychotic illness with predominant affective symptoms, that was thought at the time to be a good-prognosis schizophrenia. Kasanins concept of the illness was influenced by the psychoanalytic teachings of Adolf Meyer and Kasanin postulated that schizoaffective psychosis was caused by "emotional conflicts" of a "mainly sexual nature" and that psychoanalysis "would help prevent the recurrence of such attacks." He based his description on a case study of nine individuals. Other psychiatrists, before and after Kasanin, have made scientific observations of schizoaffective disorder based on assumptions of a biological and genetic cause of the illness. In 1863, German psychiatrist Karl Kahlbaum (1828–1899) described schizoaffective disorders as a separate group in his vesania typica circularis. Kahlbaum distinguished between cross-sectional and longitudinal observations. In 1920, psychiatrist Emil Kraepelin (1856–1926) observed a "great number" of cases that had characteristics of both groups of psychoses that he originally posited were two distinct and separate illnesses, dementia praecox (now called schizophrenia) and manic depressive insanity (now called bipolar disorders and recurrent depression).Kraepelin acknowledged that "there are many overlaps in this area," that is, the area between schizophrenia and mood disorders. In 1959, psychiatrist Kurt Schneider (1887–1967) began to further refine conceptualizations of the different forms that schizoaffective disorders can take since he observed "concurrent and sequential types". (The concurrent type of illness he referred to is a longitudinal course of illness with episodes of mood disorder and psychosis occurring predominantly at the same time [now called psychotic mood disorders or affective psychosis]; while his sequential type refers to a longitudinal course predominantly marked by alternating mood and psychotic episodes.) Schneider described schizoaffective disorders as "cases in-between" the traditional Kraepelinian dichotomy of schizophrenia and mood disorders.The historical clinical observation that schizoaffective disorder is an overlap of schizophrenia and mood disorders is explained by genes for both illnesses being present in individuals with schizoaffective disorder; specifically, recent research shows that schizophrenia and mood disorders share common genes and polygenic variations. Schizoaffective disorder was included as a subtype of schizophrenia in DSM-I and DSM-II, though research showed a schizophrenic cluster of symptoms in individuals with a family history of mood disorders whose illness course, other symptoms and treatment outcome were otherwise more akin to bipolar disorder than to schizophrenia. DSM-III placed schizoaffective disorder in "Psychotic Disorders Not Otherwise Specified" before being formally recognized in DSM-III-R. DSM-III-R included its own diagnostic criteria as well as the subtypes, bipolar and depressive. In DSM-IV, published in 1994, schizoaffective disorders belonged to the category "Other Psychotic Disorders" and included almost the same criteria and the same subtypes of illness as DSM-III-R, with the addition of mixed bipolar symptomatology.DSM-IV and DSM-IV-TR (published in 2000) criteria for schizoaffective disorder were poorly defined and poorly operationalized. These ambiguous and unreliable criteria lasted 19 years and led clinicians to significantly overuse the schizoaffective disorder diagnosis. Patients commonly diagnosed with DSM-IV schizoaffective disorder showed a clinical picture at time of diagnosis that appeared different from schizophrenia or psychotic mood disorders using DSM-IV criteria, but who as a group, were longitudinally determined to have outcomes indistinguishable from those with mood disorders with or without psychotic features. A poor prognosis was assumed to apply to these patients by most clinicians, and this poor prognosis was harmful to many patients. The poor prognosis for DSM-IV schizoaffective disorder was not based on patient outcomes research, but was caused by poorly defined criteria interacting with clinical tradition and belief; clinician enculturation with unscientific assumptions from the diagnosis history (discussed above), including the invalid Kraepelinian dichotomy; and by clinicians being unfamiliar with the scientific limitations of the diagnostic and classification system.The DSM-5 schizoaffective disorder workgroup analyzed all of the available research evidence on schizoaffective disorder, and concluded that "presenting symptoms of psychosis have little validity in determining diagnosis, prognosis, or treatment response." Given our understanding of overlapping genetics in bipolar disorders, schizoaffective disorder, and schizophrenia, as well as the overlap in treatments for these disorders; but given the lack of specificity of presenting symptoms for determining diagnosis, prognosis or treatment response in these psychotic illness syndromes, the limits of our knowledge are clearer: Presenting symptoms of psychosis describe only presenting symptoms to be treated, and not much more. Schizoaffective disorder was changed to a longitudinal or life course diagnosis in DSM-5 for this reason. Research Little is known of the causes and mechanisms that lead to the development of schizoaffective disorder. Whether schizoaffective disorder is a variant of schizophrenia (as in DSM-5 and ICD-10 classification systems), a variant of bipolar disorder, or part of a dimensional continuum between psychotic depression, bipolar disorders and schizophrenia is currently being investigated.More recently, some research suggests the need for a more specialized classification for schizoaffective disorder. In a 2017 examining diagnostic heterogeneity study, researchers found that when compared to a schizophrenia sample, individuals with schizoaffective disorder rate higher in suicidality and anxiety disorder comorbidity. References Further reading == External links ==

Can you describe Macrocheilia, to me Aarogya

Macrocheilia

Macrocheilia is a condition of permanent swelling of the lip that results from greatly distended lymphatic spaces. This causes an abnormal largeness of the lips. This is sometimes seen in leprosy patients. See also Nevus psiloliparus List of cutaneous conditions References External links eMedicine: Lip reduction

Hi Aarogya, could you help me understand about Spinal stenosis

Spinal stenosis

Spinal stenosis is an abnormal narrowing of the spinal canal or neural foramen that results in pressure on the spinal cord or nerve roots. Symptoms may include pain, numbness, or weakness in the arms or legs. Symptoms are typically gradual in onset and improve with leaning forward. Severe symptoms may include loss of bladder control, loss of bowel control, or sexual dysfunction.Causes may include osteoarthritis, rheumatoid arthritis, spinal tumors, trauma, Pagets disease of the bone, scoliosis, spondylolisthesis, and the genetic condition achondroplasia. It can be classified by the part of the spine affected into cervical, thoracic, and lumbar stenosis. Lumbar stenosis is the most common, followed by cervical stenosis. Diagnosis is generally based on symptoms and medical imaging.Treatment may involve medications, bracing, or surgery. Medications may include NSAIDs, acetaminophen, or steroid injections. Stretching and strengthening exercises may also be useful. Limiting certain activities may be recommended. Surgery is typically only done if other treatments are not effective, with the usual procedure being a decompressive laminectomy.Spinal stenosis occurs in as many as 8% of people. It occurs most commonly in people over the age of 50. Males and females are affected equally often. The first modern description of the condition is from 1803 by Antoine Portal, and there is evidence of the condition dating back to Ancient Egypt. Types The most common forms are lumbar spinal stenosis, at the level of the lower back, and cervical spinal stenosis, which are at the level of the neck. Thoracic spinal stenosis, at the level of the mid-back, is much less common.In lumbar stenosis, the spinal nerve roots in the lower back are compressed which can lead to symptoms of sciatica (tingling, weakness, or numbness that radiates from the low back and into the buttocks and legs).Cervical spinal stenosis can be far more dangerous by compressing the spinal cord. Cervical canal stenosis may lead to myelopathy, a serious condition causing symptoms including major body weakness and paralysis. Such severe spinal stenosis symptoms are virtually absent in lumbar stenosis, however, as the spinal cord terminates at the top end of the adult lumbar spine, with only nerve roots (cauda equina) continuing further down. Cervical spinal stenosis is a condition involving narrowing of the spinal canal at the level of the neck. It is frequently due to chronic degeneration, but may also be congenital or traumatic. Treatment frequently is surgical. Signs and symptoms Common Standing discomfort (94%) Discomfort/pain, in shoulder, arm, hand (78%) Bilateral symptoms (68%) Numbness at or below the level of involvement (63%) Weakness at or below the level of involvement (43%) Pain or weakness in buttock / thigh only (8%) Pain or weakness below the knee (3%) Neurological disorders Cervical (spondylotic) myelopathy, a syndrome caused by compression of the cervical spinal cord which is associated with "numb and clumsy hands", imbalance, loss of bladder and bowel control, and weakness that can progress to paralysis. Pinched nerve, causing numbness. Intermittent neurogenic claudication characterized by lower limb numbness, weakness, diffuse or radicular leg pain associated with paresthesia (bilaterally), weakness and/or heaviness in buttocks radiating into lower extremities with walking or prolonged standing. Symptoms occur with extension of spine and are relieved with spine flexion. Minimal to zero symptoms when seated or supine. Radiculopathy (with or without radicular pain) neurologic condition—nerve root dysfunction causes objective signs such as weakness, loss of sensation and of reflex. Cauda equina syndrome - Lower extremity pain, weakness, numbness that may involve perineum and buttocks, associated with bladder and bowel dysfunction. Lower back pain due to degenerative disc or joint changes. Causes Aging Any of the factors below may cause the spaces in the spine to narrow. Spinal ligaments can thicken (ligamenta flava) Bone spurs develop on the bone and into the spinal canal or foraminal openings Intervertebral discs may bulge or herniate into the canal or foraminal openings Degenerative disc disease causes narrowing of the spaces. Facet joints break down Facet joints may hypertrophy Compression fractures of the spine, which are common in osteoporosis Synovial cysts form on the facet joints causing compression of the spinal sac of nerves (thecal sac) Arthritis Osteoarthritis Rheumatoid arthritis—much less common cause of spinal problems Congenital Spinal canal is too small at birth Structural deformities of the vertebrae may cause narrowing of the spinal canal. Instability of the spine A vertebra slips forward on another (spondylolisthesis) Trauma Accidents and injuries may dislocate the spine and the spinal canal or cause burst fractures that yield fragments of bone that go through the canal. Patients with cervical myelopathy caused by narrowing of the spinal canal are at higher risks of acute spinal cord injury if involved in accidents. Tumors Irregular growths of soft tissue will cause inflammation. Growth of tissue into the canal pressing on nerves, the sac of nerves, or the spinal cord. Diagnosis The diagnosis of spinal stenosis involves a complete evaluation of the spine. The process usually begins with a medical history and physical examination. X-ray and MRI scans are typically used to determine the extent and location of the nerve compression. Medical history The medical history is the most important aspect of the examination as it will tell the physician about subjective symptoms, possible causes for spinal stenosis, and other possible causes of back pain. Physical examination The physical examination of a patient with spinal stenosis will give the physician information about exactly where nerve compression is occurring. Some important factors that should be investigated are any areas of sensory abnormalities, numbness, irregular reflexes, and any muscular weakness. MRI MRI has become the most frequently used study to diagnose spinal stenosis. The MRI uses electromagnetic signals to produce images of the spine. MRIs are helpful because they show more structures, including nerves, muscles, and ligaments, than seen on X-rays or CT scans. MRIs are helpful at showing exactly what is causing spinal nerve compression. Myelography In CT myelography, spinal tap is performed in the low back with dye injected into the spinal fluid. X-rays are performed followed by a CT scan of the spine to help see narrowing of the spinal canal. This is a very effective study in cases of lateral recess stenosis. It is also necessary for patients in which MRI is contraindicated, such as those with implanted pacemakers. Red flags Fever Nocturnal pain Gait disturbance Structural deformity Unexplained weight loss Previous carcinoma Severe pain upon lying down Recent trauma with suspicious fracture Presence of severe or progressive neurologic deficit Treatments Treatment options are either surgical or non-surgical. Overall evidence is inconclusive whether non-surgical or surgical treatment is the better for lumbar spinal stenosis. Non-surgical treatments The effectiveness of non-surgical treatments is unclear as they have not been well studied. Education about the course of the condition and how to relieve symptoms Medicines to relieve pain and inflammation, such as acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs) Exercise, to maintain or achieve overall good health, aerobic exercise, such as riding a stationary bicycle, which allows for a forward lean, walking, or swimming can relieve symptoms Weight loss, to relieve symptoms and slow progression of the stenosis Physical therapy to support self-care. Also may give instructs on stretching and strength exercises that may lead to a decrease in pain and other symptoms. Lumbar epidural steroid or anesthetic injections have low quality evidence to support their use. Surgery Lumbar decompressive laminectomy: This involves removing the roof of bone overlying the spinal canal and thickened ligaments in order to decompress the nerves and sac of nerves. 70-90% of people have good results. Interlaminar implant: This is a non-fusion U-shaped device that is placed between two bones in the lower back that maintains motion in the spine and keeps the spine stable after a lumbar decompressive surgery. The U-shaped device maintains height between the bones in the spine so nerves can exit freely and extend to lower extremities. Surgery for cervical myelopathy is either conducted from the front or from the back, depending on several factors such as where the compression occurs and how the cervical spine is aligned. Anterior cervical discectomy and fusion: A surgical treatment of nerve root or spinal cord compression by decompressing the spinal cord and nerve roots of the cervical spine with a discectomy in order to stabilize the corresponding vertebrae. Posterior approaches seek to generate space around the spinal cord by removing parts of the posterior elements of the spine. Techniques include laminectomy, laminectomy and fusion, and laminoplasty.Decompression plus fusion appears no better than decompression alone, while spinal spacers appears better than decompression plus fusion but not better than decompression alone. No differences were found in the type of decompression. Epidemiology The NAMCS data shows the incidence in the U.S. population to be 3.9% of 29,964,894 visits for mechanical back problems. The Longitudinal Framingham Heart Study found 1% of men and 1.5% of women had vertebral slippage at a mean age of 54. Over the next 25 years, 11% of men and 25% of women developed degenerative vertebral slippage. Research A RCT is being conducted in Sweden, to compare surgery versus non-surgical treatment for lumbar spinal stenosis. See also Spinal cord compression References External links "Spinal Stenosis". PubMed Health. National Center for Biotechnology Information, U.S. National Library of Medicine. 25 May 2010. Archived from the original on 8 February 2011. "Questions and Answers about Spinal Stenosis". US National Institute of Arthritis and Musculoskeletal and Skin Diseases. 11 April 2017.

Hello Aarogya , Do you know what is Liver disease,

Liver disease

Liver disease, or hepatic disease, is any of many diseases of the liver. If long-lasting it is termed chronic liver disease. Although the diseases differ in detail, liver diseases often have features in common. Signs and symptoms Some of the signs and symptoms of a liver disease are the following: Jaundice Confusion and altered consciousness caused by hepatic encephalopathy. Thrombocytopenia and coagulopathy. Risk of bleeding symptoms particularly taking place in gastrointestinal tract Liver diseases There are more than a hundred different liver diseases. Some of the most common are: Fascioliasis, a parasitic infection of liver caused by a liver fluke of the genus Fasciola, mostly Fasciola hepatica. Hepatitis, inflammation of the liver, is caused by various viruses (viral hepatitis) also by some liver toxins (e.g. alcoholic hepatitis), autoimmunity (autoimmune hepatitis) or hereditary conditions. Alcoholic liver disease is a hepatic manifestation of alcohol overconsumption, including fatty liver disease, alcoholic hepatitis, and cirrhosis. Analogous terms such as "drug-induced" or "toxic" liver disease are also used to refer to disorders caused by various drugs. Fatty liver disease (hepatic steatosis) is a reversible condition where large vacuoles of triglyceride fat accumulate in liver cells. Non-alcoholic fatty liver disease is a spectrum of disease associated with obesity and metabolic syndrome. Hereditary diseases that cause damage to the liver include hemochromatosis, involving accumulation of iron in the body, and Wilsons disease. Liver damage is also a clinical feature of alpha 1-antitrypsin deficiency and glycogen storage disease type II. In transthyretin-related hereditary amyloidosis, the liver produces a mutated transthyretin protein which has severe neurodegenerative or cardiopathic effects. Liver transplantation can be curative. Gilberts syndrome, a genetic disorder of bilirubin metabolism found in a small percent of the population, can cause mild jaundice. Cirrhosis is the formation of fibrous tissue (fibrosis) in the place of liver cells that have died due to a variety of causes, including viral hepatitis, alcohol overconsumption, and other forms of liver toxicity. Cirrhosis causes chronic liver failure. Primary liver cancer most commonly manifests as hepatocellular carcinoma or cholangiocarcinoma; rarer forms include angiosarcoma and hemangiosarcoma of the liver. (Many liver malignancies are secondary lesions that have metastasized from primary cancers in the gastrointestinal tract and other organs, such as the kidneys, lungs.) Primary biliary cirrhosis is a serious autoimmune disease of the bile capillaries. Primary sclerosing cholangitis is a serious chronic inflammatory disease of the bile duct, which is believed to be autoimmune in origin. Budd–Chiari syndrome is the clinical picture caused by occlusion of the hepatic vein. Mechanisms Liver diseases can develop through several mechanisms: DNA damage One general mechanism, increased DNA damage, is shared by some of the major liver diseases, including infection by hepatitis B virus or hepatitis C virus, heavy alcohol consumption, and obesity.Viral infection by hepatitis B virus, or hepatitis C virus causes an increase of reactive oxygen species. The increase in intracellular reactive oxygen species is about 10,000-fold with chronic hepatitis B virus infection and 100,000-fold following hepatitis C virus infection. This increase in reactive oxygen species causes inflammation and more than 20 types of DNA damage. Oxidative DNA damage is mutagenic and also causes epigenetic alterations at the sites of DNA repair. Epigenetic alterations and mutations affect the cellular machinery that may cause the cell to replicate at a higher rate or result in the cell avoiding apoptosis, and thus contribute to liver disease. By the time accumulating epigenetic and mutational changes eventually cause hepatocellular carcinoma, epigenetic alterations appear to have an even larger role in carcinogenesis than mutations. Only one gene, TP53, is mutated in more than 20% of liver cancers while 41 genes each have hypermethylated promoters (repressing gene expression) in more than 20% of liver cancers.Alcohol consumption in excess causes a build-up of acetaldehyde. Acetaldehyde and free radicals generated by metabolizing alcohol induce DNA damage and oxidative stress. In addition, activation of neutrophils in alcoholic liver disease contributes to the pathogenesis of hepatocellular damage by releasing reactive oxygen species (which can damage DNA). The level of oxidative stress and acetaldehyde-induced DNA adducts due to alcohol consumption does not appear sufficient to cause increased mutagenesis. However, as reviewed by Nishida et al., alcohol exposure, causing oxidative DNA damage (which is repairable), can result in epigenetic alterations at the sites of DNA repair. Alcohol-induced epigenetic alterations of gene expression appear to lead to liver injury and ultimately carcinoma.Obesity is associated with a higher risk of primary liver cancer. As shown with mice, obese mice are prone to liver cancer, likely due to two factors. Obese mice have increased pro-inflammatory cytokines. Obese mice also have higher levels of deoxycholic acid, a product of bile acid alteration by certain gut microbes, and these microbes are increased with obesity. The excess deoxycholic acid causes DNA damage and inflammation in the liver, which, in turn, can lead to liver cancer. Other relevant aspects Several liver diseases are due to viral infection. Viral hepatitides such as Hepatitis B virus and Hepatitis C virus can be vertically transmitted during birth via contact with infected blood. According to a 2012 NICE publication, "about 85% of hepatitis B infections in newborns become chronic". In occult cases, Hepatitis B virus is present by hepatitis B virus DNA, but testing for HBsAg is negative. High consumption of alcohol can lead to several forms of liver disease including alcoholic hepatitis, alcoholic fatty liver disease, cirrhosis, and liver cancer. In the earlier stages of alcoholic liver disease, fat builds up in the livers cells due to increased creation of triglycerides and fatty acids and a decreased ability to break down fatty acids. Progression of the disease can lead to liver inflammation from the excess fat in the liver. Scarring in the liver often occurs as the body attempts to heal and extensive scarring can lead to the development of cirrhosis in more advanced stages of the disease. Approximately 3–10% of individuals with cirrhosis develop a form of liver cancer known as hepatocellular carcinoma. According to Tilg, et al., gut microbiome could very well have an effect, be involved in the pathophysiology, on the various types of liver disease which an individual may encounter. Insight into the exact causes and mechanisms mediating pathophysiology of the liver is quickly progressing due to the introduction new technological approaches like Single cell sequencing and kinome profiling Air pollutants Particulate matter or carbon black are common pollutants. They have a direct toxic effect on the liver; cause inflammation of liver caused by and thereby impact lipid metabolism and fatty liver disease; and can translocate from the lungs to the liver.Because particulate matter and carbon black are very diverse and each has different toxicodynamics, detailed mechanisms of translocation are not clear. Water-soluble fractions of particulate matter are the most important part of translocation to the liver, through extrapulmonary circulation. When particulate matter gets into the bloodstream, it combines with immune cells and stimulates innate immune responses. Pro-inflammatory cytokines are released and cause disease progression. Diagnosis A number of liver function tests are available to test the proper function of the liver. These test for the presence of enzymes in blood that are normally most abundant in liver tissue, metabolites or products. serum proteins, serum albumin, serum globulin, alanine transaminase, aspartate transaminase, prothrombin time, partial thromboplastin time.Imaging tests such as transient elastography, ultrasound and magnetic resonance imaging can be used to show the liver tissue and the bile ducts. Liver biopsy can be performed to examine liver tissue to distinguish between various conditions; tests such as elastography may reduce the need for biopsy in some situations.In liver disease, prothrombin time is longer than usual. In addition, the amounts of both coagulation factors and anticoagulation factors are reduced as a diseased liver cannot productively synthesize them as it did when healthy. Nonetheless, there are two exceptions in this falling tendency: coagulation factor VIII and von Willebrand factor, a platelet adhesive protein. Both inversely rise in the setting of hepatic insufficiency, thanks to the drop of hepatic clearance and compensatory productions from other sites of the body. Fibrinolysis generally proceeds faster with acute liver failure and advanced stage liver disease, unlike chronic liver disease in which concentration of fibrinogen remains unchanged.A previously undiagnosed liver disease may become evident first after autopsy. Following are gross pathology images: Treatment Anti-viral medications are available to treat infections such as hepatitis B. Other conditions may be managed by slowing down disease progression, for example: By using steroid-based drugs in autoimmune hepatitis. Regularly removing a quantity of blood from a vein (venesection) in the iron overload condition, hemochromatosis. Wilson’s disease, a condition where copper builds up in the body, can be managed with drugs that bind copper, allowing it to be passed from the body in urine. In cholestatic liver disease, (where the flow of bile is affected due to cystic fibrosis) a medication called ursodeoxycholic acid may be given. See also Model for end-stage liver disease (MELD) References Further reading Friedman, Lawrence S.; Keeffe, Emmet B. (2011-08-03). Handbook of Liver Disease. Elsevier Health Sciences. ISBN 978-1455723164. == External links ==

Aarogya, What does Mittelschmerz mean

Mittelschmerz

Mittelschmerz (German: "middle pain") is a colloquial term for "ovulation pain" or "midcycle pain". About 20% of women experience mittelschmerz, some every cycle, some intermittently. Signs and symptoms Mittelschmerz is characterized by lower abdominal and pelvic pain that occurs roughly midway through a womans menstrual cycle. The pain can appear suddenly and usually subsides within hours, although it may sometimes last two or three days. In some cases it can last up to the following cycle. In some women, the mittelschmerz is localized enough so that they can tell which of their two ovaries provided the egg in a given month. Because ovulation occurs on a random ovary each cycle, the pain may switch sides or stay on the same side from one cycle to another. Other ovulation symptoms Women may notice other physical symptoms associated with their mittelschmerz, during or near ovulation. The most common sign is the appearance of fertile cervical mucus in the days leading up to ovulation. Cervical mucus is one of the primary signs used by various fertility awareness methods. Other symptoms are sometimes called secondary fertility signs to distinguish from the three primary signs. Mid-cycle or ovulatory bleeding is thought to result from the sudden drop in estrogen that occurs just before ovulation. This drop in hormones can trigger withdrawal bleeding in the same way that switching from active to placebo birth control pills does. The rise in hormones that occurs after ovulation prevents such mid-cycle spotting from becoming as heavy or long lasting as a typical menstruation. Spotting is more common in longer cycles. A womans vulva may swell just prior to ovulation, especially the side on which ovulation will occur. One of the groin lymph nodes (on the side on which ovulation will occur) will swell to about the size of a pea, and may become tender. Causes Mittelschmerz is believed to have a variety of causes: Follicular swelling: The swelling of follicles in the ovaries prior to ovulation. While only one or two eggs mature to the point of being released, a number of follicles grow during the follicular phase of the menstrual cycle (non-dominant follicles atrophy prior to ovulation). Because follicles develop on both sides, this theory explains mittelschmerz that occurs simultaneously on both sides of the abdomen.Ovarian wall rupture: The ovaries have no openings; at ovulation the egg breaks through the ovarys wall. This may make ovulation itself painful for some women. Fallopian tube contraction: After ovulation, the fallopian tubes contract (similar to peristalsis of the esophagus), which may cause pain in some women. Smooth muscle cell contraction: At ovulation, this pain may be related to smooth muscle cell contraction in the ovary as well as in its ligaments. These contractions occur in response to an increased level of prostaglandin F2-alpha, itself mediated by the surge of luteinizing hormone (LH).Irritation: At the time of ovulation, blood or other fluid is released from the ruptured egg follicle. This fluid may cause irritation of the abdominal lining. Diagnosis Diagnosis of mittelschmerz is generally made if a woman is mid-cycle and a pelvic examination shows no abnormalities. If the pain is prolonged and/or severe, other diagnostic procedures such as an abdominal ultrasound may be performed to rule out other causes of abdominal pain. The pain of mittelschmerz is sometimes mistaken for appendicitis and is one of the differential diagnoses for appendicitis in women of child-bearing age. Treatment The pain is not harmful and does not signify the presence of disease. No treatment is usually necessary. Pain relievers (analgesics) such as NSAIDS (Non-steroidal anti inflammatories) may be needed in cases of prolonged or intense pain.Hormonal forms of contraception can be taken to prevent ovulation—and therefore ovulatory pain—but otherwise there is no known prevention. Usefulness Women charting with some form of fertility awareness may find mittelschmerz to be a helpful secondary sign in detecting ovulation. Because normal sperm life is up to five days, however, mittelschmerz alone does not provide sufficient advance warning to avoid pregnancy. Because other causes of minor abdominal pain are common, mittelschmerz alone also cannot be used to confirm the beginning of the post-ovulatory infertile period. References == External links ==

Hi Aarogya , Do you know what is Intestinal capillariasis,

Intestinal capillariasis

Capillariasis is a disease in the group of helminthiasis diseases caused by the nematode Capillaria philippinensis. Symptoms and signs Symptoms in infested humans include watery diarrhea, abdominal pain, edema, weight loss, borborygmus (stomach growling), and depressed levels of potassium and albumin in the blood. In humans, the parasites damage the cells of the intestinal wall. This damage interferes with the absorption of nutrients and the maintenance of a proper electrolyte balance. Untreated C. philippinensis infestations are often fatal. Diagnosis Diagnosis usually involves finding the eggs and/or adults of C. philippinensis in stool samples. Prevention Prevention is as simple as avoiding eating small, whole, uncooked fish. However, in C. philippinensis endemic areas, such dietary habits are common and have been practiced for many generations. Treatment Anthelmintics such as mebendazole and albendazole have been reported to eliminate infestation of humans more effectively than thiabendazole. References == External links ==

Hello Aarogya, what is Dural tear

Dural tear

Dural tear is a tear occurring in the dura mater of the brain. It is usually caused as a result of trauma or as a complication following surgery. Diagnosis In case of head injury, a dural tear is likely in case of a depressed skull fracture. A burr hole is made through the normal skull near the fractured portion, and Adsons elevator is introduced. Underlying dura is separated carefully from the overlying depressed bone fragments. The dura that is now visible is carefully examined to exclude any dural tear. Treatment The whole extent of the dural tear is exposed by removing the overlying skull. The ragged edges of the tear are excised. However, care should be taken not to excise too much dura as it may increase the chances for spread of infection into the subarachnoid space. Removing too much dura will also make it difficult to close the tear. If there is not much dural loss, interrupted sutures are made with non-absorbable material. In case of dural loss, the defect is closed using a transplant from fascia lata or pericranium given that there is not much contamination of the dura. In case of contamination, the defect is left alone and a primary suture is performed at a later date. If dural tear is associated with haemorrhage from dural vessels, they are coagulated using diathermy. This technique is preferred because the vessels are too small to be picked up by an artery forceps. Large vessels, if present, can be under-run with suture. When the dural tear is associated with a dural sinus hemorrhage, a graft of pericranium is used for a small tear and a muscle graft from temporalis is used for a large tear. The muscle graft is flattened by hammering before using it for grafting. If dural tear is associated with a brain injury, wide exposure of the wound is done to examine the extent of brain damage. All devitalized brain tissues are removed along with extravasated blood, foreign bodies and pieces of bone. All devitalized tissue and foreign bodies are removed by a combination of irrigation and suction. Following dural repair, skull deficit is treated by using moulded tantalum plates or acrylic inlays, three to six months after the head injury. == References ==

Aarogya , Do you know what is Flatulence,

Flatulence

Flatulence, in humans, is the expulsion of gas from the intestines via the anus, commonly referred to as farting. "Flatus" is the medical word for gas generated in the stomach or bowels. A proportion of intestinal gas may be swallowed environmental air, and hence flatus is not entirely generated in the stomach or bowels. The scientific study of this area of medicine is termed flatology.Flatus is brought to the rectum and pressurized by muscles in the intestines. It is normal to pass flatus ("to fart"), though volume and frequency vary greatly among individuals. It is also normal for intestinal gas to have a feculent or unpleasant odor, which may be intense. The noise commonly associated with flatulence ("blowing a raspberry") is produced by the anus and buttocks, which act together in a manner similar to that of an embouchure. Both the sound and odor are sources of embarrassment, annoyance or amusement (flatulence humor). There are several general symptoms related to intestinal gas: pain, bloating and abdominal distension, excessive flatus volume, excessive flatus odor, and gas incontinence. Furthermore, eructation (colloquially known as "burping") is sometimes included under the topic of flatulence. When excessive or malodorous, flatus can be a sign of a health disorder, such as irritable bowel syndrome, celiac disease or lactose intolerance. Terminology Non-medical definitions of the term include "the uncomfortable condition of having gas in the stomach and bowels", or "a state of excessive gas in the alimentary canal". These definitions highlight that many people consider "bloating", abdominal distension or increased volume of intestinal gas, to be synonymous with the term flatulence (although this is technically inaccurate). Colloquially, flatulence may be referred to as "farting", "pumping", "trumping", "blowing off", "pooting", "passing gas", "breaking wind", "backfiring", or simply (in American English) "gas" or (British English) "wind". Derived terms include vaginal flatulence, otherwise known as a queef. Signs and symptoms Generally speaking, there are four different types of complaints that relate to intestinal gas, which may present individually or in combination. Bloating and pain Patients may complain of bloating as abdominal distension, discomfort and pain from "trapped wind". In the past, functional bowel disorders such as irritable bowel syndrome that produced symptoms of bloating were attributed to increased production of intestinal gas. However, three significant pieces of evidence refute this theory. First, in normal subjects, even very high rates of gas infusion into the small intestine (30 mL/min) is tolerated without complaints of pain or bloating and harmlessly passed as flatus per rectum. Secondly, studies aiming to quantify the total volume of gas produced by patients with irritable bowel syndrome (some including gas emitted from the mouth by eructation) have consistently failed to demonstrate increased volumes compared to healthy subjects. The proportion of hydrogen produced may be increased in some patients with irritable bowel syndrome, but this does not affect the total volume. Thirdly, the volume of flatus produced by patients with irritable bowel syndrome who have pain and abdominal distension would be tolerated in normal subjects without any complaints of pain. Patients who complain of bloating frequently can be shown to have objective increases in abdominal girth, often increased throughout the day and then resolving during sleep. The increase in girth combined with the fact that the total volume of flatus is not increased led to studies aiming to image the distribution of intestinal gas in patients with bloating. They found that gas was not distributed normally in these patients: there was segmental gas pooling and focal distension. In conclusion, abdominal distension, pain and bloating symptoms are the result of abnormal intestinal gas dynamics rather than increased flatus production. Excessive volume The normal range of volumes of flatus in normal individuals varies hugely (476–1,491 mL/24 h). All intestinal gas is either swallowed environmental air, present intrinsically in foods and beverages, or the result of gut fermentation. Swallowing small amounts of air occurs while eating and drinking. This is emitted from the mouth by eructation (burping) and is normal. Excessive swallowing of environmental air is called aerophagia, and has been shown in a few case reports to be responsible for increased flatus volume. This is, however, considered a rare cause of increased flatus volume. Gases contained in food and beverages are likewise emitted largely through eructation, e.g., carbonated beverages. Endogenously produced intestinal gases make up 74 percent of flatus in normal subjects. The volume of gas produced is partially dependent upon the composition of the intestinal microbiota, which is normally very resistant to change, but is also very different in different individuals. Some patients are predisposed to increased endogenous gas production by virtue of their gut microbiota composition. The greatest concentration of gut bacteria is in the colon, while the small intestine is normally nearly sterile. Fermentation occurs when unabsorbed food residues arrive in the colon. Therefore, even more than the composition of the microbiota, diet is the primary factor that dictates the volume of flatus produced. Diets that aim to reduce the amount of undigested fermentable food residues arriving in the colon have been shown to significantly reduce the volume of flatus produced. Again, increased volume of intestinal gas will not cause bloating and pain in normal subjects. Abnormal intestinal gas dynamics will create pain, distension, and bloating, regardless of whether there is high or low total flatus volume. Odor Although flatus possesses an odor, this may be abnormally increased in some patients and cause social distress to the patient. Increased odor of flatus presents a distinct clinical issue from other complaints related to intestinal gas. Some patients may exhibit over-sensitivity to bad flatus odor, and in extreme forms, olfactory reference syndrome may be diagnosed. Recent informal research found a correlation between flatus odor and both loudness and humidity content. Incontinence of flatus "Gas incontinence" could be defined as loss of voluntary control over the passage of flatus. It is a recognised subtype of faecal incontinence, and is usually related to minor disruptions of the continence mechanisms. Some consider gas incontinence to be the first, sometimes only, symptom of faecal incontinence. Cause Intestinal gas is composed of varying quantities of exogenous sources and endogenous sources. The exogenous gases are swallowed (aerophagia) when eating or drinking or increased swallowing during times of excessive salivation (as might occur when nauseated or as the result of gastroesophageal reflux disease). The endogenous gases are produced either as a by-product of digesting certain types of food, or of incomplete digestion, as is the case during steatorrhea. Anything that causes food to be incompletely digested by the stomach or small intestine may cause flatulence when the material arrives in the large intestine, due to fermentation by yeast or prokaryotes normally or abnormally present in the gastrointestinal tract. Flatulence-producing foods are typically high in certain polysaccharides, especially oligosaccharides such as inulin. Those foods include beans, lentils, dairy products, onions, garlic, spring onions, leeks, turnips, swedes, radishes, sweet potatoes, potatoes, cashews, Jerusalem artichokes, oats, wheat, and yeast in breads. Cauliflower, broccoli, cabbage, Brussels sprouts and other cruciferous vegetables that belong to the genus Brassica are commonly reputed to not only increase flatulence, but to increase the pungency of the flatus.In beans, endogenous gases seem to arise from complex oligosaccharides (carbohydrates) that are particularly resistant to digestion by mammals, but are readily digestible by microorganisms (methane-producing archaea; Methanobrevibacter smithii) that inhabit the digestive tract. These oligosaccharides pass through the small intestine largely unchanged, and when they reach the large intestine, bacteria ferment them, producing copious amounts of flatus.When excessive or malodorous, flatus can be a sign of a health disorder, such as irritable bowel syndrome, celiac disease, non-celiac gluten sensitivity or lactose intolerance. It can also be caused by certain medicines, such as ibuprofen, laxatives, antifungal medicines or statins. Some infections, such as giardiasis, are also associated with flatulence.Interest in the causes of flatulence was spurred by high-altitude flight and human spaceflight; the low atmospheric pressure, confined conditions, and stresses peculiar to those endeavours were cause for concern. In the field of mountaineering, the phenomenon of high altitude flatus expulsion was first recorded over two hundred years ago. Mechanism Production, composition, and odor Flatus (intestinal gas) is mostly produced as a byproduct of bacterial fermentation in the gastrointestinal (GI) tract, especially the colon. There are reports of aerophagia (excessive air swallowing) causing excessive intestinal gas, but this is considered rare.Over 99% of the volume of flatus is composed of odorless gases. These include oxygen, nitrogen, carbon dioxide, hydrogen and methane. Nitrogen is not produced in the gut, but a component of environmental air. Patients who have excessive intestinal gas that is mostly composed of nitrogen have aerophagia. Hydrogen, carbon dioxide and methane are all produced in the gut and contribute 74% of the volume of flatus in normal subjects. Methane and hydrogen are flammable, and so flatus can be ignited if it contains adequate amounts of these components.Not all humans produce flatus that contains methane. For example, in one study of the faeces of nine adults, only five of the samples contained archaea capable of producing methane. The prevalence of methane over hydrogen in human flatus may correlate with obesity, constipation and irritable bowel syndrome, as archaea that oxidise hydrogen into methane promote the metabolisms ability to absorb fatty acids from food.The remaining trace (<1% volume) compounds contribute to the odor of flatus. Historically, compounds such as indole, skatole, ammonia and short chain fatty acids were thought to cause the odor of flatus. More recent evidence proves that the major contribution to the odor of flatus comes from a combination of volatile sulfur compounds. Hydrogen sulfide, methyl mercaptan (also known as methanethiol), dimethyl sulfide, dimethyl disulfide and dimethyl trisulfide are present in flatus. The benzopyrrole volatiles indole and skatole have an odor of mothballs, and therefore probably do not contribute greatly to the characteristic odor of flatus. In one study, hydrogen sulfide concentration was shown to correlate convincingly with perceived bad odor of flatus, followed by methyl mercaptan and dimethyl sulfide. This is supported by the fact that hydrogen sulfide may be the most abundant volatile sulfur compound present. These results were generated from subjects who were eating a diet high in pinto beans to stimulate flatus production. Others report that methyl mercaptan was the greatest contributor to the odor of flatus in patients not under any specific dietary alterations. It has now been demonstrated that methyl mercaptan, dimethyl sulfide, and hydrogen sulfide (described as decomposing vegetables, unpleasantly sweet/wild radish and rotten eggs respectively) are all present in human flatus in concentrations above their smell perception thresholds.It is recognized that increased dietary sulfur-containing amino acids significantly increases the odor of flatus. It is therefore likely that the odor of flatus is created by a combination of volatile sulfur compounds, with minimal contribution from non-sulfur volatiles. This odor can also be caused by the presence of large numbers of microflora bacteria or the presence of faeces in the rectum. Diets high in protein, especially sulfur-containing amino acids, have been demonstrated to significantly increase the odor of flatus. Volume and intestinal gas dynamics Normal flatus volume is 476 to 1491 mL per 24 hours. This variability between individuals is greatly dependent upon diet. Similarly, the number of flatus episodes per day is variable; the normal range is given as 8–20 per day. The volume of flatus associated with each flatulence event again varies (5–375 mL). The volume of the first flatulence upon waking in the morning is significantly larger than those during the day. This may be due to buildup of intestinal gas in the colon during sleep, the peak in peristaltic activity in the first few hours after waking or the strong prokinetic effect of rectal distension on the rate of transit of intestinal gas. It is now known that gas is moved along the gut independently of solids and liquids, and this transit is more efficient in the erect position compared to when supine. It is thought that large volumes of intestinal gas present low resistance, and can be propelled by subtle changes in gut tone, capacitance and proximal contraction and distal relaxation. This process is thought not to affect solid and liquid intra-lumenal contents.Researchers investigating the role of sensory nerve endings in the anal canal did not find them to be essential for retaining fluids in the anus, and instead speculate that their role may be to distinguish between flatus and faeces, thereby helping detect a need to defecate or to signal the end of defecation.The sound varies depending on the tightness of the sphincter muscle and velocity of the gas being propelled, as well as other factors, such as water and body fat. The auditory pitch (sound) of the flatulence outburst can also be affected by the anal embouchure. Among humans, flatulence occasionally happens accidentally, such as incidentally to coughing or sneezing or during orgasm; on other occasions, flatulence can be voluntarily elicited by tensing the rectum or "bearing down" on stomach or bowel muscles and subsequently relaxing the anal sphincter, resulting in the expulsion of flatus. Management Since problems involving intestinal gas present as different (but sometimes combined) complaints, the management is cause-related. Pain and bloating While not affecting the production of the gases themselves, surfactants (agents that lower surface tension) can reduce the disagreeable sensations associated with flatulence, by aiding the dissolution of the gases into liquid and solid faecal matter. Preparations containing simethicone reportedly operate by promoting the coalescence of smaller bubbles into larger ones more easily passed from the body, either by burping or flatulence. Such preparations do not decrease the total amount of gas generated in or passed from the colon, but make the bubbles larger and thereby allowing them to be passed more easily.Other drugs including prokinetics, lubiprostone, antibiotics and probiotics are also used to treat bloating in patients with functional bowel disorders such as irritable bowel syndrome, and there is some evidence that these measures may reduce symptoms.A flexible tube, inserted into the rectum, can be used to collect intestinal gas in a flatus bag. This method is occasionally needed in a hospital setting, when the patient is unable to pass gas normally. Volume One method of reducing the volume of flatus produced is dietary modification, reducing the amount of fermentable carbohydrates. This is the theory behind diets such as the low-FODMAP diet (a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, alcohols, and polyols).Most starches, including potatoes, corn, noodles, and wheat, produce gas as they are broken down in the large intestine. Intestinal gas can be reduced by fermenting the beans, and making them less gas-inducing, or by cooking them in the liquor from a previous batch. For example, the fermented bean product miso is less likely to produce as much intestinal gas. Some legumes also stand up to prolonged cooking, which can help break down the oligosaccharides into simple sugars. Fermentative lactic acid bacteria such as Lactobacillus casei and Lactobacillus plantarum reduce flatulence in the human intestinal tract.Probiotics (live yogurt, kefir, etc.) are reputed to reduce flatulence when used to restore balance to the normal intestinal flora. Live (bioactive) yogurt contains, among other lactic bacteria, Lactobacillus acidophilus, which may be useful in reducing flatulence. L. acidophilus may make the intestinal environment more acidic, supporting a natural balance of the fermentative processes. L. acidophilus is available in supplements. Prebiotics, which generally are non-digestible oligosaccharides, such as fructooligosaccharide, generally increase flatulence in a similar way as described for lactose intolerance. Digestive enzyme supplements may significantly reduce the amount of flatulence caused by some components of foods not being digested by the body and thereby promoting the action of microbes in the small and large intestines. It has been suggested that alpha-galactosidase enzymes, which can digest certain complex sugars, are effective in reducing the volume and frequency of flatus. The enzymes alpha-galactosidase, lactase, amylase, lipase, protease, cellulase, glucoamylase, invertase, malt diastase, pectinase, and bromelain are available, either individually or in combination blends, in commercial products. The antibiotic rifaximin, often used to treat diarrhea caused by the microorganism E. coli, may reduce both the production of intestinal gas and the frequency of flatus events. Odor Bismuth The odor created by flatulence is commonly treated with bismuth subgallate, available over-the-counter in the US as Devrom. Bismuth subgallate is commonly used by individuals who have had ostomy surgery, bariatric surgery, faecal incontinence and irritable bowel syndrome. Bismuth subsalicylate is a compound that binds hydrogen sulfide, and one study reported a dose of 524 mg four times a day for 3–7 days bismuth subsalicylate yielded a >95% reduction in faecal hydrogen sulfide release in both humans and rats. Another bismuth compound, bismuth subnitrate was also shown to bind to hydrogen sulfide. Another study showed that bismuth acted synergistically with various antibiotics to inhibit sulfate-reducing gut bacteria and sulfide production. Some authors proposed a theory that hydrogen sulfide was involved in the development of ulcerative colitis and that bismuth might be helpful in the management of this condition. However, bismuth administration in rats did not prevent them from developing ulcerative colitis despite reduced hydrogen sulfide production. Also, evidence suggests that colonic hydrogen sulfide is largely present in bound forms, probably sulfides of iron and other metals. Rarely, serious bismuth toxicity may occur with higher doses. Activated charcoal Despite being an ancient treatment for various digestive complaints, activated charcoal did not produce reduction in both the total flatus volume nor the release of sulfur-containing gasses, and there was no reduction in abdominal symptoms (after 0.52 g activated charcoal four times a day for one week). The authors suggested that saturation of charcoal binding sites during its passage through the gut was the reason for this. A further study concluded that activated charcoal (4 g) does not influence gas formation in vitro or in vivo. Other authors reported that activated charcoal was effective. A study in 8 dogs concluded activated charcoal (unknown oral dose) reduced hydrogen sulfide levels by 71%. In combination with yucca schidigera, and zinc acetate, this was increased to an 86% reduction in hydrogen sulfide, although flatus volume and number was unchanged. An early study reported activated charcoal (unknown oral dose) prevented a large increase in the number of flatus events and increased breath hydrogen concentrations that normally occur following a gas-producing meal.Garments and external devices In 1998, Chester "Buck" Weimer of Pueblo, Colorado, received a patent for the first undergarment that contained a replaceable charcoal filter. The undergarments are air-tight and provide a pocketed escape hole in which a charcoal filter can be inserted. In 2001 Weimer received the Ig Nobel Prize for Biology for his invention.A similar product was released in 2002, but rather than an entire undergarment, consumers are able to purchase an insert similar to a pantiliner that contains activated charcoal. The inventors, Myra and Brian Conant of Mililani, Hawaii, still claim on their website to have discovered the undergarment product in 2002 (four years after Chester Weimer filed for a patent for his product), but state that their tests "concluded" that they should release an insert instead. Incontinence Flatus incontinence where there is involuntary passage of gas, is a type of faecal incontinence, and is managed similarly. Society and culture In many cultures, flatulence in public is regarded as embarrassing, but, depending on context, may also be considered humorous. People will often strain to hold in the passing of gas when in polite company, or position themselves to silence or conceal the passing of gas. In other cultures, it may be no more embarrassing than coughing. While the act of passing flatus in some cultures is generally considered to be an unfortunate occurrence in public settings, flatulence may, in casual circumstances and especially among children, be used as either a humorous supplement to a joke ("pull my finger"), or as a comic activity in and of itself. The social acceptability of flatulence-based humour in entertainment and the mass media varies over the course of time and between cultures. A sufficient number of entertainers have performed using their flatus to lead to the coining of the term flatulist. The whoopee cushion is a joking device invented in the early 20th century for simulating a fart. In 2008, a farting application for the iPhone earned nearly $10,000 in one day.A farting game named Touch Wood was documented by John Gregory Bourke in the 1890s. It existed under the name of Safety in the 20th century in the U.S., and has been found being played in 2011.In January 2011, the Malawi Minister of Justice, George Chaponda, said that Air Fouling Legislation would make public "farting" illegal in his country. When reporting the story, the media satirised Chapondas statement with punning headlines. Later, the minister withdrew his statement. Environmental impact Flatulence is often blamed as a significant source of greenhouse gases, owing to the erroneous belief that the methane released by livestock is in the flatus. While livestock account for around 20% of global methane emissions, 90–95% of that is released by exhaling or burping. In cows, gas and burps are produced by methane-generating microbes called methanogens, that live inside the cows digestive system. Proposals for reducing methane production in cows include the feeding of supplements such as oregano and seaweed, and the genetic engineering of gut biome microbes to produce less methane.Since New Zealand produces large amounts of agricultural products, it is in the unique position of having high methane emissions from livestock compared to other greenhouse gas sources. The New Zealand government is a signatory to the Kyoto Protocol and therefore attempts are being made to reduce greenhouse emissions. To achieve this, an agricultural emissions research levy was proposed, which promptly became known as a "fart tax" or "flatulence tax". It encountered opposition from farmers, farming lobby groups and opposition politicians. Entertainment Historical comment on the ability to fart at will is observed as early as Saint Augustines The City of God (5th century A.D.). Augustine mentions men who "have such command of their bowels, that they can break wind continuously at will, so as to produce the effect of singing". Intentional passing of gas and its use as entertainment for others appear to have been somewhat well known in pre-modern Europe, according to mentions of it in medieval and later literature, including Rabelais. Le Pétomane ("the Fartomaniac") was a famous French performer in the 19th century who, as well as many professional farters before him, did flatulence impressions and held shows. The performer Mr. Methane carries on le Pétomanes tradition today. Also, a 2002 fiction film Thunderpants revolves around a boy named Patrick Smash who has an ongoing flatulence problem from the time of his birth.Since the 1970s, farting has increasingly been featured in film, especially comedies such as Blazing Saddles and Scooby-Doo. Religion In Islam, flatulence, if audible or odorous, invalidates wudu (ritual purity). Personal experiences People find other peoples flatus unpleasant, but are unfazed by, and may even enjoy, the scent of their own. While there has been little research carried out upon the subject, some speculative guesses have been made as to why this might be so. For example, one explanation for this phenomenon is that people are very familiar with the scent of their own flatus, and that survival in nature may depend on the detection of and reaction to foreign scents. See also References Citations General and cited references Allen, V. (2007). On Farting: Language and Laughter in the Middle Ages. Palgrave MacMillan. ISBN 978-0-312-23493-5. Bolin, T. D. & Stanton, R. (1997). Wind Breaks. Allen & Unwin. ISBN 978-1-86448-321-5. Dawson, Jim (1999). Who Cut the Cheese?: A Cultural History of the Fart. Ten Speed Press. ISBN 1-58008-011-1. Dawson, Jim (2006). Blame it on the Dog: A Modern History of the Fart. Ten Speed Press. ISBN 1-58008-751-5. Franklin, Benjamin (2003). Japikse, Carl (ed.). Fart Proudly ((Reprint) ed.). Frog Ltd/Blue Snake. ISBN 1-58394-079-0. Persels, J., & Ganim, R. (2004). Fecal Matters in Early Modern Literature and Art: Studies in Scatology. (Chap. 1: "The Honorable Art of Farting in Continental Renaissance"). ISBN 0-7546-4116-3. von Schmausen, D. (2002). Official Rules, New World Odor International Freestyle Farting Championship. LULU. ISBN 1435709195. External links The Merck Manual of Diagnosis and Therapy, Gas Dictionary of Fart Slang Invisible College of Experimental Flatology

Aarogya, could you share information about a health condition involving Worry

Worry

Worry refers to the thoughts, images, emotions, and actions of a negative nature in a repetitive, uncontrollable manner that results from a proactive cognitive risk analysis made to avoid or solve anticipated potential threats and their potential consequences. Introduction Psychologically, worry is part of Perseverative Cognition (a collective term for continuous thinking about negative events in the past or in the future). As an emotion "worry" is experienced from anxiety or concern about a real or imagined issue, often personal issues such as health or finances, or external broader issues such as environmental pollution, social structure or technological change. It is a natural response to anticipated future problems. Excessive worry is a primary diagnostic feature of generalized anxiety disorder, but also is pervasive in other psychological disorders, like schizophrenia. Most people experience short-lived periods of worry in their lives without incident; indeed, a mild amount of worrying have positive effects, if it prompts people to take precautions (e.g., fastening their seat belt or buying insurance) or avoid risky behaviors (e.g., angering dangerous animals, or binge drinking), but with excessive worrisome people they overestimate future dangers in their assessments and in its extremities tend to magnify the situation as a dead end which results stress. Overestimation happens because analytic resources are a combination of external locus of control, personal experience and belief fallacies. Chronically worried individuals are also more likely to lack confidence in their problem solving ability, perceive problems as threats, become easily frustrated when dealing with a problem, and are pessimistic about the outcome of problem-solving efforts.Seriously anxious people find it difficult to control their worry and typically experience symptoms like restlessness, fatigue, difficulty in concentrating, irritability, muscle tension and sleep disturbance. Theories Avoidance model The avoidance model of worry (AMW) theorizes that worry is a verbal linguistic, thought based activity, which arises as an attempt to inhibit vivid mental imagery and associated somatic and emotional activation. This inhibition precludes the emotional processing of fear that is theoretically necessary for successful habituation and extinction of feared stimuli. Worry is reinforced as a coping technique due to the fact that most worries never actually occur, leaving the worrier with a feeling of having successfully controlled the feared situation, without the unpleasant sensations associated with exposure. Noteworthy, studies also show that visual worry, i.e. worrying that occurs in visual modality, is also associated with increased anxiety and other psychopathology symptoms. Cognitive model This model explains pathological worry to be an interaction between involuntary (bottom-up) processes, such as habitual biases in attention and interpretation favoring threat content, and voluntary (top-down) processes, such as attentional control. Emotional processing biases influence the probability of threat representations into the awareness as intruding negative or positive thoughts. At a pre-conscious level, these processes influence the competition among mental representations in which some correspond to the assertive power of worry with impaired cognitive process and others to the preventive power of worry with attentional control or exhaustive vigilance. The biases determine threatening degree and nature of worry content the worrier attempts to resolve the perceived threat and the redirection of anticipations, responses and coping in such situations.There are some who respond to mental representations in an uncertain or ambiguous state in regard to the stressful or upsetting event. In this state the worrier is held in a perpetual state of worry. This is because availability of an overwhelming number(maybe 2 or 3, depending upon the worry-prone individual) of possibilities of outcomes which can be generated, it puts the worrier in a threatening crisis and they focus their attentional control voluntarily on the potential negative outcomes, whereas others engage in a constructive problem solving manner and in a benign approach rather than to engage with heightened anticipation on the possible negative outcome. Philosophical perspectives Greek thinkers such as stoic philosopher Epictetus and Seneca advised against worry. Albert Ellis, the creator of Rational Emotive Behavior Therapy, was inspired by the Stoics’ therapeutic ideas. Religious perspectives The biblical word used in Hebrew for worry (Hebrew: דָּאַג, daag) regards worry as a combined form of fear and sorrow which affects nephesh, the totality of our being. The bible takes a fortitude-strengthening approach regarding worrying e.g. Psalm 94: In the multitude of my anxieties within me, your comforts delight my soul.In the New Testament, the Gospel of Matthew encourages: And can any of you by worrying add a single hour to your span of life? ... So do not worry about tomorrow, for tomorrow will bring worries of its own. Today’s trouble is enough for today.The Greek word used for worry in Matthew is merimnaō, which means to be anxious about, or to be troubled with cares. St. Paul writes to the Philippian church, "There is no need to worry" and in the pastoral epistles, 2 Timothy 1:7 emboldens: For God did not give us a spirit of cowardice, but rather a spirit of power and of love and of self-discipline.Similarly James 1:2-4 motivates to face trials of any kind with joy, because they produce endurance (strength and courage). Further Saint Peter reveals his understanding of healthy living in Second Peter 1:3,5–7: We have a sure hope ... this is a cause of great joy for us.A late Indian spiritual teacher Meher Baba stated that worry is caused by desires and can be overcome through detachment: Worry is the product of feverish imagination working under the stimulus of desires ... (It) is a necessary resultant of attachment to the past or to the anticipated future, and it always persists in some form or other until the mind is completely detached from everything. Management The worry system is activated from exposure to a potential triggering event, traumatic experience or vulnerability, this brings worrisome thoughts and feelings which bring about physical stress reactions and response to avoid worrisome behavior, to ensure allostasis. But under the crisis this activity feeds back into the first worrisome thoughts and feelings which generates and strengthens the vicious worry cycle. Relaxation, risk assessment, worry exposure and behavior prevention have been proven effective in curbing the excessive worry, a chief feature of generalized anxiety disorder. Cognitive behavioral techniques hasnt branched out enough to address the problem holistically but therapy can control or diminish worry. See also References Further reading Kate Sweeny; Michael D. Dooley (18 April 2017). "The surprising upsides of worry". Social and Personality Psychology Compass. 11 (4): e12311. doi:10.1111/spc3.12311. External links Current theoretical models of generalized anxiety disorder (GAD): Conceptual review and treatment implications

Can you describe Neisseria meningitidis, to me Aarogya

Neisseria meningitidis

Neisseria meningitidis, often referred to as meningococcus, is a Gram-negative bacterium that can cause meningitis and other forms of meningococcal disease such as meningococcemia, a life-threatening sepsis. The bacterium is referred to as a coccus because it is round, and more specifically a diplococcus because of its tendency to form pairs. About 10% of adults are carriers of the bacteria in their nasopharynx. As an exclusively human pathogen, it is the main cause of bacterial meningitis in children and young adults, causing developmental impairment and death in about 10% of cases. It causes the only form of bacterial meningitis known to occur epidemically, mainly in Africa and Asia. It occurs worldwide in both epidemic and endemic form.N. meningitidis is spread through saliva and respiratory secretions during coughing, sneezing, kissing, chewing on toys and through sharing a source of fresh water. It has also been reported to be transmitted through oral sex and cause urethritis in men. It infects its host cells by sticking to them with long thin extensions called pili and the surface-exposed proteins Opa and Opc and has several virulence factors. Signs and symptoms Meningococcus can cause meningitis and other forms of meningococcal disease. It initially produces general symptoms like fatigue, fever, and headache and can rapidly progress to neck stiffness, coma and death in 10% of cases. Petechiae occur in about 50% of cases. Chance of survival is highly correlated with blood cortisol levels, with lower levels prior to steroid administration corresponding with increased patient mortality. Symptoms of meningococcal meningitis are easily confused with those caused by other bacteria, such as Haemophilus influenzae and Streptococcus pneumoniae. Suspicion of meningitis is a medical emergency and immediate medical assessment is recommended. Current guidance in the United Kingdom is that if a case of meningococcal meningitis or septicaemia (infection of the blood) is suspected, intravenous antibiotics should be given and the ill person admitted to the hospital. This means that laboratory tests may be less likely to confirm the presence of Neisseria meningitidis as the antibiotics will dramatically lower the number of bacteria in the body. The UK guidance is based on the idea that the reduced ability to identify the bacteria is outweighed by reduced chance of death. Septicaemia caused by Neisseria meningitidis has received much less public attention than meningococcal meningitis even though septicaemia has been linked to infant deaths. Meningococcal septicaemia typically causes a purpuric rash, that does not lose its color when pressed with a glass slide ("non-blanching") and does not cause the classical symptoms of meningitis. This means the condition may be ignored by those not aware of the significance of the rash. Septicaemia carries an approximate 50% mortality rate over a few hours from initial onset. Other severe complications include Waterhouse–Friderichsen syndrome, a massive, usually bilateral, hemorrhage into the adrenal glands caused by fulminant meningococcemia, adrenal insufficiency, and disseminated intravascular coagulation.Not all instances of a purpura-like rash are due to meningococcal septicaemia; other possible causes, such as idiopathic thrombocytopenic purpura (ITP; a platelet disorder) and Henoch–Schönlein purpura, also need prompt investigation. Microbiology N. meningitidis is a Gram-negative diplococcus since it has an outer and inner membranes with a thin layer of peptidoglycan in between. It is 0.6–1.0 micrometers in size. It tests positive for the enzyme cytochrome c oxidase. Habitat N. meningitidis is a part of the normal nonpathogenic flora in the nasopharynx of up to 8–25% of adults. It colonizes and infects only humans, and has never been isolated from other animals. This is thought to result from the bacteriums inability to get iron from sources other than human transferrin and lactoferrin. Subtypes Disease-causing strains are classified according to the antigenic structure of their polysaccharide capsule. Serotype distribution varies markedly around the world. Among the 13 identified capsular types of N. meningitidis, six (A, B, C, W135, X, and Y) account for most disease cases worldwide. Type A has been the most prevalent in Africa and Asia, but is rare/practically absent in North America. In the United States, serogroup B is the predominant cause of disease and mortality, followed by serogroup C. The multiple subtypes have hindered development of a universal vaccine for meningococcal disease. Pathogenesis Virulence Lipooligosaccharide (LOS) is a component of the outer membrane of N. meningitidis. This acts as an endotoxin and is responsible for septic shock and hemorrhage due to the destruction of red blood cells. Other virulence factors include a polysaccharide capsule which prevents host phagocytosis and aids in evasion of the host immune response. Adhesion is another key virulence strategy to successfully invade host cell. There are several known proteins that are involved in adhesion and invasion, or mediate interactions with specific host cell receptors. These include the Type IV pilin adhesin which mediates attachment of the bacterium to the epithelial cells of the nasopharynx, surface-exposed Opa and Opc proteins which mediate interactions with specific host cell receptors, and NadA which is involved in adhesion.Pathogenic meningococci that have invaded into the bloodstream must be able to survive in the new niche, this is facilitated by acquisition and utilisation of iron (FetA and Hmbr), resisting intracellular oxidative killing by producing catalase and superoxide dismutase and ability to avoid complement mediated killing (fHbp). Meningococci produce an IgA protease, an enzyme that cleaves IgA class antibodies and thus allows the bacteria to evade a subclass of the humoral immune system. A hypervirulent strain was discovered in China. Its impact is yet to be determined. Complement inhibition Factor H binding protein (fHbp) that is exhibited in N. meningitidis and some commensal species is the main inhibitor of the alternative complement pathway. fHbp protects meningococci from complement-mediated death in human serum experiments, but has also been shown to protect meningococci from antimicrobial peptides in vitro. Factor H binding protein is key to the pathogenesis of N. meningitidis, and is, therefore, important as a potential vaccine candidate. Porins are also an important factor for complement inhibition for both pathogenic and commensal species. Porins are important for nutrient acquisition. Porins are also recognized by TLR2, they bind complement factors (C3b, C4b, factor H, and C4bp (complement factor 4b-binding protein)). Cooperation with pili for CR3-mediated internalization is another function of porins. Ability to translocate into host cells and modulate reactive oxygen species production and apoptosis is made possible by porins, as well. Strains of the same species can express different porins. Genome At least 8 complete genomes of Neisseria meningitidis strains have been determined which encode about 2,100 to 2,500 proteins.The genome of strain MC58 (serogroup B) has 2,272,351-base pairs. When sequenced in 2000, it was found to contain 2158 open reading frames (ORFs). Of these, a biological function was predicted for 1158 (53.7%). There were three major islands of horizontal DNA transfer found. Two encode proteins involved in pathogenicity. The third island only codes for hypothetical proteins. They also found more genes that undergo phase variation than any pathogen then known. Phase variation is a mechanism that helps the pathogen to evade the immune system of the host.The genome size of strain H44/76 is 2.18 Mb, and encodes 2,480 open reading frames (ORFs), compared to 2.27 Mb and 2,465 ORFs for MC58. Both strains have a GC content of 51.5%. A comparison with MC58 showed that four genes are uniquely present in H44/76 and nine genes are only present in MC58. Of all ORFs in H44/76, 2,317 (93%) show more than 99% sequence identity.The complete genome sequence of strain NMA510612 (serogroup A) consists of one circular chromosome with a size of 2,188,020 bp, and the average GC content is 51.5%. The chromosome is predicted to possess 4 rRNA operons, 163 insertion elements (IS), 59 tRNAs, and 2,462 ORFs.There is a public database available for N. meningitidis core genome multilocus sequence typing (cMILST). Available at: https://pubmlst.org/bigsdb?db=pubmlst_neisseria_seqdef Genetic transformation Genetic transformation is the process by which a recipient bacterial cell takes up DNA from a neighboring cell and integrates this DNA into the recipients genome by recombination. In N. meningitidis, DNA transformation requires the presence of short DNA sequences (9–10 mers residing in coding regions) of the donor DNA. These sequences are called DNA uptake sequences (DUSs). Specific recognition of these sequences is mediated by a type IV pilin. In N. meningitidis DUSs occur at a significantly higher density in genes involved in DNA repair and recombination (as well as in restriction-modification and replication) than in other annotated gene groups. The over-representation of DUS in DNA repair and recombination genes may reflect the benefit of maintaining the integrity of the DNA repair and recombination machinery by preferentially taking up genome maintenance genes, that could replace their damaged counterparts in the recipient cell.N. meningititis colonizes the nasopharyngeal mucosa, which is rich in macrophages. Upon their activation, macrophages produce superoxide (O2−) and hydrogen peroxide (H2O2). Thus N. meningitidis is likely to encounter oxidative stress during its life cycle. Consequently, an important benefit of genetic transformation to N. meningitidis may be the maintenance of the recombination and repair machinery of the cell that removes oxidative DNA damages such as those caused by reactive oxygen. This is consistent with the more general idea that transformation benefits bacterial pathogens by facilitating repair of DNA damages produced by the oxidative defenses of the host during infection.Meningococci population is extensively diverse genetically, this is due to horizontal gene transfers while in the nasophanrynx. Gene transfer can occur within and between genomes of Neisseria species, and it is the main mechanism of acquiring new traits. This is facilitated by the natural competence of the meningococci to take up foreign DNA. The commensal species of Neisseria can act as a reservoir of genes that can be acquired, for example, this is how capsule switching can occur as a means of hiding from the immune system. An invasive N. meningitidis strain of serogroup C broke out in Nigeria in 2013 - the strain was a new sequence type, ST-10217 determined by multilocus sequence typing. It was determined that a commensal strain of N. meningitidis acquired an 8-kb prophage, the meningococcal disease-associated island (MDAΦ), previously associated with hyper-invasiveness; and the full serogroup C capsule operon, thus becoming a hypervirulent strain. This illustrates how hypervirulent strains can arise from non-pathgenic strains due to the high propensity of gene transfers and DNA uptake by N. meningitidis. Diagnosis A small amount of cerebrospinal fluid (CSF) is sent to the laboratory as soon as possible for analysis. The diagnosis is suspected, when Gram-negative diplococci are seen on Gram stain of a centrifuged sample of CSF; sometimes they are located inside white blood cells. The microscopic identification takes around 1–2 hours after specimen arrival in the laboratory.The gold standard of diagnosis is microbiological isolation of N. meningitidis by growth from a sterile body fluid, which could be CSF or blood. Diagnosis is confirmed when the organism has grown, most often on a chocolate agar plate, but also on Thayer-Martin agar. To differentiate any bacterial growth from other species a small amount of a bacterial colony is tested for oxidase, catalase for which all clinically relevant Neisseria show a positive reaction, and the carbohydrates maltose, sucrose, and glucose, in which N. meningitidis will ferment that is, utilize the glucose and maltose. Finally, serology determines the subgroup of the N. meningitidis, which is important for epidemiological surveillance purposes; this may often only be done in specialized laboratories. The above tests take a minimum of 48–72 hours turnaround time for growing the organism, and up to a week more for serotyping. Growth can and often does fail, either because antibiotics have been given preemptively, or because specimens have been inappropriately transported, as the organism is extremely susceptible to antibiotics and fastidious in its temperature, CO2 and growth medium requirements. Polymerase chain reaction (PCR) tests where available, mostly in industrialized countries, have been increasingly used; PCR can rapidly identify the organism, and works even after antibiotics have been given. Prevention All recent contacts of the infected patient over the 7 days before onset should receive medication to prevent them from contracting the infection. This especially includes young children and their child caregivers or nursery-school contacts, as well as anyone who had direct exposure to the patient through kissing, sharing utensils, or medical interventions such as mouth-to-mouth resuscitation. Anyone who frequently ate, slept or stayed at the patients home during the 7 days before the onset of symptom, or those who sat beside the patient on an airplane flight or classroom for 8 hours or longer, should also receive chemoprophylaxis. The agent of choice is usually oral rifampicin for a few days.Receiving a dose of the Meningococcal vaccine before traveling to a country in the "meningitis belt" or having a booster meningitis vaccine, normally five years apart could prevent someone from getting an infection from the pathogen. Vaccination United States A number of vaccines are available in the U.S. to prevent meningococcal disease. Some of the vaccines cover serogroup B, while others cover A, C, W, and Y. The Centers for Disease Control and Prevention (CDC) recommends all teenagers receive MenACWY vaccine and booster, with optional MenB. MenACWY and MenB are also recommended for people of other ages with various medical conditions and social risk factors.A meningococcal polysaccharide vaccine (MPSV4) has been available since the 1970s and is the only meningococcal vaccine licensed for people older than 55. MPSV4 may be used in people 2–55 years old if the MCV4 vaccines are not available or contraindicated. Two meningococcal conjugate vaccines (MCV4) are licensed for use in the U.S. The first conjugate vaccine was licensed in 2005, the second in 2010. Conjugate vaccines are the preferred vaccine for people 2 through 55 years of age. It is indicated in those with impaired immunity, such as nephrotic syndrome or splenectomy. In June 2012, the U.S. Food and Drug Administration (FDA) approved a combination vaccine against two types of meningococcal diseases and Hib disease for infants and children 6 weeks to 18 months old. The vaccine, Menhibrix, was designed to prevent disease caused by Neisseria meningitidis serogroups C and Y, and Haemophilus influenzae type b (Hib). It was the first meningococcal vaccine that could be given to infants as young as six weeks old.In October 2014 the FDA approved the first vaccine effective against serogroup B, named Trumenba, for use in 10- to 25-year-old individuals. Africa In 2010, the Meningitis Vaccine Project introduced a vaccine called MenAfriVac in the African meningitis belt. It was made by generic drug maker Serum Institute of India and cost 50 U.S. cents per injection. Beginning in Burkina Faso in 2010, it has been given to 215 million people across Benin, Cameroon, Chad, Ivory Coast, Ethiopia, Ghana, Mali, Niger, Mauritania, Nigeria, Senegal, Sudan, Togo and Gambia. The vaccination campaign has resulted in near-elimination of serogroup A meningitis from the participating countries. Treatment Persons with confirmed N. meningitidis infection should be hospitalized immediately for treatment with antibiotics. Because meningococcal disease can disseminate very rapidly, a single dose of intramuscular antibiotic is often given at the earliest possible opportunity, even before hospitalization, if disease symptoms look suspicious enough. Third-generation cephalosporin antibiotics (i.e. cefotaxime, ceftriaxone) should be used to treat a suspected or culture-proven meningococcal infection before antibiotic susceptibility results are available. Clinical practice guidelines endorse empirical treatment in the event a lumbar puncture to collect cerebrospinal fluid (CSF) for laboratory testing cannot first be performed. Antibiotic treatment may affect the results of microbiology tests, but a diagnosis may be made on the basis of blood-cultures and clinical examination. Epidemiology N. meningitidis is a major cause of illness, developmental impairment and death during childhood in industrialized countries and has been responsible for epidemics in Africa and in Asia. Every year, about 2,500 to 3,500 people become infected with N. meningitidis in the US, with a frequency of about 1 in 100,000. Children younger than 5 years are at greatest risk, followed by teenagers of high school age. Rates in the African meningitis belt were as high as 1 in 1,000 to 1 in 100 before introduction of a vaccine in 2010. The incidence of meningococcal disease is highest among infants (children younger than 1-year-old) whose immune system is relatively immature. In industrialized countries there is a second peak of incidence in young adults, who are congregating closely, living in dormitories or smoking. Vaccine development is ongoing.It is spread through saliva and other respiratory secretions during coughing, sneezing, kissing, and chewing on toys. Inhalation of respiratory droplets from a carrier which may be someone who is themselves in the early stages of disease can transmit the bacteria. Close contact with a carrier is the predominant risk factor. Other risk factors include a weakened general or local immune response, such as a recent upper respiratory infection, smoking, and complement deficiency. The incubation period is short, from 2 to 10 days. In susceptible individuals, N. meningitidis may invade the bloodstream and cause a systemic infection, sepsis, disseminated intravascular coagulation, breakdown of circulation, and septic shock. History In 1884 Ettore Marchiafava and Angelo Celli first observed the bacterium inside cells in the cerebral spinal fluid (CSF). In 1887 Anton Weichselbaum isolated the bacterium from the CSF of patients with bacterial meningitis. He named the bacterium Diplococcus intracellularis meningitidis. Biotechnology Components from Neisseria meningitidis are being harnessed in biotechnology. Its Cas9 enzyme is a useful tool in CRISPR gene editing because the enzyme is small and has distinct targeting features to the commonly used enzyme from Streptococcus pyogenes. The cell-surface protein FrpC from Neisseria meningitidis has been engineered to allow covalent coupling between proteins, because it generates a reactive anhydride when exposed to calcium. The bacterium also expresses unique enzymes able to cleave IgA antibodies. See also DNA uptake sequence DNA taken up by Neisseria NmVac4-A/C/Y/W-135 polysaccharide vaccine Sara Branham Matthews microbiologist Shwartzman phenomenon Sepsis References External links "Neisseria meningitidis". NCBI Taxonomy Browser. 487. Type strain of Neisseria meningitidis at BacDive - the Bacterial Diversity Metadatabase

Aarogya, Please give me a short description about Clonorchiasis

Clonorchiasis

Clonorchiasis is an infectious disease caused by the Chinese liver fluke (Clonorchis sinensis) and two related species. Clonorchiasis is a known risk factor for the development of cholangiocarcinoma, a neoplasm of the biliary system.Symptoms of opisthorchiasis caused by Opisthorchis viverrini and by O. felineus are indistinguishable from clonorchiasis caused by Clonorchis sinensis, leading some to argue that the disease by these three parasites should be referred to collectively as clonorchiasis. Signs and symptoms Cause Clonorchiasis sinensis is a trematode (fluke) which is part of the phylum Platyhelminthes. The parasitic worm is as long as 10 to 25 mm and lives in the bile ducts of the liver. It is a hermaphroditic fluke that requires two intermediate hosts. The eggs of the worms are passed in fecal matter into a body of water and are then ingested by mollusks. The water snail is the first intermediate host, in which a miracidium (an embryonated egg discharged in stool) goes through its developmental stages (sporocyst, rediae and cercariae). Freshwater fish are a second intermediate host for the parasitic worm. They become infected when the larva (cercaria) of the worm leaves the snail and penetrates the flesh of the fish. Humans then become infected by eating infected fish that has been undercooked, smoked, pickled, or salted, and from there the cycle repeats. Clonorchiasis is endemic in the Far East, especially in Korea, Japan, Taiwan, and Southern China. Clonorchiasis has been reported in areas to which it is not endemic (including the United States). In such cases, the infection follows the ingestion of undercooked or pickled freshwater fish imported from one of the endemic areas and containing metacercariae. Diagnosis Adult C. sinensis worms can inhabit the bile ducts of humans for 20–25 years without any clear clinical symptoms. This, in addition to the nonspecific symptoms infected persons may develop, can lead to missed diagnoses.Patients are diagnosed when C. sinensis eggs are found in stools. The formalin-ether concentration technique (FECT) method of stool examination is most effective at diagnosing light cases of infection, while the Kato-Katz (KK) method is more suitable for the diagnosing of persons with clonorchiasis. Serological methods that use enzyme-linked immunosorbent assay (ELISA) can help differentiate the eggs of C. sinensis from other flukes. Treatment Praziquantel is the treatment of choice for clonorchiasis. References == External links ==

Can you describe Tuberculous meningitis, to me Aarogya

Tuberculous meningitis

Tuberculous meningitis, also known as TB meningitis or tubercular meningitis, is a specific type of bacterial meningitis caused by the Mycobacterium tuberculosis infection of the meninges—the system of membranes which envelop the central nervous system. Signs and symptoms Fever and headache are the cardinal features; confusion is a late feature and coma bears a poor prognosis. Meningism is absent in a fifth of patients with TB meningitis. Patients may also have focal neurological deficits. Causes Mycobacterium tuberculosis of the meninges is the cardinal feature and the inflammation is concentrated towards the base of the brain. When the inflammation is in the brain stem subarachnoid area, cranial nerve roots may be affected. The symptoms will mimic those of space-occupying lesions.Blood-borne spread certainly occurs, presumably by crossing the blood–brain barrier; but a proportion of patients may get TB meningitis from rupture of a cortical focus in the brain; an even smaller proportion get it from rupture of a bony focus in the spine. Pathophysiology The pathophysiology of tuberculous meningitis involves bacterial invasion of the brain parenchyma meninges or cortex, causing the formation of small subpial foci. These foci, termed Rich foci, are necrotic and expand as the colonies within them multiply. Tubercle (focal) rupture in the subarachnoid space causes meningitis. Diagnosis Diagnosis of TB meningitis is made by analysing cerebrospinal fluid collected by lumbar puncture. When collecting CSF for suspected TB meningitis, a minimum of 1ml of fluid should be taken (preferably 5 to 10ml). The CSF usually has a high protein, low glucose and a raised number of lymphocytes. Acid-fast bacilli are sometimes seen on a CSF smear, but more commonly, M. tuberculosis is grown in culture. A spiderweb clot in the collected CSF is characteristic of TB meningitis, but is a rare finding. ELISPOT testing is not useful for the diagnosis of acute TB meningitis and is often false negative, but may paradoxically become positive after treatment has started, which helps to confirm the diagnosis. Nucleic acid amplification tests (NAAT) This is a group of tests that use polymerase chain reaction (PCR) to detect mycobacterial nucleic acid. These test vary in which nucleic acid sequence they detect and vary in their accuracy. The two most common commercially available tests are the amplified mycobacterium tuberculosis direct test (MTD, Gen-Probe) and Amplicor. In 2007, review concluded that for diagnosing tuberculous meningitis "Individually, the AMTD test appears to perform the best (sensitivity 74% and specificity 98%)", they found the pooled prevalence of TB meningitis to be 29%. Treatment The treatment of TB meningitis is isoniazid, rifampicin, pyrazinamide and ethambutol for two months, followed by isoniazid and rifampicin alone for a further ten months. Steroids help reduce the risk of death in those without HIV. Steroids can be used in the first six weeks of treatment, A few people may require immunomodulatory agents such as thalidomide. Hydrocephalus occurs as a complication in about a third of people with TB meningitis. The addition of aspirin may reduce or delay mortality, possibly by reducing complications such as infarcts. References == External links ==

Please give me a short description about Major depressive disorder , Aarogya

Major depressive disorder

Major depressive disorder (MDD), also known as clinical depression, is a mental disorder characterized by at least two weeks of pervasive low mood, low self-esteem, and loss of interest or pleasure in normally enjoyable activities. Introduced by a group of US clinicians in the mid-1970s, the term was adopted by the American Psychiatric Association for this symptom cluster under mood disorders in the 1980 version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), and has become widely used since. The diagnosis of major depressive disorder is based on the persons reported experiences, behavior reported by relatives or friends, and a mental status examination. There is no laboratory test for the disorder, but testing may be done to rule out physical conditions that can cause similar symptoms. The most common time of onset is in a persons 20s, with females affected about twice as often as males. The course of the disorder varies widely, from one episode lasting months to a lifelong disorder with recurrent major depressive episodes. Those with major depressive disorder are typically treated with psychotherapy and antidepressant medication. Medication appears to be effective, but the effect may be significant only in the most severely depressed. Hospitalization (which may be involuntary) may be necessary in cases with associated self-neglect or a significant risk of harm to self or others. Electroconvulsive therapy (ECT) may be considered if other measures are not effective.Major depressive disorder is believed to be caused by a combination of genetic, environmental, and psychological factors, with about 40% of the risk being genetic. Risk factors include a family history of the condition, major life changes, certain medications, chronic health problems, and substance use disorders. It can negatively affect a persons personal life, work life, or education, and cause issues with a persons sleeping habits, eating habits, and general health. Major depressive disorder affected approximately 163 million people (2% of the worlds population) in 2017. The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France. Lifetime rates are higher in the developed world (15%) compared to the developing world (11%). The disorder causes the second-most years lived with disability, after lower back pain. Symptoms and signs Major depression significantly affects a persons family and personal relationships, work or school life, sleeping and eating habits, and general health. A person having a major depressive episode usually exhibits a low mood, which pervades all aspects of life, and an inability to experience pleasure in previously enjoyable activities. Depressed people may be preoccupied with—or ruminate over—thoughts and feelings of worthlessness, inappropriate guilt or regret, helplessness or hopelessness. Other symptoms of depression include poor concentration and memory, withdrawal from social situations and activities, reduced sex drive, irritability, and thoughts of death or suicide. Insomnia is common; in the typical pattern, a person wakes very early and cannot get back to sleep. Hypersomnia, or oversleeping, can also happen. Some antidepressants may also cause insomnia due to their stimulating effect. In severe cases, depressed people may have psychotic symptoms. These symptoms include delusions or, less commonly, hallucinations, usually unpleasant. People who have had previous episodes with psychotic symptoms are more likely to have them with future episodes.A depressed person may report multiple physical symptoms such as fatigue, headaches, or digestive problems; physical complaints are the most common presenting problem in developing countries, according to the World Health Organizations criteria for depression. Appetite often decreases, resulting in weight loss, although increased appetite and weight gain occasionally occur. Family and friends may notice agitation or lethargy. Older depressed people may have cognitive symptoms of recent onset, such as forgetfulness, and a more noticeable slowing of movements.Depressed children may often display an irritable rather than a depressed mood; most lose interest in school and show a steep decline in academic performance. Diagnosis may be delayed or missed when symptoms are interpreted as "normal moodiness." Elderly people may not present with classical depressive symptoms. Diagnosis and treatment is further complicated in that the elderly are often simultaneously treated with a number of other drugs, and often have other concurrent diseases. Cause The biopsychosocial model proposes that biological, psychological, and social factors all play a role in causing depression. The diathesis–stress model specifies that depression results when a preexisting vulnerability, or diathesis, is activated by stressful life events. The preexisting vulnerability can be either genetic, implying an interaction between nature and nurture, or schematic, resulting from views of the world learned in childhood. American psychiatrist Aaron Beck suggested that a triad of automatic and spontaneous negative thoughts about the self, the world or environment, and the future may lead to other depressive signs and symptoms.Adverse childhood experiences (incorporating childhood abuse, neglect and family dysfunction) markedly increase the risk of major depression, especially if more than one type. Childhood trauma also correlates with severity of depression, poor responsiveness to treatment and length of illness. Some are more susceptible than others to developing mental illness such as depression after trauma, and various genes have been suggested to control susceptibility. Genetics Family and twin studies find that nearly 40% of individual differences in risk for major depressive disorder can be explained by genetic factors. Like most psychiatric disorders, major depressive disorder is likely influenced by many individual genetic changes. In 2018, a genome-wide association study discovered 44 genetic variants linked to risk for major depression; a 2019 study found 102 variants in the genome linked to depression. Research focusing on specific candidate genes has been criticized for its tendency to generate false positive findings. There are also other efforts to examine interactions between life stress and polygenic risk for depression. Other health problems Depression can also arise after a chronic or terminal medical condition, such as HIV/AIDS or asthma, and may be labeled "secondary depression." It is unknown whether the underlying diseases induce depression through effect on quality of life, or through shared etiologies (such as degeneration of the basal ganglia in Parkinsons disease or immune dysregulation in asthma). Depression may also be iatrogenic (the result of healthcare), such as drug-induced depression. Therapies associated with depression include interferons, beta-blockers, isotretinoin, contraceptives, cardiac agents, anticonvulsants, antimigraine drugs, antipsychotics, and hormonal agents such as gonadotropin-releasing hormone agonist. Substance use in early age is associated with increased risk of developing depression later in life. Depression occurring after giving birth is called postpartum depression and is thought to be the result of hormonal changes associated with pregnancy. Seasonal affective disorder, a type of depression associated with seasonal changes in sunlight, is thought to be triggered by decreased sunlight. Vitamin B2, B6 and B12 deficiency may cause depression in females. Pathophysiology The pathophysiology of depression is not completely understood, but current theories center around monoaminergic systems, the circadian rhythm, immunological dysfunction, HPA-axis dysfunction and structural or functional abnormalities of emotional circuits. Derived from the effectiveness of monoaminergic drugs in treating depression, the monoamine theory posits that insufficient activity of monoamine neurotransmitters is the primary cause of depression. Evidence for the monoamine theory comes from multiple areas. First, acute depletion of tryptophan—a necessary precursor of serotonin and a monoamine—can cause depression in those in remission or relatives of people who are depressed, suggesting that decreased serotonergic neurotransmission is important in depression. Second, the correlation between depression risk and polymorphisms in the 5-HTTLPR gene, which codes for serotonin receptors, suggests a link. Third, decreased size of the locus coeruleus, decreased activity of tyrosine hydroxylase, increased density of alpha-2 adrenergic receptor, and evidence from rat models suggest decreased adrenergic neurotransmission in depression. Furthermore, decreased levels of homovanillic acid, altered response to dextroamphetamine, responses of depressive symptoms to dopamine receptor agonists, decreased dopamine receptor D1 binding in the striatum, and polymorphism of dopamine receptor genes implicate dopamine, another monoamine, in depression. Lastly, increased activity of monoamine oxidase, which degrades monoamines, has been associated with depression. However, the monoamine theory is inconsistent with observations that serotonin depletion does not cause depression in healthy persons, that antidepressants instantly increase levels of monoamines but take weeks to work, and the existence of atypical antidepressants which can be effective despite not targeting this pathway. One proposed explanation for the therapeutic lag, and further support for the deficiency of monoamines, is a desensitization of self-inhibition in raphe nuclei by the increased serotonin mediated by antidepressants. However, disinhibition of the dorsal raphe has been proposed to occur as a result of decreased serotonergic activity in tryptophan depletion, resulting in a depressed state mediated by increased serotonin. Further countering the monoamine hypothesis is the fact that rats with lesions of the dorsal raphe are not more depressive than controls, the finding of increased jugular 5-HIAA in people who are depressed that normalized with selective serotonin reuptake inhibitor (SSRI) treatment, and the preference for carbohydrates in people who are depressed. Already limited, the monoamine hypothesis has been further oversimplified when presented to the general public. A 2022 review found no consistent evidence supporting the serotonin hypothesis, linking serotonin levels and depression.Immune system abnormalities have been observed, including increased levels of cytokines involved in generating sickness behavior (which shares overlap with depression). The effectiveness of nonsteroidal anti-inflammatory drugs (NSAIDs) and cytokine inhibitors in treating depression, and normalization of cytokine levels after successful treatment further suggest immune system abnormalities in depression.HPA-axis abnormalities have been suggested in depression given the association of CRHR1 with depression and the increased frequency of dexamethasone test non-suppression in people who are depressed. However, this abnormality is not adequate as a diagnosis tool, because its sensitivity is only 44%. These stress-related abnormalities are thought to be the cause of hippocampal volume reductions seen in people who are depressed. Furthermore, a meta-analysis yielded decreased dexamethasone suppression, and increased response to psychological stressors. Further abnormal results have been obscured with the cortisol awakening response, with increased response being associated with depression.Theories unifying neuroimaging findings have been proposed. The first model proposed is the limbic-cortical model, which involves hyperactivity of the ventral paralimbic regions and hypoactivity of frontal regulatory regions in emotional processing. Another model, the cortico-striatal model, suggests that abnormalities of the prefrontal cortex in regulating striatal and subcortical structures result in depression. Another model proposes hyperactivity of salience structures in identifying negative stimuli, and hypoactivity of cortical regulatory structures resulting in a negative emotional bias and depression, consistent with emotional bias studies. Diagnosis Clinical assessment A diagnostic assessment may be conducted by a suitably trained general practitioner, or by a psychiatrist or psychologist, who records the persons current circumstances, biographical history, current symptoms, family history, and alcohol and drug use. The assessment also includes a mental state examination, which is an assessment of the persons current mood and thought content, in particular the presence of themes of hopelessness or pessimism, self-harm or suicide, and an absence of positive thoughts or plans. Specialist mental health services are rare in rural areas, and thus diagnosis and management is left largely to primary-care clinicians. This issue is even more marked in developing countries. Rating scales are not used to diagnose depression, but they provide an indication of the severity of symptoms for a time period, so a person who scores above a given cut-off point can be more thoroughly evaluated for a depressive disorder diagnosis. Several rating scales are used for this purpose; these include the Hamilton Rating Scale for Depression, the Beck Depression Inventory or the Suicide Behaviors Questionnaire-Revised.Primary-care physicians have more difficulty with underrecognition and undertreatment of depression compared to psychiatrists. These cases may be missed because for some people with depression, physical symptoms often accompany depression. In addition, there may also be barriers related to the person, provider, and/or the medical system. Non-psychiatrist physicians have been shown to miss about two-thirds of cases, although there is some evidence of improvement in the number of missed cases.A doctor generally performs a medical examination and selected investigations to rule out other causes of depressive symptoms. These include blood tests measuring TSH and thyroxine to exclude hypothyroidism; basic electrolytes and serum calcium to rule out a metabolic disturbance; and a full blood count including ESR to rule out a systemic infection or chronic disease. Adverse affective reactions to medications or alcohol misuse may be ruled out, as well. Testosterone levels may be evaluated to diagnose hypogonadism, a cause of depression in men. Vitamin D levels might be evaluated, as low levels of vitamin D have been associated with greater risk for depression. Subjective cognitive complaints appear in older depressed people, but they can also be indicative of the onset of a dementing disorder, such as Alzheimers disease. Cognitive testing and brain imaging can help distinguish depression from dementia. A CT scan can exclude brain pathology in those with psychotic, rapid-onset or otherwise unusual symptoms. No biological tests confirm major depression. In general, investigations are not repeated for a subsequent episode unless there is a medical indication. DSM and ICD criteria The most widely used criteria for diagnosing depressive conditions are found in the American Psychiatric Associations Diagnostic and Statistical Manual of Mental Disorders (DSM) and the World Health Organizations International Statistical Classification of Diseases and Related Health Problems (ICD). The latter system is typically used in European countries, while the former is used in the US and many other non-European nations, and the authors of both have worked towards conforming one with the other. Both DSM and ICD mark out typical (main) depressive symptoms. The most recent edition of the DSM is the Fifth Edition, Text Revision (DSM-5-TR), and the most recent edition of the ICD is the Eleventh Edition (ICD-11).Under mood disorders, ICD-11 classifies major depressive disorder as either single episode depressive disorder (where there is no history of depressive episodes, or of mania) or recurrent depressive disorder (where there is a history of prior episodes, with no history of mania). ICD-11 symptoms, present nearly every day for at least two weeks, are a depressed mood or anhedonia, accompanied by other symptoms such as "difficulty concentrating, feelings of worthlessness or excessive or inappropriate guilt, hopelessness, recurrent thoughts of death or suicide, changes in appetite or sleep, psychomotor agitation or retardation, and reduced energy or fatigue." These symptoms must affect work, social, or domestic activities. The ICD-11 system allows further specifiers for the current depressive episode: the severity (mild, moderate, severe, unspecified); the presence of psychotic symptoms (with or without psychotic symptoms); and the degree of remission if relevant (currently in partial remission, currently in full remission). These two disorders are classified as "Depressive disorders", in the category of "Mood disorders".According to DSM-5, there are two main depressive symptoms: a depressed mood, and loss of interest/pleasure in activities (anhedonia). These symptoms, as well as five out of the nine more specific symptoms listed, must frequently occur for more than two weeks (to the extent in which it impairs functioning) for the diagnosis. Major depressive disorder is classified as a mood disorder in DSM-5. The diagnosis hinges on the presence of single or recurrent major depressive episodes. Further qualifiers are used to classify both the episode itself and the course of the disorder. The category Unspecified Depressive Disorder is diagnosed if the depressive episodes manifestation does not meet the criteria for a major depressive episode. Major depressive episode A major depressive episode is characterized by the presence of a severely depressed mood that persists for at least two weeks. Episodes may be isolated or recurrent and are categorized as mild (few symptoms in excess of minimum criteria), moderate, or severe (marked impact on social or occupational functioning). An episode with psychotic features—commonly referred to as psychotic depression—is automatically rated as severe. If the person has had an episode of mania or markedly elevated mood, a diagnosis of bipolar disorder is made instead. Depression without mania is sometimes referred to as unipolar because the mood remains at one emotional state or "pole".Bereavement is not an exclusion criterion in DSM-5, and it is up to the clinician to distinguish between normal reactions to a loss and MDD. Excluded are a range of related diagnoses, including dysthymia, which involves a chronic but milder mood disturbance; recurrent brief depression, consisting of briefer depressive episodes; minor depressive disorder, whereby only some symptoms of major depression are present; and adjustment disorder with depressed mood, which denotes low mood resulting from a psychological response to an identifiable event or stressor. Subtypes The DSM-5 recognizes six further subtypes of MDD, called specifiers, in addition to noting the length, severity and presence of psychotic features: "Melancholic depression" is characterized by a loss of pleasure in most or all activities, a failure of reactivity to pleasurable stimuli, a quality of depressed mood more pronounced than that of grief or loss, a worsening of symptoms in the morning hours, early-morning waking, psychomotor retardation, excessive weight loss (not to be confused with anorexia nervosa), or excessive guilt. "Atypical depression" is characterized by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite (comfort eating), excessive sleep or sleepiness (hypersomnia), a sensation of heaviness in limbs known as leaden paralysis, and significant long-term social impairment as a consequence of hypersensitivity to perceived interpersonal rejection. "Catatonic depression" is a rare and severe form of major depression involving disturbances of motor behavior and other symptoms. Here, the person is mute and almost stuporous, and either remains immobile or exhibits purposeless or even bizarre movements. Catatonic symptoms also occur in schizophrenia or in manic episodes, or may be caused by neuroleptic malignant syndrome. "Depression with anxious distress" was added into the DSM-5 as a means to emphasize the common co-occurrence between depression or mania and anxiety, as well as the risk of suicide of depressed individuals with anxiety. Specifying in such a way can also help with the prognosis of those diagnosed with a depressive or bipolar disorder. "Depression with peri-partum onset" refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth or while a woman is pregnant. DSM-IV-TR used the classification "postpartum depression," but this was changed to not exclude cases of depressed woman during pregnancy. Depression with peripartum onset has an incidence rate of 3–6% among new mothers. The DSM-V mandates that to qualify as depression with peripartum onset, onset occurs during pregnancy or within one month of delivery. "Seasonal affective disorder" (SAD) is a form of depression in which depressive episodes come on in the autumn or winter, and resolve in spring. The diagnosis is made if at least two episodes have occurred in colder months with none at other times, over a two-year period or longer. Differential diagnoses To confirm major depressive disorder as the most likely diagnosis, other potential diagnoses must be considered, including dysthymia, adjustment disorder with depressed mood, or bipolar disorder. Dysthymia is a chronic, milder mood disturbance in which a person reports a low mood almost daily over a span of at least two years. The symptoms are not as severe as those for major depression, although people with dysthymia are vulnerable to secondary episodes of major depression (sometimes referred to as double depression). Adjustment disorder with depressed mood is a mood disturbance appearing as a psychological response to an identifiable event or stressor, in which the resulting emotional or behavioral symptoms are significant but do not meet the criteria for a major depressive episode.Other disorders need to be ruled out before diagnosing major depressive disorder. They include depressions due to physical illness, medications, and substance use disorders. Depression due to physical illness is diagnosed as a mood disorder due to a general medical condition. This condition is determined based on history, laboratory findings, or physical examination. When the depression is caused by a medication, non-medical use of a psychoactive substance, or exposure to a toxin, it is then diagnosed as a specific mood disorder (previously called substance-induced mood disorder). Screening and prevention Preventive efforts may result in decreases in rates of the condition of between 22 and 38%. Since 2016, the United States Preventive Services Task Force (USPSTF) has recommended screening for depression among those over the age 12; though a 2005 Cochrane review found that the routine use of screening questionnaires has little effect on detection or treatment. Screening the general population is not recommended by authorities in the UK or Canada.Behavioral interventions, such as interpersonal therapy and cognitive-behavioral therapy, are effective at preventing new onset depression. Because such interventions appear to be most effective when delivered to individuals or small groups, it has been suggested that they may be able to reach their large target audience most efficiently through the Internet.The Netherlands mental health care system provides preventive interventions, such as the "Coping with Depression" course (CWD) for people with sub-threshold depression. The course is claimed to be the most successful of psychoeducational interventions for the treatment and prevention of depression (both for its adaptability to various populations and its results), with a risk reduction of 38% in major depression and an efficacy as a treatment comparing favorably to other psychotherapies. Management The most common and effective treatments for depression are psychotherapy, medication, and electroconvulsive therapy (ECT); a combination of treatments is the most effective approach when depression is resistant to treatment. American Psychiatric Association treatment guidelines recommend that initial treatment should be individually tailored based on factors including severity of symptoms, co-existing disorders, prior treatment experience, and personal preference. Options may include pharmacotherapy, psychotherapy, exercise, ECT, transcranial magnetic stimulation (TMS) or light therapy. Antidepressant medication is recommended as an initial treatment choice in people with mild, moderate, or severe major depression, and should be given to all people with severe depression unless ECT is planned. There is evidence that collaborative care by a team of health care practitioners produces better results than routine single-practitioner care.Psychotherapy is the treatment of choice (over medication) for people under 18, and cognitive behavioral therapy (CBT), third wave CBT and interpersonal therapy may help prevent depression. The UK National Institute for Health and Care Excellence (NICE) 2004 guidelines indicate that antidepressants should not be used for the initial treatment of mild depression because the risk-benefit ratio is poor. The guidelines recommend that antidepressants treatment in combination with psychosocial interventions should be considered for: People with a history of moderate or severe depression Those with mild depression that has been present for a long period As a second line treatment for mild depression that persists after other interventions As a first line treatment for moderate or severe depression.The guidelines further note that antidepressant treatment should be continued for at least six months to reduce the risk of relapse, and that SSRIs are better tolerated than tricyclic antidepressants.Treatment options are more limited in developing countries, where access to mental health staff, medication, and psychotherapy is often difficult. Development of mental health services is minimal in many countries; depression is viewed as a phenomenon of the developed world despite evidence to the contrary, and not as an inherently life-threatening condition. There is insufficient evidence to determine the effectiveness of psychological versus medical therapy in children. Lifestyle Physical exercise has been found to be effective for major depression, and may be recommended to people who are willing, motivated, and healthy enough to participate in an exercise program as treatment. It is equivalent to the use of medications or psychological therapies in most people. In older people it does appear to decrease depression. Sleep and diet may also play a role in depression, and interventions in these areas may be an effective add-on to conventional methods. In observational studies, smoking cessation has benefits in depression as large as or larger than those of medications. Talking therapies Talking therapy (psychotherapy) can be delivered to individuals, groups, or families by mental health professionals, including psychotherapists, psychiatrists, psychologists, clinical social workers, counselors, and psychiatric nurses. A 2012 review found psychotherapy to be better than no treatment but not other treatments. With more complex and chronic forms of depression, a combination of medication and psychotherapy may be used. There is moderate-quality evidence that psychological therapies are a useful addition to standard antidepressant treatment of treatment-resistant depression in the short term. Psychotherapy has been shown to be effective in older people. Successful psychotherapy appears to reduce the recurrence of depression even after it has been stopped or replaced by occasional booster sessions. The most-studied form of psychotherapy for depression is CBT, which teaches clients to challenge self-defeating, but enduring ways of thinking (cognitions) and change counter-productive behaviors. CBT can perform as well as antidepressants in people with major depression. CBT has the most research evidence for the treatment of depression in children and adolescents, and CBT and interpersonal psychotherapy (IPT) are preferred therapies for adolescent depression. In people under 18, according to the National Institute for Health and Clinical Excellence, medication should be offered only in conjunction with a psychological therapy, such as CBT, interpersonal therapy, or family therapy. Several variables predict success for cognitive behavioral therapy in adolescents: higher levels of rational thoughts, less hopelessness, fewer negative thoughts, and fewer cognitive distortions. CBT is particularly beneficial in preventing relapse. Cognitive behavioral therapy and occupational programs (including modification of work activities and assistance) have been shown to be effective in reducing sick days taken by workers with depression. Several variants of cognitive behavior therapy have been used in those with depression, the most notable being rational emotive behavior therapy, and mindfulness-based cognitive therapy. Mindfulness-based stress reduction programs may reduce depression symptoms. Mindfulness programs also appear to be a promising intervention in youth. Problem solving therapy, cognitive behavioral therapy, and interpersonal therapy are effective interventions in the elderly.Psychoanalysis is a school of thought, founded by Sigmund Freud, which emphasizes the resolution of unconscious mental conflicts. Psychoanalytic techniques are used by some practitioners to treat clients presenting with major depression. A more widely practiced therapy, called psychodynamic psychotherapy, is in the tradition of psychoanalysis but less intensive, meeting once or twice a week. It also tends to focus more on the persons immediate problems, and has an additional social and interpersonal focus. In a meta-analysis of three controlled trials of Short Psychodynamic Supportive Psychotherapy, this modification was found to be as effective as medication for mild to moderate depression. Antidepressants Conflicting results have arisen from studies that look at the effectiveness of antidepressants in people with acute, mild to moderate depression. A review commissioned by the National Institute for Health and Care Excellence (UK) concluded that there is strong evidence that SSRIs, such as escitalopram, paroxetine, and sertraline, have greater efficacy than placebo on achieving a 50% reduction in depression scores in moderate and severe major depression, and that there is some evidence for a similar effect in mild depression. Similarly, a Cochrane systematic review of clinical trials of the generic tricyclic antidepressant amitriptyline concluded that there is strong evidence that its efficacy is superior to placebo. Antidepressants work less well for the elderly than for younger individuals with depression.To find the most effective antidepressant medication with minimal side-effects, the dosages can be adjusted, and if necessary, combinations of different classes of antidepressants can be tried. Response rates to the first antidepressant administered range from 50 to 75%, and it can take at least six to eight weeks from the start of medication to improvement. Antidepressant medication treatment is usually continued for 16 to 20 weeks after remission, to minimize the chance of recurrence, and even up to one year of continuation is recommended. People with chronic depression may need to take medication indefinitely to avoid relapse.SSRIs are the primary medications prescribed, owing to their relatively mild side-effects, and because they are less toxic in overdose than other antidepressants. People who do not respond to one SSRI can be switched to another antidepressant, and this results in improvement in almost 50% of cases. Another option is to switch to the atypical antidepressant bupropion. Venlafaxine, an antidepressant with a different mechanism of action, may be modestly more effective than SSRIs. However, venlafaxine is not recommended in the UK as a first-line treatment because of evidence suggesting its risks may outweigh benefits, and it is specifically discouraged in children and adolescents as it increases the risk of suicidal thoughts or attempts.For children and adolescents with moderate-to-severe depressive disorder, fluoxetine seems to be the best treatment (either with or without cognitive behavioural therapy) but more research is needed to be certain. Sertraline, escitalopram, duloxetine might also help in reducing symptoms. Some antidepressants have not been shown to be effective. Medications are not recommended in children with mild disease.There is also insufficient evidence to determine effectiveness in those with depression complicated by dementia. Any antidepressant can cause low blood sodium levels; nevertheless, it has been reported more often with SSRIs. It is not uncommon for SSRIs to cause or worsen insomnia; the sedating atypical antidepressant mirtazapine can be used in such cases.Irreversible monoamine oxidase inhibitors, an older class of antidepressants, have been plagued by potentially life-threatening dietary and drug interactions. They are still used only rarely, although newer and better-tolerated agents of this class have been developed. The safety profile is different with reversible monoamine oxidase inhibitors, such as moclobemide, where the risk of serious dietary interactions is negligible and dietary restrictions are less strict.It is unclear whether antidepressants affect a persons risk of suicide. For children, adolescents, and probably young adults between 18 and 24 years old, there is a higher risk of both suicidal ideations and suicidal behavior in those treated with SSRIs. For adults, it is unclear whether SSRIs affect the risk of suicidality. One review found no connection; another an increased risk; and a third no risk in those 25–65 years old and a decreased risk in those more than 65. A black box warning was introduced in the United States in 2007 on SSRIs and other antidepressant medications due to the increased risk of suicide in people younger than 24 years old. Similar precautionary notice revisions were implemented by the Japanese Ministry of Health. Other medications and supplements The combined use of antidepressants plus benzodiazepines demonstrates improved effectiveness when compared to antidepressants alone, but these effects may not endure. The addition of a benzodiazepine is balanced against possible harms and other alternative treatment strategies when antidepressant mono-therapy is considered inadequate.Ketamine may have a rapid antidepressant effect lasting less than two weeks; there is limited evidence of any effect after that, common acute side effects, and longer-term studies of safety and adverse effects are needed. A nasal spray form of esketamine was approved by the FDA in March 2019 for use in treatment-resistant depression when combined with an oral antidepressant; risk of substance use disorder and concerns about its safety, serious adverse effects, tolerability, effect on suicidality, lack of information about dosage, whether the studies on it adequately represent broad populations, and escalating use of the product have been raised by an international panel of experts.There is insufficient high quality evidence to suggest omega-3 fatty acids are effective in depression. There is limited evidence that vitamin D supplementation is of value in alleviating the symptoms of depression in individuals who are vitamin D-deficient. Lithium appears effective at lowering the risk of suicide in those with bipolar disorder and unipolar depression to nearly the same levels as the general population. There is a narrow range of effective and safe dosages of lithium thus close monitoring may be needed. Low-dose thyroid hormone may be added to existing antidepressants to treat persistent depression symptoms in people who have tried multiple courses of medication. Limited evidence suggests stimulants, such as amphetamine and modafinil, may be effective in the short term, or as adjuvant therapy. Also, it is suggested that folate supplements may have a role in depression management. There is tentative evidence for benefit from testosterone in males. Electroconvulsive therapy Electroconvulsive therapy (ECT) is a standard psychiatric treatment in which seizures are electrically induced in a person with depression to provide relief from psychiatric illnesses.: 1880  ECT is used with informed consent as a last line of intervention for major depressive disorder. A round of ECT is effective for about 50% of people with treatment-resistant major depressive disorder, whether it is unipolar or bipolar. Follow-up treatment is still poorly studied, but about half of people who respond relapse within twelve months. Aside from effects in the brain, the general physical risks of ECT are similar to those of brief general anesthesia.: 259  Immediately following treatment, the most common adverse effects are confusion and memory loss. ECT is considered one of the least harmful treatment options available for severely depressed pregnant women.A usual course of ECT involves multiple administrations, typically given two or three times per week, until the person no longer has symptoms. ECT is administered under anesthesia with a muscle relaxant. Electroconvulsive therapy can differ in its application in three ways: electrode placement, frequency of treatments, and the electrical waveform of the stimulus. These three forms of application have significant differences in both adverse side effects and symptom remission. After treatment, drug therapy is usually continued, and some people receive maintenance ECT.ECT appears to work in the short term via an anticonvulsant effect mostly in the frontal lobes, and longer term via neurotrophic effects primarily in the medial temporal lobe. Other Transcranial magnetic stimulation (TMS) or deep transcranial magnetic stimulation is a noninvasive method used to stimulate small regions of the brain. TMS was approved by the FDA for treatment-resistant major depressive disorder (trMDD) in 2008 and as of 2014 evidence supports that it is probably effective. The American Psychiatric Association, the Canadian Network for Mood and Anxiety Disorders, and the Royal Australia and New Zealand College of Psychiatrists have endorsed TMS for trMDD. Transcranial direct current stimulation (tDCS) is another noninvasive method used to stimulate small regions of the brain with a weak electric current. Several meta-analyses have concluded that active tDCS was useful for treating depression.There is a small amount of evidence that sleep deprivation may improve depressive symptoms in some individuals, with the effects usually showing up within a day. This effect is usually temporary. Besides sleepiness, this method can cause a side effect of mania or hypomania. There is insufficient evidence for Reiki and dance movement therapy in depression. Cannabis is specifically not recommended as a treatment. Prognosis Studies have shown that 80% of those with a first major depressive episode will have at least one more during their life, with a lifetime average of four episodes. Other general population studies indicate that around half those who have an episode recover (whether treated or not) and remain well, while the other half will have at least one more, and around 15% of those experience chronic recurrence. Studies recruiting from selective inpatient sources suggest lower recovery and higher chronicity, while studies of mostly outpatients show that nearly all recover, with a median episode duration of 11 months. Around 90% of those with severe or psychotic depression, most of whom also meet criteria for other mental disorders, experience recurrence. Cases when outcome is poor are associated with inappropriate treatment, severe initial symptoms including psychosis, early age of onset, previous episodes, incomplete recovery after one year of treatment, pre-existing severe mental or medical disorder, and family dysfunction.A high proportion of people who experience full symptomatic remission still have at least one not fully resolved symptom after treatment. Recurrence or chronicity is more likely if symptoms have not fully resolved with treatment. Current guidelines recommend continuing antidepressants for four to six months after remission to prevent relapse. Evidence from many randomized controlled trials indicates continuing antidepressant medications after recovery can reduce the chance of relapse by 70% (41% on placebo vs. 18% on antidepressant). The preventive effect probably lasts for at least the first 36 months of use.Major depressive episodes often resolve over time, whether or not they are treated. Outpatients on a waiting list show a 10–15% reduction in symptoms within a few months, with approximately 20% no longer meeting the full criteria for a depressive disorder. The median duration of an episode has been estimated to be 23 weeks, with the highest rate of recovery in the first three months. According to a 2013 review, 23% of untreated adults with mild to moderate depression will remit within 3 months, 32% within 6 months and 53% within 12 months. Ability to work Depression may affect peoples ability to work. The combination of usual clinical care and support with return to work (like working less hours or changing tasks) probably reduces sick leave by 15%, and leads to fewer depressive symptoms and improved work capacity, reducing sick leave by an annual average of 25 days per year. Helping depressed people return to work without a connection to clinical care has not been shown to have an effect on sick leave days. Additional psychological interventions (such as online cognitive behavioral therapy) lead to fewer sick days compared to standard management only. Streamlining care or adding specific providers for depression care may help to reduce sick leave. Life expectancy and the risk of suicide Depressed individuals have a shorter life expectancy than those without depression, in part because people who are depressed are at risk of dying of suicide. About 50% of people who die of suicide have a mood disorder such as major depression, and the risk is especially high if a person has a marked sense of hopelessness or has both depression and borderline personality disorder. About 2–8% of adults with major depression die by suicide. In the US, the lifetime risk of suicide associated with a diagnosis of major depression is estimated at 7% for men and 1% for women, even though suicide attempts are more frequent in women.Depressed people have a higher rate of dying from other causes. There is a 1.5- to 2-fold increased risk of cardiovascular disease, independent of other known risk factors, and is itself linked directly or indirectly to risk factors such as smoking and obesity. People with major depression are less likely to follow medical recommendations for treating and preventing cardiovascular disorders, further increasing their risk of medical complications. Cardiologists may not recognize underlying depression that complicates a cardiovascular problem under their care. Epidemiology Major depressive disorder affected approximately 163 million people in 2017 (2% of the global population). The percentage of people who are affected at one point in their life varies from 7% in Japan to 21% in France. In most countries the number of people who have depression during their lives falls within an 8–18% range.In the United States, 8.4% of adults (21 million individuals) have at least one episode within a year-long period; the probability of having a major depressive episode is higher for females than males (10.5% to 6.2%), and highest for those aged 18 to 25 (17%). Among adolescents between the ages of 12 and 17, 17% of the U.S. population (4.1 million individuals) had a major depressive episode in 2020 (females 25.2%, males 9.2%). Among individuals reporting two or more races, the US prevalence is highest.Major depression is about twice as common in women as in men, although it is unclear why this is so, and whether factors unaccounted for are contributing to this. The relative increase in occurrence is related to pubertal development rather than chronological age, reaches adult ratios between the ages of 15 and 18, and appears associated with psychosocial more than hormonal factors. In 2019, major depressive disorder was identified (using either the DSM-IV-TR or ICD-10) in the Global Burden of Disease Study as the fifth most common cause of years lived with disability and the 18th most common for disability-adjusted life years.People are most likely to develop their first depressive episode between the ages of 30 and 40, and there is a second, smaller peak of incidence between ages 50 and 60. The risk of major depression is increased with neurological conditions such as stroke, Parkinsons disease, or multiple sclerosis, and during the first year after childbirth. It is also more common after cardiovascular illnesses, and is related more to those with a poor cardiac disease outcome than to a better one. Depressive disorders are more common in urban populations than in rural ones and the prevalence is increased in groups with poorer socioeconomic factors, e.g., homelessness. Depression is common among those over 65 years of age and increases in frequency beyond this age. The risk of depression increases in relation to the frailty of the individual. Depression is one of the most important factors which negatively impact quality of life in adults, as well as the elderly. Both symptoms and treatment among the elderly differ from those of the rest of the population.Major depression was the leading cause of disease burden in North America and other high-income countries, and the fourth-leading cause worldwide as of 2006. In the year 2030, it is predicted to be the second-leading cause of disease burden worldwide after HIV, according to the WHO. Delay or failure in seeking treatment after relapse and the failure of health professionals to provide treatment are two barriers to reducing disability. Comorbidity Major depression frequently co-occurs with other psychiatric problems. The 1990–92 National Comorbidity Survey (US) reported that half of those with major depression also have lifetime anxiety and its associated disorders, such as generalized anxiety disorder. Anxiety symptoms can have a major impact on the course of a depressive illness, with delayed recovery, increased risk of relapse, greater disability and increased suicidal behavior. Depressed people have increased rates of alcohol and substance use, particularly dependence, and around a third of individuals diagnosed with attention deficit hyperactivity disorder (ADHD) develop comorbid depression. Post-traumatic stress disorder and depression often co-occur. Depression may also coexist with ADHD, complicating the diagnosis and treatment of both. Depression is also frequently comorbid with alcohol use disorder and personality disorders. Depression can also be exacerbated during particular months (usually winter) in those with seasonal affective disorder. While overuse of digital media has been associated with depressive symptoms, using digital media may also improve mood in some situations.Depression and pain often co-occur. One or more pain symptoms are present in 65% of people who have depression, and anywhere from 5 to 85% of people who are experiencing pain will also have depression, depending on the setting—a lower prevalence in general practice, and higher in specialty clinics. Depression is often underrecognized, and therefore undertreated, in patients presenting with pain. Depression often coexists with physical disorders common among the elderly, such as stroke, other cardiovascular diseases, Parkinsons disease, and chronic obstructive pulmonary disease. History The Ancient Greek physician Hippocrates described a syndrome of melancholia (μελαγχολία, melankholía) as a distinct disease with particular mental and physical symptoms; he characterized all "fears and despondencies, if they last a long time" as being symptomatic of the ailment. It was a similar but far broader concept than todays depression; prominence was given to a clustering of the symptoms of sadness, dejection, and despondency, and often fear, anger, delusions and obsessions were included. The term depression itself was derived from the Latin verb deprimere, meaning "to press down". From the 14th century, "to depress" meant to subjugate or to bring down in spirits. It was used in 1665 in English author Richard Bakers Chronicle to refer to someone having "a great depression of spirit", and by English author Samuel Johnson in a similar sense in 1753. The term also came into use in physiology and economics. An early usage referring to a psychiatric symptom was by French psychiatrist Louis Delasiauve in 1856, and by the 1860s it was appearing in medical dictionaries to refer to a physiological and metaphorical lowering of emotional function. Since Aristotle, melancholia had been associated with men of learning and intellectual brilliance, a hazard of contemplation and creativity. The newer concept abandoned these associations and through the 19th century, became more associated with women.Although melancholia remained the dominant diagnostic term, depression gained increasing currency in medical treatises and was a synonym by the end of the century; German psychiatrist Emil Kraepelin may have been the first to use it as the overarching term, referring to different kinds of melancholia as depressive states. Freud likened the state of melancholia to mourning in his 1917 paper Mourning and Melancholia. He theorized that objective loss, such as the loss of a valued relationship through death or a romantic break-up, results in subjective loss as well; the depressed individual has identified with the object of affection through an unconscious, narcissistic process called the libidinal cathexis of the ego. Such loss results in severe melancholic symptoms more profound than mourning; not only is the outside world viewed negatively but the ego itself is compromised. The persons decline of self-perception is revealed in his belief of his own blame, inferiority, and unworthiness. He also emphasized early life experiences as a predisposing factor. Adolf Meyer put forward a mixed social and biological framework emphasizing reactions in the context of an individuals life, and argued that the term depression should be used instead of melancholia. The first version of the DSM (DSM-I, 1952) contained depressive reaction and the DSM-II (1968) depressive neurosis, defined as an excessive reaction to internal conflict or an identifiable event, and also included a depressive type of manic-depressive psychosis within Major affective disorders.The term unipolar (along with the related term bipolar) was coined by the neurologist and psychiatrist Karl Kleist, and subsequently used by his disciples Edda Neele and Karl Leonhard.The term Major depressive disorder was introduced by a group of US clinicians in the mid-1970s as part of proposals for diagnostic criteria based on patterns of symptoms (called the "Research Diagnostic Criteria", building on earlier Feighner Criteria), and was incorporated into the DSM-III in 1980. The American Psychiatric Association added "major depressive disorder" to the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), as a split of the previous depressive neurosis in the DSM-II, which also encompassed the conditions now known as dysthymia and adjustment disorder with depressed mood. To maintain consistency the ICD-10 used the same criteria, with only minor alterations, but using the DSM diagnostic threshold to mark a mild depressive episode, adding higher threshold categories for moderate and severe episodes. The ancient idea of melancholia still survives in the notion of a melancholic subtype. The new definitions of depression were widely accepted, albeit with some conflicting findings and views. There have been some continued empirically based arguments for a return to the diagnosis of melancholia. There has been some criticism of the expansion of coverage of the diagnosis, related to the development and promotion of antidepressants and the biological model since the late 1950s. Society and culture Terminology The term "depression" is used in a number of different ways. It is often used to mean this syndrome but may refer to other mood disorders or simply to a low mood. Peoples conceptualizations of depression vary widely, both within and among cultures. "Because of the lack of scientific certainty," one commentator has observed, "the debate over depression turns on questions of language. What we call it—disease, disorder, state of mind—affects how we view, diagnose, and treat it." There are cultural differences in the extent to which serious depression is considered an illness requiring personal professional treatment, or an indicator of something else, such as the need to address social or moral problems, the result of biological imbalances, or a reflection of individual differences in the understanding of distress that may reinforce feelings of powerlessness, and emotional struggle. Stigma Historical figures were often reluctant to discuss or seek treatment for depression due to social stigma about the condition, or due to ignorance of diagnosis or treatments. Nevertheless, analysis or interpretation of letters, journals, artwork, writings, or statements of family and friends of some historical personalities has led to the presumption that they may have had some form of depression. People who may have had depression include English author Mary Shelley, American-British writer Henry James, and American president Abraham Lincoln. Some well-known contemporary people with possible depression include Canadian songwriter Leonard Cohen and American playwright and novelist Tennessee Williams. Some pioneering psychologists, such as Americans William James and John B. Watson, dealt with their own depression. There has been a continuing discussion of whether neurological disorders and mood disorders may be linked to creativity, a discussion that goes back to Aristotelian times. British literature gives many examples of reflections on depression. English philosopher John Stuart Mill experienced a several-months-long period of what he called "a dull state of nerves", when one is "unsusceptible to enjoyment or pleasurable excitement; one of those moods when what is pleasure at other times, becomes insipid or indifferent". He quoted English poet Samuel Taylor Coleridges "Dejection" as a perfect description of his case: "A grief without a pang, void, dark and drear, / A drowsy, stifled, unimpassioned grief, / Which finds no natural outlet or relief / In word, or sigh, or tear." English writer Samuel Johnson used the term "the black dog" in the 1780s to describe his own depression, and it was subsequently popularized by British Prime Minister Sir Winston Churchill, who also had the disorder. Johann Wolfgang von Goethe in his Faust, Part I, published in 1808, has Mephistopheles assume the form of a black dog, specifically a poodle. Social stigma of major depression is widespread, and contact with mental health services reduces this only slightly. Public opinions on treatment differ markedly to those of health professionals; alternative treatments are held to be more helpful than pharmacological ones, which are viewed poorly. In the UK, the Royal College of Psychiatrists and the Royal College of General Practitioners conducted a joint Five-year Defeat Depression campaign to educate and reduce stigma from 1992 to 1996; a MORI study conducted afterwards showed a small positive change in public attitudes to depression and treatment. References === Cited works ===

Aarogya, give me a short description about MERRF syndrome

MERRF syndrome

MERRF syndrome (or myoclonic epilepsy with ragged red fibers) is a mitochondrial disease. It is extremely rare, and has varying degrees of expressivity owing to heteroplasmy. MERRF syndrome affects different parts of the body, particularly the muscles and nervous system. The signs and symptoms of this disorder appear at an early age, generally childhood or adolescence. The causes of MERRF syndrome are difficult to determine, but because it is a mitochondrial disorder, it can be caused by the mutation of nuclear DNA or mitochondrial DNA. The classification of this disease varies from patient to patient, since many individuals do not fall into one specific disease category. The primary features displayed on a person with MERRF include myoclonus, seizures, cerebellar ataxia, myopathy, and ragged red fibers (RRF) on muscle biopsy, leading to the diseases name. Secondary features include dementia, optic atrophy, bilateral deafness, peripheral neuropathy, spasticity, or multiple lipomata. Mitochondrial disorders, including MERRFS, may present at any age. Symptoms and signs An individual displaying MERRFs syndrome will manifest not only a single symptom, but patients regularly display more than one affected body part at a time. It has been observed that patients with MERRF syndrome will primarily display myoclonus as a first symptom. There may also be seizures, cerebellar ataxia and myopathy. Secondary features can include dementia, optic atrophy, bilateral deafness, peripheral neuropathy, spasticity, multiple lipomata, and/or cardiomyopathy with Wolff Parkinson-White syndrome. Most patients will not exhibit all of these symptoms, but more than one of these symptoms will be present in a patient who has been diagnosed with MERRF disease. Mitochondrial disorders, including MERRF, may present at any age. Due to the multiple symptoms presented by the individual, the severity of the syndrome is very difficult to evaluate. Causes The cause of MERRF disorder is due to mutations in the mitochondrial genome. This means that it is a pathological variant in mtDNA (mitochondrial DNA) and is transmitted by maternal inheritance. Four point mutations in the genome can be identified that are associated with MERRF: m.A8344G, m.T8356C, m.G8361A, and m.G8363A. The point mutation m.A8344G is most commonly associated with MERRF, in a study published by Paul Jose Lorenzoni from the Department of neurology at University of Panama stated that 80% of the patients with MERRF disease exhibited this point mutation. This point mutation disrupts the mitochondrial gene for tRNA-Lys. This disrupts the synthesis of proteins. The remaining mutations only account for 10% of cases, and the remaining 10% of the patients with MERRF did not have an identifiable mutation in the mitochondrial DNA.Many genes are involved. These genes include: MT-TK MT-TL1 MT-TH MT-TS1 MT-TS2 MT-TFIt involves the following characteristics: progressive myoclonic epilepsy "Ragged Red Fibers" - clumps of diseased mitochondria accumulate in the subsarcolemmal region of the muscle fiber and appear as "Ragged Red Fibers" when muscle is stained with modified Gömöri trichrome stain.There is currently no cure for MERRF. Mechanism The mechanism by which MERRFs syndrome occur is not yet well understood. The human mitochondrial tRNA mutations are associated with a variety of diseases including mitochondrial myopathies. However, it is understood that defects in the mitochondrial DNA (mtDNA) have been associated with these diseases, and studies have been able to assign biochemical defects. One of these defects has to do with the decreased energy available for cell processes. As muscles are stained with Gömöri trichrome, characteristic ragged red fibers are visible under the microscope. This appearance is due to the accumulation of abnormal mitochondria below the plasma membrane of the muscle fiber. These may extend throughout the muscle fiber as the disease severity increases. The mitochondrial aggregates cause the contour of the muscle fiber to become irregular, leading to the "ragged" appearance. Diagnosis The diagnosis varies from individual to individual. Each is evaluated and diagnosed according to age, clinical phenotype, and pressed inheritance pattern. If the individual has been experiencing myoclonus, the doctor will run a series of genetic studies to determine if it is a mitochondrial disorder.The molecular genetic studies are run to identify the reason of for the mutations underlying the mitochondrial dysfunction. This approach will avoid the need for a muscle biopsy or an exhaustive metabolic evaluation. After sequencing the mitochondrial genomes, four points mutations in the genome can be identified which are associated with MERRF: A8344G, T8356C, G8361A, and G8363A. The point mutation A8344G is mostly associated with MERRF, in a study published by Paul Jose Lorenzoni from the Department of neurology at University of Panama stated that 80% of the patients with MERRF disease exhibited this point mutation. The remaining mutations only account for 10% of cases, and the remaining 10% of the patients with MERRF did not have an identifiable mutation in the mitochondrial DNA.If a patient does not exhibit mitochondrial DNA mutations, there are other ways that they can be diagnosed with MERRF. They can go through computed tomography (CT) or magnetic resonance imaging (MRI).The classification for the severity of MERRF syndrome is difficult to distinguish since most individuals will exhibit multi-symptoms. This is often necessary for children with complex neurologic or multi-system involvement, as described below. History and physical examination of the patient A detailed family history should be obtained from at least three generations, particularly if there have been any neonatal and childhood deaths. A family history may also indicate if any family members exhibit features of the multi-system disease, specifically if there has been maternal inheritance. This would show transmission of the disease only to females, or if there is a family member who experienced a multi-system involvement such as: brain condition that a family member has been record to have such as seizures, dystonia, ataxia, or stroke-like episodes. There may also be optic atrophy, skeletal muscle with a history of myalgia, weakness, or ptosis. Family history may also include neuropathy and dysautonomia, or heart conditions such as cardiomyopathy. The patients history might also exhibit kidney problems, such as proximal nephron dysfunction. There may also be endocrine conditions, such as diabetes or hypoparathyroidism. The patient might have also had a gastrointestinal condition which could have been due to liver disease, as well as episodes of nausea or vomiting. Multiple lipomas in the skin, sideroblastic anemia and pancytopenia in the metabolic system, or short stature might all be examples of patients with possible symptoms of MERRF disease. Treatment Like many mitochondrial diseases, there is no cure for MERRF, no matter the means for diagnosis of the disease. The treatment is primarily symptomatic. High doses of coenzyme Q10, B complex vitamins, and L-Carnitine are used for the altered metabolic processing that results in the disease. There is very little success with these treatments as therapies in hopes of improving mitochondrial function. The treatment only alleviates symptoms, and these do not prevent the disease from progressing. Patients with concomitant disease, such as diabetes, deafness, or cardiac disease, are treated in combination to manage symptoms. Research The Journal of Child Neurology published a paper that discusses possible new methods to test for MERRF and other mitochondrial diseases through a simple swabbing technique. This is a less invasive technique which allows for an analysis of buccal mitochondrial DNA, and showed significant amounts of the common 5 kb and 7.4 kb mitochondrial DNA deletions, which are also detectable in blood. This study suggests that a buccal swab approach can be used to informatively examine mitochondrial dysfunction in children with seizures and may be applicable to screening mitochondrial disease with other clinical presentations.Proceedings of the National Academy of Science of the United States of America published an article investigating the human mitochondrial tRNA (hmt-tRNA) mutations which are associated with mitochondrial myopathies. Since the current understanding of the precise molecular mechanisms of these mutations is limited, there is no efficient method to treat their associated mitochondrial diseases. All pathogenic mutants displayed pleiotropic phenotypes, with the exception of the G34A anticodon mutation, which solely affected aminoacylation. See also Epilepsy Mitochondrial disease Myoclonus Ragged red fibers References External links MERRF+Syndrome at the US National Library of Medicine Medical Subject Headings (MeSH) merrf at NIH/UW GeneTests

Hey Aarogya, could you help me understand about Acute pericarditis

Acute pericarditis

Acute pericarditis is a type of pericarditis (inflammation of the sac surrounding the heart, the pericardium) usually lasting less than 6 weeks. It is the most common condition affecting the pericardium. Signs and symptoms Chest pain is one of the common symptoms of acute pericarditis. It is usually of sudden onset, occurring in the anterior chest and often has a sharp quality that worsens with breathing in or coughing, due to inflammation of the pleural surface at the same time. The pain may be reduced with sitting up and leaning forward while worsened with lying down, and also may radiate to the back, to one or both trapezius ridges. However, the pain can also be dull and steady, resembling the chest pain in an acute myocardial infarction. As with any chest pain, other causes must also be ruled out, such as GERD, pulmonary embolism, muscular pain, etc. A pericardial friction rub is a very specific sign of acute pericarditis, meaning the presence of this sign invariably indicates presence of disease. However, absence of this sign does not rule out disease. This rub can be best heard by the diaphragm of the stethoscope at the left sternal border arising as a squeaky or scratching sound, resembling the sound of leather rubbing against each other. This sound should be distinguished from the sound of a murmur, which is similar but sounds more like a "swish" sound than a scratching sound. The pericardial rub is said to be generated from the friction generated by the two inflamed layers of the pericardium; however, even a large pericardial effusion does not necessarily present a rub. The rub is best heard during the maximal movement of the heart within the pericardial sac, namely, during atrial systole, ventricular systole, and the filling phase of early ventricular diastole. Fever may be present since this is an inflammatory process. Causes There are several causes of acute pericarditis. In developed nations, the cause of most (80–90%) cases of acute pericarditis is unknown but a viral cause is suspected in the majority of such cases. The other 10–20% of acute pericarditis cases have various causes including connective tissue diseases (e.g., systemic lupus erythematosus), cancer, or involve an inflammatory reaction of the pericardium following trauma to the heart such as after a heart attack such as Dresslers syndrome. Familial mediterranean fever and TNF receptor associated periodic syndrome are rare inherited autoimmune diseases capable of causing recurring episodes of acute pericarditis. Pathophysiology Clinical presentation of diseases of pericardium may vary between: Acute and recurrent pericarditis Pericardial effusion without major hemodynamic compromise Cardiac tamponade Constrictive pericarditis Effusive-constrictive pericarditis Diagnosis For acute pericarditis to formally be diagnosed, two or more of the following criteria must be present: chest pain consistent with a diagnosis of acute pericarditis (sharp chest pain worsened by breathing in or a cough), a pericardial friction rub, a pericardial effusion, and changes on electrocardiogram (ECG) consistent with acute pericarditis.A complete blood count may show an elevated white count and a serum C-reactive protein may be elevated. Acute pericarditis is associated with a modest increase in serum creatine kinase MB (CK-MB). and cardiac troponin I (cTnI), both of which are also markers for injury to the muscular layer of the heart. Therefore, it is imperative to also rule out acute myocardial infarction in the face of these biomarkers. The elevation of these substances may occur when inflammation of the hearts muscular layer in addition to acute pericarditis. Also, ST elevation on EKG (see below) is more common in those patients with a cTnI > 1.5 µg/L. Coronary angiography in those patients should indicate normal vascular perfusion. Troponin levels increase in 35-50% of people with pericarditis.Electrocardiogram (ECG) changes in acute pericarditis mainly indicates inflammation of the epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes stage 1 -- diffuse, positive, ST elevations with reciprocal ST depression in aVR and V1. Elevation of PR segment in aVR and depression of PR in other leads especially left heart V5, V6 leads indicates atrial injury. stage 2 -- normalization of ST and PR deviations stage 3 -- diffuse T wave inversions (may not be present in all patients) stage 4 -- EKG becomes normal OR T waves may be indefinitely invertedThe two most common clinical conditions where ECG findings may mimic pericarditis are acute myocardial infarction (AMI) and generalized early repolarization. As opposed to pericarditis, AMI usually causes localized convex ST-elevation usually associated with reciprocal ST-depression which may also be frequently accompanied by Q-waves, T-wave inversions (while ST is still elevated unlike pericarditis), arrhythmias and conduction abnormalities. In AMI, PR-depressions are rarely present. Early repolarization usually occurs in young males (age <40 years) and ECG changes are characterized by terminal R-S slurring, temporal stability of ST-deviations and J-height/ T-amplitude ratio in V5 and V6 of <25% as opposed to pericarditis where terminal R-S slurring is very uncommon and J-height/ T-amplitude ratio is ≥ 25%. Very rarely, ECG changes in hypothermia may mimic pericarditis, however differentiation can be helpful by a detailed history and presence of an Osborne wave in hypothermia.Another important diagnostic electrocardiographic sign in acute pericarditis is the Spodick sign. It signifies to the PR-depressions in a usual (but not always) association with downsloping TP segment in patients with acute pericarditis and is present in up to 80% of the patients affected with acute pericarditis. The sign is often best visualized in lead II and lateral precordial leads. In addition, Spodicks sign may also serve as an important distinguishing electrocardiographic tool between the acute pericarditis and acute coronary syndrome. The presence of a classical Spodicks sign is often a giveaway to the diagnosis.Rarely, electrical alternans may be seen, depending on the size of the effusion.A chest x-ray is usually normal in acute pericarditis but can reveal the presence of an enlarged heart if a pericardial effusion is present and is greater than 200 mL in volume. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis.An echocardiogram is typically normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis. Treatment Patients with uncomplicated acute pericarditis can generally be treated and followed up in an outpatient clinic. However, those with high risk factors for developing complications (see above) will need to be admitted to an inpatient service, most likely an ICU setting. High risk patients include the following: subacute onset high fever (> 100.4 F/38 C) and leukocytosis development of cardiac tamponade large pericardial effusion (echo-free space > 20 mm) resistant to NSAID treatment immunocompromised history of oral anticoagulation therapy acute trauma failure to respond to seven days of NSAID treatmentPericardiocentesis is a procedure whereby the fluid in a pericardial effusion is removed through a needle. It is performed under the following conditions: presence of moderate or severe cardiac tamponade diagnostic purpose for suspected purulent, tuberculosis, or neoplastic pericarditis persistent symptomatic pericardial effusionNSAIDs in viral or idiopathic pericarditis. In patients with underlying causes other than viral, the specific etiology should be treated. With idiopathic or viral pericarditis, NSAID is the mainstay treatment. Goal of therapy is to reduce pain and inflammation. The course of the disease may not be affected. The preferred NSAID is ibuprofen because of rare side effects, better effect on coronary flow, and larger dose range. Depending on severity, dosing is between 300 and 800 mg every 6–8 hours for days or weeks as needed. An alternative protocol is aspirin 800 mg every 6–8 hours. Dose tapering of NSAIDs may be needed. In pericarditis following acute myocardial infarction, NSAIDs other than aspirin should be avoided since they can impair scar formation. As with all NSAID use, GI protection should be engaged. Failure to respond to NSAIDs within one week (indicated by persistence of fever, worsening of condition, new pericardial effusion, or continuing chest pain) likely indicates that a cause other than viral or idiopathic is in process.Colchicine, which has been essential to treat recurrent pericarditis, has been supported for routine use in acute pericarditis by recent prospective studies. Colchicine can be given 0.6 mg twice a day (0.6 mg daily for patients <70 kg) for 3 months following an acute attack. It should be considered in all patients with acute pericarditis, preferably in combination with a short-course of NSAIDs. For patients with a first episode of acute idiopathic or viral pericarditis, they should be treated with an NSAID plus colchicine 1–2 mg on first day followed by 0.5 daily or twice daily for three months. It should be avoided or used with caution in patients with severe chronic kidney disease, hepatobiliary dysfunction, blood dyscrasias, and gastrointestinal motility disorders.Corticosteroids are usually used in those cases that are clearly refractory to NSAIDs and colchicine and a specific cause has not been found. Systemic corticosteroids are usually reserved for those with autoimmune disease. Prognosis One of the most feared complications of acute pericarditis is cardiac tamponade. Cardiac tamponade is accumulation of enough fluid in the pericardial space --- pericardial effusion --- to cause serious obstruction to the inflow of blood to the heart. Signs of cardiac tamponade include distended neck veins, muffled heart sounds when listening with a stethoscope, and low blood pressure (together known as Becks triad). This condition can be fatal if not immediately treated. Another longer term complication of pericarditis, if it recurs over a longer period of time (normally more than 3 months), is progression to constrictive pericarditis. Recent studies have shown this to be an uncommon complication. The definitive treatment for constrictive pericarditis is pericardial stripping, which is a surgical procedure where the entire pericardium is peeled away from the heart. References Further reading Chugh, S. N. (2014-05-14). Textbook of Clinical Electrocardiography. Jaypee Brothers Publishers. ISBN 9789350906088. == External links ==

Aarogya, can you share information about a health condition involving Ulcerative colitis

Ulcerative colitis

Ulcerative colitis (UC) is a long-term condition that results in inflammation and ulcers of the colon and rectum. The primary symptoms of active disease are abdominal pain and diarrhea mixed with blood (hematochezia). Weight loss, fever, and anemia may also occur. Often, symptoms come on slowly and can range from mild to severe. Symptoms typically occur intermittently with periods of no symptoms between flares. Complications may include abnormal dilation of the colon (megacolon), inflammation of the eye, joints, or liver, and colon cancer.The cause of UC is unknown. Theories involve immune system dysfunction, genetics, changes in the normal gut bacteria, and environmental factors. Rates tend to be higher in the developed world with some proposing this to be the result of less exposure to intestinal infections, or to a Western diet and lifestyle. The removal of the appendix at an early age may be protective. Diagnosis is typically by colonoscopy with tissue biopsies. It is a type of inflammatory bowel disease (IBD) along with Crohns disease and microscopic colitis.Dietary changes, such as maintaining a high-calorie diet or lactose-free diet, may improve symptoms. Several medications are used to treat symptoms and bring about and maintain remission, including aminosalicylates such as mesalazine or sulfasalazine, steroids, immunosuppressants such as azathioprine, and biologic therapy. Removal of the colon by surgery may be necessary if the disease is severe, does not respond to treatment, or if complications such as colon cancer develop. Removal of the colon and rectum generally cures the condition.Together with Crohns disease, about 11.2 million people were affected as of 2015. Each year it newly occurs in 1 to 20 per 100,000 people, and 5 to 500 per 100,000 individuals are affected. The disease is more common in North America and Europe than other regions. Often it begins in people aged 15 to 30 years, or among those over 60. Males and females appear to be affected in equal proportions. It has also become more common since the 1950s. Together, ulcerative colitis and Crohns disease affect about a million people in the United States. With appropriate treatment the risk of death appears the same as that of the general population. The first description of ulcerative colitis occurred around the 1850s. Signs and symptoms Gastrointestinal People with ulcerative colitis usually present with diarrhea mixed with blood, of gradual onset that persists for an extended period of time (weeks). Additional symptoms may include fecal incontinence, increased frequency of bowel movements, mucus discharge, and nocturnal defecations. With proctitis (inflammation of the rectum), people with UC may experience urgency or rectal tenesmus, which is the urgent desire to evacuate the bowels but with the passage of little stool. Tenesmus may be misinterpreted as constipation, due to the urge to defecate despite small volume of stool passage. Bloody diarrhea and abdominal pain may be more prominent features in severe disease. The severity of abdominal pain with UC varies from mild discomfort to very painful bowel movements and abdominal cramping. High frequency of bowel movements, weight loss, nausea, fatigue, and fever are also common during disease flares. Chronic bleeding from the GI tract, chronic inflammation, and iron deficiency often leads to anemia, which can affect quality of life.The clinical presentation of ulcerative colitis depends on the extent of the disease process. Up to 15% of individuals may have severe disease upon initial onset of symptoms. A substantial proportion (up to 45%) of people with a history of UC without any ongoing symptoms (clinical remission) have objective evidence of ongoing inflammation. Ulcerative colitis is associated with a generalized inflammatory process that can affect many parts of the body. Sometimes, these associated extra-intestinal symptoms are the initial signs of the disease. Extent of involvement In contrast to Crohns disease, which can affect areas of the gastrointestinal tract outside of the colon, ulcerative colitis is usually confined to the colon. Inflammation in ulcerative colitis is usually continuous, typically involving the rectum, with involvement extending proximally (to sigmoid colon, ascending colon, etc.). In contrast, inflammation with Crohns disease is often patchy, with so-called "skip lesions" (intermittent regions of inflamed bowel).The disease is classified by the extent of involvement, depending on how far the disease extends: proctitis (rectal inflammation), left sided colitis (inflammation extending to descending colon), and extensive colitis (inflammation proximal to the descending colon). Proctosigmoiditis describes inflammation of the rectum and sigmoid colon. Pancolitis describes involvement of the entire colon, extending from the rectum to the cecum. While usually associated with Crohns disease, ileitis (inflammation of the ileum) also occurs in UC. About 17% of individuals with UC have ileitis. Ileitis more commonly occurs in the setting of pancolitis (occurring in 20% of cases of pancolitis), and tends to correlate with the activity of colitis. This so-called "backwash ileitis" can occur in 10–20% of people with pancolitis and is believed to be of little clinical significance. Severity of disease In addition to the extent of involvement, UC is also characterized by severity of disease. Severity of disease is defined by symptoms, objective markers of inflammation (endoscopic findings, blood tests), disease course, and the impact of the disease on day-to-day life. Most patients are categorized through endoscopy and fecal calprotectin levels. Indicators of low risk for future complications in mild and moderate UC include the following parameters: exhibiting less than 6 stools daily and lack of fever/weight loss. Other indicators include lack of extraintestinal symptoms, none to little elevation in CRP, ESR, and calprotectin, and later age of diagnosis (over 40 years). Mild disease correlates with fewer than four stools daily; in addition, mild urgency and rectal bleeding may occur intermittently. Mild disease lacks systemic signs of toxicity (eg. fever, chills, weight changes) and exhibits normal levels of serum inflammatory markers (erythrocyte sedimentation rate and C-reactive protein).Moderate to severe disease correlates with more than six stools daily, frequent bloody stools and urgency. Moderate abdominal pain, low-grade fever, 38 to 39 °C (100 to 102 °F), and anemia may develop (75% of normal). Toxicity is present, as demonstrated by fever, tachycardia, anemia or an elevated ESR or CRP.Fulminant disease correlates with more than 10 bowel movements daily, continuous bleeding, toxicity, abdominal tenderness and distension, blood transfusion requirement, and colonic dilation (expansion). People with fulminant UC may have inflammation extending beyond just the mucosal layer, causing impaired colonic motility and leading to toxic megacolon. Toxic megacolon is defined by diameter of colon (>6 cm) or cecum (>9 cm) and represents a medical emergency, one often treated surgically. If the serous membrane is involved, a colonic perforation may ensue, which has a 50% mortality rate in patients afflicted with UC.Ulcerative colitis may improve and enter remission. Remission of disease is characterized by formed stools, the absence of bloody diarrhea, resolution of urgency, and normal levels of serum inflammatory markers. Extraintestinal manifestations and complications UC is characterized by immune dysregulation and systemic inflammation, which may result in symptoms and complications outside the colon. Commonly affected organs include: eyes, joints, skin, and liver. The frequency of such extraintestinal manifestations has been reported as between 6 and 47%.UC may affect the mouth. About 8% of individuals with UC develop oral manifestations. The two most common oral manifestations are aphthous stomatitis and angular cheilitis. Aphthous stomatitis is characterized by ulcers in the mouth, which are benign, noncontagious and often recurrent. Angular chelitis is characterized by redness at the corners of the mouth, which may include painful sores or breaks in the skin. Very rarely, benign pustules may occur in the mouth (pyostomatitis vegetans).UC may affect the eyes manifesting in scleritis, iritis, and conjunctivitis. Patients may be asymptomatic or experience redness, burning, or itching in eyes (CITE CMDP). Inflammation may occur in the interior portion of the eye, leading to uveitis and iritis. Uveitis can cause blurred vision and eye pain, especially when exposed to light (photophobia). Untreated, uveitis can lead to permanent vision loss. Inflammation may also involve the white part of the eye (sclera) or the overlying connective tissue (episclera), causing conditions called scleritis and episcleritis. Ulcerative colitis is most commonly associated with uveitis and episcleritis.UC may cause several joint manifestations, including a type of rheumatologic disease known as seronegative arthritis, which may affect few large joints (oligoarthritis), the vertebra (ankylosing spondylitis) or several small joints of the hands and feet (peripheral arthritis). Often the insertion site where muscle attaches to bone (entheses) becomes inflamed (enthesitis). Inflammation may affect the sacroiliac joint (sacroiliitis). It is estimated that round 50% of IBD patients suffer from migratory arthritis. Synovitis, or inflammation of the synovial fluid surrounding a joint, can occur for months and recur in later times but usually does not erode the joint. The symptoms of arthritis include joint pain, swelling, and effusion, and often leads to significant morbidity. The severity of joint symptoms often does not correspond with severity of IBD. Ulcerative colitis may affect the skin. The most common type of skin manifestation, erythema nodosum, presents in up to 3% of UC patients and almost 8% in patients afflicted with Crohns disease. It develops as raised, tender red nodules usually appearing on the outer areas of the arms or legs, especially in the anterior tibial area (shins). The nodules have diameters that measure approximately 1–5 cm. Erythema nodosum is due to inflammation of the underlying subcutaneous tissue (panniculitis), and biopsy will display focal panniculitis (although is often unnecessary in diagnosis). In contrast to joint-related manifestations, erythema nodosum often occurs alongside intestinal disease. Thus, treatment of UC can often lead to resolution of skin nodules.A lesser common skin complication associated with UC, pyoderma gangrenosum, is typically more severe. One study discovered this skin manifestation in only 0.75% pf patients. Pyoderma gangrenosum is characterized by painful lesions or nodules that become ulcers which progressively grow. It often starts as many small raised red spots (papules) or pus-filled lesions (pustules) that are usually detected on lower extremities. The inner layer of the skin, or dermis, slowly undergoes necrosis (process of dying) causing the ulcerations that are typical of pyoderma gangrenosum. The ulcers are often filled with sterile pus-like material, so biopsy often displays an abscess that is sterile. Whereas erythema nodosum tends to correlate with the activity of the ulcerative colitis and often improves with treatment of the colonic inflammation, pyoderma gangrenosum may occur independently of UC disease activity. In some cases, pyoderma gangrenosum may require injection with corticosteroids. Treatment may also involve inhibitors of tumor necrosis factor (TNF), a cytokine that promotes cell survival.Other associations determined between the skin and ulcerative colitis include a skin condition known as hidradenitis suppurativa (HS). This condition represents a chronic process in which follicles become occluded leading to recurring inflammation of nodules and abscesses and even tunnels in the skin that drain fluid.Ulcerative colitis may affect the blood and endocrine system. UC increases the risk of blood clots in both arteries and veins; painful swelling of the lower legs can be a sign of deep venous thrombosis, while difficulty breathing may be a result of pulmonary embolism (blood clots in the lungs). The risk of blood clots is about threefold higher in individuals with IBD. The risk of venous thromboembolism is high in ulcerative colitis due to hypercoagulability from inflammation, especially with active or extensive disease. Additional risk factors may include surgery, hospitalization, pregnancy, the use of corticosteroids and tofacitinib, a JAK inhibitor.The immune system may also attack red blood cells, leading to autoimmune hemolytic anemia. In addition to autoimmune destruction, anemia may occur due to chronic blood loss from rectal bleeding and bone marrow suppression due to inflammation (anemia of chronic disease). Anemic patients can present asymptomatically. However, 75% of individuals exhibit symptoms such as shortness of breath, fatigue, and tachycardia (racing heart). About 1/3rd of patients show signs of jaundice (yellowing of the skin) or darkened urine from loss of bilirubin in urine. A smaller percentage may present with chest pain or a concurrent immune cytopenia, most commonly immune thrombocytopenia (ITP) (CITE WAHA). Osteoporosis may occur related to systemic inflammation, which increases the risk of bone fractures. Clubbing, a deformity of the ends of the fingers, may occur. Amyloidosis may occur, especially with severe and poorly controlled disease, which usually presents with protein in the urine (proteinuria) and nephritic syndrome. Primary sclerosing cholangitis Ulcerative colitis has a significant association with primary sclerosing cholangitis (PSC), a progressive inflammatory disorder of small and large bile ducts. Up to 70-90% of people with primary sclerosing cholangitis have ulcerative colitis. As many as 5% of people with ulcerative colitis may progress to develop primary sclerosing cholangitis. PSC is more common in men, and often begins between 30 and 40 years of age. It can present asymptomatically or exhibit symptoms of itchiness (pruritis) and fatigue. Other symptoms include systemic signs such as fever and night sweats. Such symptoms are often associated with a bacterial episodic version of PSC. Upon physical exam, one may discern enlarged liver contours (hepatomegaly) or enlarged spleen (splenomegaly) as well as areas of excoriation. Yellow coloring of the skin, or jaundice, may also be present due to excess of bile byproduct buildup (bilirubin) from the biliary tract. In diagnosis, lab results often reveal a pattern indicative of biliary disease (cholestatic pattern). This is often displayed by markedly elevated alkaline phosphatase levels and milder or no elevation in liver enzyme levels. Xray results often show bile ducts with thicker walls, areas of dilation or narrowing.In some cases, primary sclerosing cholangitis occurs several years before the bowel symptoms of ulcerative colitis develop. PSC does not parallel the onset, extent, duration, or activity of the colonic inflammation in ulcerative colitis. In addition, colectomy does not have an impact on the course of primary sclerosing cholangitis in individuals with UC. PSC is associated with an increased risk of colorectal cancer and cholangiocarcinoma (bile duct cancer). PSC is a progressive condition, and may result in cirrhosis of the liver. No specific therapy has been proven to affect the long term course of PSC.Other liver-related manifestations of UC include fatty liver disease and autoimmune liver disease. Causes Ulcerative colitis is an autoimmune disease characterized by T-cells infiltrating the colon. No direct causes for UC are known, but factors such as genetics, environment, and an overactive immune system play a role. UC is associated with comorbidities that produce symptoms in many areas of the body outside the digestive system. Genetic factors A genetic component to the cause of UC can be hypothesized based on aggregation of UC in families, variation of prevalence between different ethnicities, genetic markers and linkages. In addition, the identical twin concordance rate is 10%, whereas the dizygotic twin concordance rate is only 3%. Between 8 and 14% of people with ulcerative colitis have a family history of inflammatory bowel disease. In addition, people with a first degree relative with UC have a four-fold increase in their risk of developing the disease.Twelve regions of the genome may be linked to UC, including, in the order of their discovery, chromosomes 16, 12, 6, 14, 5, 19, 1, and 3, but none of these loci has been consistently shown to be at fault, suggesting that the disorder is influenced by multiple genes. For example, chromosome band 1p36 is one such region thought to be linked to inflammatory bowel disease. Some of the putative regions encode transporter proteins such as OCTN1 and OCTN2. Other potential regions involve cell scaffolding proteins such as the MAGUK family. Human leukocyte antigen associations may even be at work. In fact, this linkage on chromosome 6 may be the most convincing and consistent of the genetic candidates.Multiple autoimmune disorders are associated with ulcerative colitis, including celiac disease, psoriasis, lupus erythematosus, rheumatoid arthritis, episcleritis, and scleritis. Ulcerative colitis is also associated with acute intermittent porphyria. Environmental factors Many hypotheses have been raised for environmental factors contributing to the pathogenesis of ulcerative colitis, including diet, breastfeeding and medications. Breastfeeding may have a protective effect in the development of ulcerative colitis. One study of isotretinoin found a small increase in the rate of UC.As the colon is exposed to many dietary substances which may encourage inflammation, dietary factors have been hypothesized to play a role in the pathogenesis of both ulcerative colitis and Crohns disease. However, current research does not show a link between diet and the development of ulcerative colitis. Few studies have investigated such an association; one study showed no association of refined sugar on the number of people affected of ulcerative colitis. High intake of unsaturated fat and vitamin B6 may enhance the risk of developing ulcerative colitis. Other identified dietary factors that may influence the development and/or relapse of the disease include meat protein and alcoholic beverages. Specifically, sulfur has been investigated as being involved in the cause of ulcerative colitis, but this is controversial. Sulfur restricted diets have been investigated in people with UC and animal models of the disease. The theory of sulfur as an etiological factor is related to the gut microbiota and mucosal sulfide detoxification in addition to the diet.As a result of a class-action lawsuit and community settlement with DuPont, three epidemiologists conducted studies on the population surrounding a chemical plant that was exposed to PFOA at levels greater than in the general population. The studies concluded that there was an association between PFOA exposure and six health outcomes, one of which being ulcerative colitis. Alternative theories Levels of sulfate-reducing bacteria tend to be higher in persons with ulcerative colitis, which could indicate higher levels of hydrogen sulfide in the intestine. An alternative theory suggests that the symptoms of the disease may be caused by toxic effects of the hydrogen sulfide on the cells lining the intestine.Infection by mycobacterium avium, subspecies paratuberculosis, has been proposed as the ultimate cause of both ulcerative colitis and Crohns disease. Pathophysiology An increased amount of colonic sulfate-reducing bacteria has been observed in some people with ulcerative colitis, resulting in higher concentrations of the toxic gas hydrogen sulfide. Human colonic mucosa is maintained by the colonic epithelial barrier and immune cells in the lamina propria (see intestinal mucosal barrier). N-butyrate, a short-chain fatty acid, gets oxidized through the beta oxidation pathway into carbon dioxide and ketone bodies. It has been shown that N-butyrate helps supply nutrients to this epithelial barrier. Studies have proposed that hydrogen sulfide plays a role in impairing this beta-oxidation pathway by interrupting the short chain acetyl-CoA dehydrogenase, an enzyme within the pathway. Furthermore, it has been suggested that the protective benefit of smoking in ulcerative colitis is due to the hydrogen cyanide from cigarette smoke reacting with hydrogen sulfide to produce the non-toxic isothiocyanate, thereby inhibiting sulfides from interrupting the pathway. An unrelated study suggested that the sulfur contained in red meats and alcohol may lead to an increased risk of relapse for people in remission. Diagnosis The initial diagnostic workup for ulcerative colitis consists of a complete history and physical examination, assessment of signs and symptoms, laboratory tests and endoscopy. Severe UC can exhibit high erythrocyte sedimentation rate (ESR), decreased albumin (a protein produced by the liver), and various changes in electrolytes. As discussed previously, UC patients often also display elevated alkaline phosphatase. Inflammation in the intestine may also cause higher levels of fecal calprotectin or lactoferrin.Specific testing may include the following: A complete blood count is done to check for anemia; thrombocytosis, a high platelet count, is occasionally seen Electrolyte studies and kidney function tests are done, as chronic diarrhea may be associated with hypokalemia, hypomagnesemia and kidney injury. Liver function tests are performed to screen for bile duct involvement: primary sclerosing cholangitis. Imaging such as x-ray or CT scan to evaluate for possible perforation or toxic megacolon Stool culture and Clostridioides difficile stool assay to rule out infectious colitis Inflammatory markers, such as erythrocyte sedimentation rate or C-reactive protein Lower endoscopy to evaluate the rectum and distal large intestine (sigmoidoscopy) or entire colon and end of the small intestine (colonoscopy) for ulcers and inflammationAlthough ulcerative colitis is a disease of unknown causation, inquiry should be made as to unusual factors believed to trigger the disease.The simple clinical colitis activity index was created in 1998 and is used to assess the severity of symptoms. Endoscopic The best test for diagnosis of ulcerative colitis remains endoscopy, which is examination of the internal surface of the bowel using a flexible camera. Initially, a flexible sigmoidoscopy may be completed to establish the diagnosis. The physician may elect to limit the extent of the initial exam if severe colitis is encountered to minimize the risk of perforation of the colon. However, a complete colonoscopy with entry into the terminal ileum should be performed to rule out Crohns disease, and assess extent and severity of disease. Endoscopic findings in ulcerative colitis include: erythema (redness of the mucosa), friability of the mucosa, superficial ulceration, and loss of the vascular appearance of the colon. When present, ulcerations may be confluent. Pseudopolyps may be observed.Ulcerative colitis is usually continuous from the rectum, with the rectum almost universally being involved. Perianal disease is rare. The degree of involvement endoscopically ranges from proctitis (rectal inflammation) to left sided colitis (extending to descending colon), to extensive colitis (extending proximal to descending colon). Histologic Biopsies of the mucosa are taken during endoscopy to confirm the diagnosis of UC and differentiate it from Crohns disease, which is managed differently clinically. Histologic findings in ulcerative colitis includes: distortion of crypt architecture, crypt abscesses, and inflammatory cells in the mucosa (lymphocytes, plasma cells, and granulocytes). Unlike the transmural inflammation seen in Crohns disease, the inflammation of ulcerative colitis is limited to the mucosa. Laboratory tests Blood and stool tests serve primarily to assess disease severity, level of inflammation and rule out causes of infectious colitis. All individuals with suspected ulcerative colitis should have stool testing to rule out infection.A complete blood count may demonstrate anemia, leukocytosis, or thrombocytosis. Anemia may be caused by inflammation or bleeding. Chronic blood loss may lead to iron deficiency as a cause for anemia, particularly microcytic anemia (small red blood cells), which can be evaluated with a serum ferritin, iron, total iron-binding capacity and transferrin saturation. Anemia may be due to a complication of treatment from azathioprine, which can cause low blood counts, or sulfasalazine, which can result in folate deficiency. Thiopurine metabolites (from azathioprine) and a folate level can help.UC may cause high levels of inflammation throughout the body, which may be quantified with serum inflammatory markers, such as CRP and ESR. However, elevated inflammatory markers are not specific for UC and elevations are commonly seen in other conditions, including infection. In addition, inflammatory markers are not uniformly elevated in people with ulcerative colitis. Twenty five percent of individuals with confirmed inflammation on endoscopic evaluation have a normal CRP level. Serum albumin may also be low related to inflammation, in addition to loss of protein in the GI tract associated with bleeding and colitis. Low serum levels of vitamin D are associated with UC, although the significance of this finding is unclear.Specific antibody markers may be elevated in ulcerative colitis. Specifically, perinuclear antineutrophil cytoplasmic antibodies (pANCA) are found in 70 percent of cases of UC. Antibodies against Saccharomyces cerevisiae may be present, but are more often positive in Crohns disease compared with ulcerative colitis. However, due to poor accuracy of these serolologic tests, they are not helpful in the diagnostic evaluation of possible inflammatory bowel disease.Several stool tests may help quantify the extent of inflammation present in the colon and rectum. Fecal calprotectin is elevated in inflammatory conditions affecting the colon, and is useful in distinguishing irritable bowel syndrome (noninflammatory) from a flare in inflammatory bowel disease. Fecal calprotectin is 88% sensitive and 79% specific for the diagnosis of ulcerative colitis. If the fecal calprotectin is low, the likelihood of inflammatory bowel disease are less than 1 percent. Lactoferrin is an additional nonspecific marker of intestinal inflammation. Imaging Overall, imaging tests, such as x-ray or CT scan, may be helpful in assessing for complications of ulcerative colitis, such as perforation or toxic megacolon. Bowel ultrasound (US) is a cost-effective, well-tolerated, non-invasive and readily available tool for the management of patients with inflammatory bowel disease (IBD), including UC, in clinical practice. Some recent studies demonstrated that US is an accurate tool for assessing disease activity in patients with UC. Imaging is otherwise of limited use in diagnosing ulcerative colitis. Magnetic resonance imaging (MRI) is necessary to diagnose underlying PSC.Abdominal xray is often the test of choice and may display nonspecific findings in cases of mild or moderate ulcerative colitis. In circumstances of severe UC, radiographic findings may include thickening of the mucosa, often termed "thumbprinting," which indicates swelling due to fluid displacement (edema). Other findings may include colonic dilation and stool buildup evidencing constipation.Similar to xray, in mild ulcerative colitis, double contrast barium enema often shows nonspecific findings. Conversely, barium enema may display small buildups of barium in microulcerations. Severe UC can be characterized by various polyps, colonic shortening, loss of haustrae (the small bulging pouches in the colon),and narrowing of the colon. It is important to note that barium enema should not be conducted in patients exhibiting very severe symptoms as this may slow or stop stool passage through the colon causing ileus and toxic megacolon.Other methods of imaging include computed tomography (CT) and magnetic resonance imaging (MRI). Both may depict colonic wall thickening but have decreased ability to find early signs of wall changes when compared to barium enema. In cases of severe ulcerative colitis, however, they often exhibit equivalent ability to detect colonic changes.Doppler ultrasound is the last means of imaging that may be used. Similar to the imaging methods mentioned earlier, this may show some thickened bowel wall layers. In severe cases, this may show thickening in all bowel wall layers (transmural thickness). Differential diagnosis Several conditions may present in a similar manner as ulcerative colitis, and should be excluded. Such conditions include: Crohns disease, infectious colitis, nonsteroidal anti-inflammatory drug enteropathy, and irritable bowel syndrome. Alternative causes of colitis should be considered, such as ischemic colitis (inadequate blood flow to the colon), radiation colitis (if prior exposure to radiation therapy), or chemical colitis. Pseudomembranous colitis may occur due to Clostridioides difficile infection following administration of antibiotics. Entamoeba histolytica is a protozoan parasite that causes intestinal inflammation. A few cases have been misdiagnosed as UC with poor outcomes occurring due to the use of corticosteroids.The most common disease that mimics the symptoms of ulcerative colitis is Crohns disease, as both are inflammatory bowel diseases that can affect the colon with similar symptoms. It is important to differentiate these diseases since their courses and treatments may differ. In some cases, however, it may not be possible to tell the difference, in which case the disease is classified as indeterminate colitis. Crohns disease can be distinguished from ulcerative colitis in several ways. Characteristics that indicate Crohns include evidence of disease around the anus (perianal disease). This includes anal fissures and abscesses as well as fistulas, which are abnormal connections between various bodily structures.Infectious colitis is another condition that may present in similar manner to ulcerative colitis. Endoscopic findings are also oftentimes similar. One can discern whether a patient has infectious colitis by employing tissue cultures and stool studies. Biopsy of the colon is another beneficial test but is more invasive. Other forms of colitis that may present similarly include radiation and diversion colitis. Radiation colitis occurs after irradiation and often affects the rectum or sigmoid colon, similar to ulcerative colitis. Upon histology radiation colitis may indicate eosinophilic infiltrates, abnormal epithelial cells, or fibrosis. Diversion colitis, on the other hand, occurs after portions of bowel loops have been removed. Histology in this condition often shows increased growth of lymphoid tissue. In patients who have undergone transplantation, graft versus host disease may also be a differential diagnosis. This response to transplantation often causes prolonged diarrhea if the colon is affected. Typical symptoms also include rash. Involvement of the upper gastrointestinal tract may lead to difficulty swallowing or ulceration. Upon histology, graft versus host disease may present with crypt cell necrosis and breakdown products within the crypts themselves. Management Standard treatment for ulcerative colitis depends on the extent of involvement and disease severity. The goal is to induce remission initially with medications, followed by the administration of maintenance medications to prevent a relapse. The concept of induction of remission and maintenance of remission is very important. The medications used to induce and maintain a remission somewhat overlap, but the treatments are different. Physicians first direct treatment to inducing remission, which involves relief of symptoms and mucosal healing of the colons lining, and then longer-term treatment to maintain remission and prevent complications. Acute severe ulcerative colitis requires hospitalisation, exclusion of infections, and corticosteroids.For acute stages of the disease, a low fiber diet may be recommended. Medication Ulcerative colitis can be treated with a number of medications, including 5-ASA drugs such as sulfasalazine and mesalazine. Corticosteroids such as prednisone can also be used due to their immunosuppressive and short-term healing properties, but because their risks outweigh their benefits, they are not used long-term in treatment. Immunosuppressive medications such as azathioprine and biological agents such as infliximab and adalimumab are given only if people cannot achieve remission with 5-ASA and corticosteroids. Infliximab, ustekinumab, or vedolizumab are recommended in those with moderate or severe disease.A formulation of budesonide was approved by the U.S. Food and Drug Administration (FDA) for treatment of active ulcerative colitis in January 2013. In 2018, tofacitinib was approved for treatment of moderately to severely active ulcerative colitis in the United States, the first oral medication indicated for long term use in this condition. The evidence on methotrexate does not show a benefit in producing remission in people with ulcerative colitis. Cyclosporine is effective for severe UC and tacrolimus has also shown benefits. Aminosalicylates Sulfasalazine has been a major agent in the therapy of mild to moderate ulcerative colitis for over 50 years. In 1977, it was shown that 5-aminosalicylic acid (5-ASA, mesalazine/mesalamine) was the therapeutically active component in sulfasalazine. Many 5-ASA drugs have been developed with the aim of delivering the active compound to the large intestine to maintain therapeutic efficacy but with reduction of the side effects associated with the sulfapyridine moiety in sulfasalazine. Oral 5-ASA drugs are particularly effective in inducing and in maintaining remission in mild to moderate ulcerative colitis. Rectal suppository, foam or liquid enema formulations of 5-ASA are used for colitis affecting the rectum, sigmoid or descending colon, and have been shown to be effective especially when combined with oral treatment. Biologics Biologic treatments such as the TNF inhibitors infliximab, adalimumab, and golimumab are commonly used to treat people with UC who are no longer responding to corticosteroids. Tofacitinib and vedolizumab can also produce good clinical remission and response rates in UC. Biologics may be used early in treatment (step down approach), or after other treatments have failed to induce remission (step up approach); the strategy should be individualized.Unlike aminosalicylates, biologics can cause serious side effects such as an increased risk of developing extra-intestinal cancers, heart failure; and weakening of the immune system, resulting in a decreased ability of the immune system to clear infections and reactivation of latent infections such as tuberculosis. For this reason, people on these treatments are closely monitored and are often tested for hepatitis and tuberculosis annually. Nicotine Unlike Crohns disease, ulcerative colitis has a lesser chance of affecting smokers than non-smokers. In select individuals with a history of previous tobacco use, resuming low dose smoking may improve signs and symptoms of active ulcerative colitis, but it is not recommended due to the overwhelmingly negative health effects of tobacco. Studies using a transdermal nicotine patch have shown clinical and histological improvement. In one double-blind, placebo-controlled study conducted in the United Kingdom, 48.6% of people with UC who used the nicotine patch, in conjunction with their standard treatment, showed complete resolution of symptoms. Another randomized, double-blind, placebo-controlled, single-center clinical trial conducted in the United States showed that 39% of people who used the patch showed significant improvement, versus 9% of those given a placebo. However, nicotine therapy is generally not recommended due to side effects and inconsistent results. Iron supplementation The gradual loss of blood from the gastrointestinal tract, as well as chronic inflammation, often leads to anemia, and professional guidelines suggest routinely monitoring for anemia with blood tests repeated every three months in active disease and annually in quiescent disease. Adequate disease control usually improves anemia of chronic disease, but iron deficiency anemia should be treated with iron supplements. The form in which treatment is administered depends both on the severity of the anemia and on the guidelines that are followed. Some advise that parenteral iron be used first because people respond to it more quickly, it is associated with fewer gastrointestinal side effects, and it is not associated with compliance issues. Others require oral iron to be used first, as people eventually respond and many will tolerate the side effects. Surgery Unlike in Crohns disease, the gastrointestinal aspects of ulcerative colitis can generally be cured by surgical removal of the large intestine, though extraintestinal symptoms may persist. This procedure is necessary in the event of: exsanguinating hemorrhage, frank perforation, or documented or strongly suspected carcinoma. Surgery is also indicated for people with severe colitis or toxic megacolon. People with symptoms that are disabling and do not respond to drugs may wish to consider whether surgery would improve the quality of life.The removal of the entire large intestine, known as a proctocolectomy, results in a permanent ileostomy – where a stoma is created by pulling the terminal ileum through the abdomen. Intestinal contents are emptied into a removable ostomy bag which is secured around the stoma using adhesive.Another surgical option for ulcerative colitis that is affecting most of the large bowel is called the ileal pouch-anal anastomosis (IPAA). This is a two- or three-step procedure. In a three-step procedure, the first surgery is a sub-total colectomy, in which the large bowel is removed, but the rectum remains in situ, and a temporary ileostomy is made. The second step is a proctectomy and formation of the ileal pouch (commonly known as a "j-pouch"). This involves removing the large majority of the remaining rectal stump and creating a new "rectum" by fashioning the end of the small intestine into a pouch and attaching it to the anus. After this procedure, a new type of ileostomy is created (known as a loop ileostomy) to allow the anastomoses to heal. The final surgery is a take-down procedure where the ileostomy is reversed and there is no longer the need for an ostomy bag. When done in two steps, a proctocolectomy – removing both the colon and rectum – is performed alongside the pouch formation and loop ileostomy. The final step is the same take-down surgery as in the three-step procedure. Time taken between each step can vary, but typically a six- to twelve-month interval is recommended between the first two steps, and a minimum of two to three months is required between the formation of the pouch and the ileostomy take-down.While the ileal pouch procedure removes the need for an ostomy bag, it does not restore normal bowel function. In the months following the final operation, patients typically experience 8–15 bowel movements a day. Over time this number decreases, with many patients reporting four-six bowel movements after one year post-op. While many patients have success with this procedure, there are a number of known complications. Pouchitis, inflammation of the ileal pouch resulting in symptoms similar to ulcerative colitis, is relatively common. Pouchitis can be acute, remitting, or chronic however treatment using antibiotics, steroids, or biologics can be highly effective. Other complications include fistulas, abscesses, and pouch failure. Depending on the severity of the condition, pouch revision surgery may need to be performed. In some cased the pouch may need to be de-functioned or removed and an ileostomy recreated.The risk of cancer arising from a ileal pouch anal anastomosis is low. However, annual surveillance with pouchoscopy may be considered in individuals with risk factors for dysplasia, such as a history of dysplasia or colorectal cancer, a history of PSC, refractory pouchitis, and severely inflamed atrophic pouch mucosa. Bacterial recolonization In a number of randomized clinical trials, probiotics have demonstrated the potential to be helpful in the treatment of ulcerative colitis. Specific types of probiotics such as Escherichia coli Nissle have been shown to induce remission in some people for up to a year. A probiotic named after its gastroenterologist medical doctor inventor, the De Simone Formulation, may be effective in inducing remission in active ulcerative colitis, and may be as effective as 5-ASAs in preventing relapse of quiescent UC. The De Simone Formulation was sold and researched under the brand name VSL#3 until 2016. Since, it has been sold and researched under various regional brand names including Visbiome in the United States and Vivomixx in Europe.Fecal microbiota transplant involves the infusion of human probiotics through fecal enemas. Ulcerative colitis typically requires a more prolonged bacteriotherapy treatment than Clostridium difficile infection to be successful, possibly due to the time needed to heal the ulcerated epithelium. The response of ulcerative colitis is potentially very favorable with one study reporting 67.7% of people experiencing complete remission. Other studies found a benefit from using fecal microbiota transplantation. Alternative medicine A variety of alternative medicine therapies have been used for ulcerative colitis, with inconsistent results. Curcumin (turmeric) therapy, in conjunction with taking the medications mesalamine or sulfasalazine, may be effective and safe for maintaining remission in people with quiescent ulcerative colitis. The effect of curcumin therapy alone on quiescent ulcerative colitis is unknown.Treatments using cannabis or cannabis oil are uncertain. So far, studies havent determined its effectiveness and safety. Abdominal pain management Many interventions have been considered to manage abdominal pain in people with ulcerative colitis, including FODMAPs diet, relaxation training, yoga, kefir diet and stellate ganglion block treatment. It is unclear whether any of these are safe or effective at improving pain or reducing anxiety and depression. Prognosis Poor prognostic factors include: age < 40 years upon diagnosis, extensive colitis, severe colitis on endoscopy, prior hospitalization, elevated CRP and low serum albumin. Progression or remission People with ulcerative colitis usually have an intermittent course, with periods of disease inactivity alternating with "flares" of disease. People with proctitis or left-sided colitis usually have a more benign course: only 15% progress proximally with their disease, and up to 20% can have sustained remission in the absence of any therapy. A subset of people experience a course of disease progress rapidly. In these cases, there is usually a failure to respond to medication and surgery often is performed within the first few years of disease onset. People with more extensive disease are less likely to sustain remission, but the rate of remission is independent of the severity of the disease. Several risk factors are associated with eventual need for colectomy, including: prior hospitalization for UC, extensive colitis, need for systemic steroids, young age at diagnosis, low serum albumin, elevated inflammatory markers (CRP & ESR), and severe inflammation seen during colonoscopy. Surgical removal of the large intestine is necessary in some cases. Colorectal cancer The risk of colorectal cancer is significantly increased in people with ulcerative colitis after ten years if involvement is beyond the splenic flexure. People with backwash ileitis might have an increased risk for colorectal carcinoma. Those people with only proctitis usually have no increased risk. It is recommended that people have screening colonoscopies with random biopsies to look for dysplasia after eight years of disease activity, at one to two year intervals. Mortality People with ulcerative colitis are at similar or perhaps slightly increased overall risk of death compared with the background population. However, the distribution of causes-of-death differs from the general population. Specific risk factors may predict worse outcomes and a higher risk of mortality in people with ulcerative colitis, including: C. difficile infection and cytomegalovirus infection (due to reactivation). Epidemiology Together with Crohns disease, about 11.2 million people were affected as of 2015. Each year, ulcerative colitis newly occurs in 1 to 20 per 100,000 people (incidence), and there are a total of 5-500 per 100,000 individuals with the disease (prevalence). In 2015, a worldwide total of 47,400 people died due to inflammatory bowel disease (UC and Crohns disease). The peak onset is between 30 and 40 years of age, with a second peak of onset occurring in the 6th decade of life. Ulcerative colitis is equally common among men and women. With appropriate treatment the risk of death appears similar to that of the general population. UC has become more common since the 1950s.The geographic distribution of UC and Crohns disease is similar worldwide, with the highest number of new cases a year of UC found in Canada, New Zealand and the United Kingdom. The disease is more common in North America and Europe than other regions. In general, higher rates are seen in northern locations compared to southern locations in Europe and the United States. UC is more common in western Europe compared with eastern Europe. Worldwide, the prevalence of UC varies from 2 - 299 per 100,000 people. Together, ulcerative colitis and Crohns disease affect about a million people in the United States.As with Crohns disease, the rates of UC are greater among Ashkenazi Jews and decreases progressively in other persons of Jewish descent, non-Jewish Caucasians, Africans, Hispanics, and Asians. Appendectomy prior to age 20 for appendicitis and current tobacco use are protective against development of UC. However, former tobacco use is associated with a higher risk of developing the disease. United States As of 2004, the number of new cases of UC in the United States was between 2.2 and 14.3 per 100,000 per year. The number of people affected in the United States in 2004 was between 37 and 246 per 100,000. Canada In Canada, between 1998 and 2000, the number of new cases per year was 12.9 per 100,000 population or 4,500 new cases. The number of people affected was estimated to be 211 per 100,000 or 104,000. United Kingdom In the United Kingdom 10 per 100,000 people newly develop the condition a year while the number of people affected is 243 per 100,000. Approximately 146,000 people in the United Kingdom have been diagnosed with UC. History The first description of ulcerative colitis occurred around the 1850s. Research Helminthic therapy using the whipworm Trichuris suis has been shown in a randomized control trial from Iowa to show benefit in people with ulcerative colitis. The therapy tests the hygiene hypothesis which argues that the absence of helminths in the colons of people in the developed world may lead to inflammation. Both helminthic therapy and fecal microbiota transplant induce a characteristic Th2 white cell response in the diseased areas, which was unexpected given that ulcerative colitis was thought to involve Th2 overproduction.Alicaforsen is a first generation antisense oligodeoxynucleotide designed to bind specifically to the human ICAM-1 messenger RNA through Watson-Crick base pair interactions in order to subdue expression of ICAM-1. ICAM-1 propagates an inflammatory response promoting the extravasation and activation of leukocytes (white blood cells) into inflamed tissue. Increased expression of ICAM-1 has been observed within the inflamed intestinal mucosa of ulcerative colitis patients, where ICAM-1 over production correlated with disease activity. This suggests that ICAM-1 is a potential therapeutic target in the treatment of ulcerative colitis.Gram positive bacteria present in the lumen could be associated with extending the time of relapse for ulcerative colitis.A series of drugs in development looks to disrupt the inflammation process by selectively targeting an ion channel in the inflammation signaling cascade known as KCa3.1. In a preclinical study in rats and mice, inhibition of KCa3.1 disrupted the production of Th1 cytokines IL-2 and TNF-∝ and decreased colon inflammation as effectively as sulfasalazine.Neutrophil extracellular traps and the resulting degradation of the extracellular matrix have been reported in the colon mucosa in ulcerative colitis patients in clinical remission, indicating the involvement of the innate immune system in the etiology.Fexofenadine, an antihistamine drug used in treatment of allergies, has shown promise in a combination therapy in some studies. Opportunely, low gastrointestinal absorption (or high absorbed drug gastrointestinal secretion) of fexofenadine results in higher concentration at the site of inflammation. Thus, the drug may locally decrease histamine secretion by involved gastrointestinal mast cells and alleviate the inflammation.There is evidence that etrolizumab is effective for ulcerative colitis, with phase 3 trials underway as of 2016. Etrolizumab is a humanized monoclonal antibody that targets he β7 subunit of integrins α4β7 and αEβ7. Etrolizumab decreases lymphocytes trafficking, similar to vedolizumab (another integrin antagonist). A type of leukocyte apheresis, known as granulocyte and monocyte adsorptive apheresis, still requires large-scale trials to determine whether or not it is effective. Results from small trials have been tentatively positive. Notable cases References Further reading External links MedlinePlus ulcerative colitis page

Aarogya, Please give me a short description about Metaphyseal dysplasia

Metaphyseal dysplasia

Metaphyseal dysplasia, or Pyle disease, is a disorder of the bones. It is a rare disease in which the outer part of the shafts of long bones is thinner than normal and there is an increased chance of fractures. Its hallmark feature is an abnormality of the long bones in the arms and legs in which the ends (metaphyses) of the bones are abnormally broad; the shape of the bones resembles a boat oar or paddle. The broad metaphyses are due to enlargement of the spongy inner layer of bone (trabecular bone). Although trabecular bone is expanded, the dense outermost layer of bone (cortical bone) is thinner than normal. As a result, the bones are fragile and fracture easily. The bone abnormalities in the legs commonly cause knock knees (genu valgum) in affected individuals.Other bone abnormalities can also occur in Pyle disease. Affected individuals may have widened collar bones (clavicles), ribs, or bones in the fingers and hands. Dental problems are common in Pyle disease, including delayed appearance (eruption) of permanent teeth and misalignment of the top and bottom teeth (malocclusion). Signs and symptoms It is an autosomal recessive disorder in which mild clinical manifestations contrast with radiological appearances of gross metaphyseal undermodeling. Most patients present with mild genu valgum. The elbows are unable to extend fully. There may be widening of the lower femora and clavicles. Bones can sometimes be fragile, but fracturing is usually not common. Patients may present with dental caries, mandibular prognathism, spinal alignment, and disproportionate limb lengthening. Mental development, physical development, and height are usually normal. Most patients with Pyles diseases will have symptoms that vary from person to person. Symptoms are:5%–29% of people have Delated eruption of teethOther people may have Abnormality of thorax Absent paranasal sinuses Arthralgia Carious teeth Genu valgum Hypoplastic frontal sinuses Limited elbow extension Mandibular prognathia Metaphyseal widening Metaphyseal dysplasia Muscle weakness Platyspondyly Reduced bone mineral density Scoliosis Thickened calvaria Cause Pyle disease is caused by mutations in the SFRP4 gene. This gene provides instructions for making a protein that blocks (inhibits) a process called Wnt signaling, which is involved in the development of several tissues and organs throughout the body. In particular, regulation of Wnt signaling by the SFRP4 protein is critical for normal bone development and remodeling. Bone remodeling is a normal process in which old bone is broken down and new bone is created to replace it. Mutations in the SFRP4 gene are thought to prevent the production of functional SFRP4 protein. The resulting dysregulation of Wnt signaling leads to the bone abnormalities characteristic of Pyle disease.Pyle disease is inherited in an autosomal recessive pattern, which means both copies of the SFRP4 gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene. While they do not develop the condition, they may have mild abnormalities of the long bones. Diagnosis There are two clinical molecular genetic test that are available to those thought to have Pyle’s Disease. Theses test are; Sequence analysis of the entire coding region and Deletion/duplication analysis. Differential diagnosis Pyle disease may be confused with craniometaphyseal dysplasia. The two, however, are clinically, radiographically, and genetically distinct from one another. Treatment People with Pyle disease are often asymptomatic. Dental anomalies may require orthodontic interventions. Skeletal anomalies may require orthopedic surgery. Epidemiology Pyle disease is thought to be a rare disorder, although its prevalence is unknown. More than 25 cases have been described in the medical literature.It has been described in four German families originating from the same town in Bohemia and in a 7-year-old Japanese girl. Research Cortical-bone fragility is a common feature in osteoporosis that is linked to nonvertebral fractures. Regulation of cortical-bone homeostasis has proved elusive. The study of genetic disorders of the skeleton can yield insights that fuel experimental therapeutic approaches to the treatment of rare disorders and common skeletal ailments. The study showed that Pyle’s disease was caused by a deficiency of sFRP4, that cortical-bone and trabecular-bone homeostasis were governed by different mechanisms, and that sFRP4-mediated cross-regulation between Wnt and BMP signaling was critical for achieving proper cortical-bone thickness and stability.Recently, homozygous mutations in secreted frizzled-related protein 4 gene (SFRP4) gene were found to underlie this condition. Sequencing of coding regions of SFRP4 gene from an 11-year-old female with PYL was performed. A novel homozygous nonsense variant, c.183C>G (p.Y61*) was observed. Segregation analysis in the patient revealed a germline mutation, resulting in reduced protein formation. References == External links ==

Hey Aarogya, could you help me understand about Amenorrhea

Amenorrhea

Amenorrhea is the absence of a menstrual period in a woman of reproductive age. Physiological states of amenorrhoea are seen, most commonly, during pregnancy and lactation (breastfeeding). Outside the reproductive years, there is absence of menses during childhood and after menopause.Amenorrhoea is a symptom with many potential causes. Primary amenorrhea is defined as an absence of secondary sexual characteristics by age 13 with no menarche or normal secondary sexual characteristics but no menarche by 15 years of age. It may be caused by developmental problems, such as the congenital absence of the uterus, failure of the ovary to receive or maintain egg cells, or delay in pubertal development. Secondary amenorrhoea, ceasing of menstrual cycles after menarche, is defined as the absence of menses for three months in a woman with previously normal menstruation, or six months for women with a history of oligomenorrhoea. It is often caused by hormonal disturbances from the hypothalamus and the pituitary gland, premature menopause, intrauterine scar formation, or eating disorders. Pathophysiology Although amenorrhea has multiple potential causes, ultimately, it is the result of hormonal imbalance or an anatomical abnormality.Physiologically, menstruation is controlled by the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. GnRH acts on the pituitary to stimulate the release of follicle stimulating hormone (FSH) and luteinizing hormone (LH). FSH and LH then act on the ovaries to stimulate the production of estrogen and progesterone which, respectively, control the proliferative and secretary phases of the menstrual cycle. Prolactin also influences the menstrual cycle as it suppresses the release of LH and FSH form the pituitary. Similarly, thyroid hormone also affects the menstrual cycle. Low levels of thyroid hormone stimulate the release of TRH from the hypothalamus, which in turn increases both TSH and prolactin release. This increase in prolactin suppresses the release of LH and FSH through a negative feedback mechanism. Amenorrhea can be caused by any mechanism that disrupts this hypothalamic-pituitary-ovarian axis, whether that it be by hormonal imbalance or by disruption of feedback mechanisms. Classification Amenorrhea is classified as either primary or secondary. Primary Amenorrhea Primary amenorrhoea is the absence of menstruation in a woman by the age of 16. Females who have not reached menarche at 14 and who have no signs of secondary sexual characteristics (thelarche or pubarche) are also considered to have primary amenorrhea. Examples of amenorrhea include constitutional delay of puberty, Turner syndrome, and Mayer–Rokitansky–Küster–Hauser (MRKH) syndrome. Secondary Amenorrhea Secondary amenorrhoea is defined as the absence of menstruation for three months in a woman with a history of regular cyclic bleeding or six months in a woman with a history of irregular menstrual periods. Examples of secondary amenorrhea include hypothyroidism, hyperthyroidism, hyperprolactinemia, polycystic ovarian syndrome, primary ovarian insufficiency, and functional hypothalamic amenorrhea. Causes Primary amenorrhea Turner syndrome Turner syndrome, monosomy 45XO, is a genetic disorder characterized by a missing, or partially missing, X chromosome. Turner syndrome is associated with a wide spectrum of features that vary with each case. However, one common feature of this syndrome is ovarian insufficiency due to gonadal dysgenesis. Most people with Turner syndrome experience ovarian insufficiency within the first few years of life, prior to menarche. Therefore, most patients with Turner syndrome will have primary amenorrhea. However, the incidence of spontaneous puberty varies between 8–40% depending on whether or not there is a complete or partial absence of the X chromosome. MRKH MRKH (Mayer–Rokitansky–Küster–Hauser) syndrome is the second-most common cause of primary amenorrhoea. The syndrome is characterized by Müllerian agenesis. In MRKH Syndrome, the Müllerian ducts develop abnormally and result in the absence of a uterus and cervix. Even though patients with MRKH have functioning ovaries, and therefore have secondary sexual characteristics, they experience primary amenorrhea since there is no functioning uterus. Constitutional delay of puberty Constitutional delay of puberty is a diagnosis of exclusion that is made when the workup for primary amenorrhea does not reveal another cause. Constitutional delay of puberty is not due to a pathologic cause. It is considered a variant of the timeline of puberty. Although more common in boys, girls with delayed puberty present with onset of secondary sexual characteristics after the age of 14, as well as menarche after the age of 16. This may be due to genetics, as some cases of constitutional delay of puberty are familial. Secondary amenorrhea Breastfeeding Physiologic amenorrhea is present before menarche, during pregnancy and breastfeeding, and after menopause.Breastfeeding or lactational amenorrhea is also a common cause of secondary amenorrhoea. Lactational amenorrhea is due to the presence of elevated prolactin and low levels of LH, which suppress ovarian hormone secretion. Breastfeeding typically prolongs postpartum lactational amenorrhoea, and the duration of amenorrhoea varies depending on how often a woman breastfeeds. Due to this reason, breastfeeding has been advocated as a method of family planning, especially in developing countries where access to other methods of contraception may be limited. Diseases of the thyroid Disturbances in thyroid hormone regulation has been a known cause of menstrual irregularities, including secondary amenorrhea.Patients with hypothyroidism frequently present with changes in their menstrual cycle. It is hypothesized that this is due to increased TRH, which goes on to stimulate the release of both TSH and prolactin. Increased prolactin inhibits the release of LH and FSH which are needed for ovulation to occur.Patients with hyperthyroidism may also present with oligomenorrhea or amenorrhea. Sex hormone binding globulin is increased in hyperthyroid states. This, in turn, increases the total levels of testosterone and estradiol. Increased levels of LH and FSH have also been reported in patients with hyperthyroidism. Hypothalamic and pituitary causes Changes in the hypothalamic-pituitary axis is a common cause of secondary amenorrhea. GnRH is released from the hypothalamus and stimulates the anterior pituitary to release FSH and LH, which in turn stimulate the ovaries to release estrogen and progesterone. Any pathology in the hypothalamus or pituitary can alter the way this feedback mechanism works and can cause secondary amenorrhea.Pituitary adenomas are a common cause of amenorrhea. Prolactin secreting pituitary adenomas cause amenorrhea due to the hyper-secretion of prolactin which inhibits FSH and LH release. Other space occupying pituitary lesions can also cause amenorrhea due to the inhibition of dopamine, an inhibitor of prolactin, due to compression of the pituitary gland. Polycystic ovary syndrome Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting 4–8% of women worldwide. It is characterized by multiple cysts on the ovary, amenorrhea or oligomenorrhea, and increased androgens. Although the exact cause remains unknown, it is hypothesized that increased levels of circulating androgens is what results in secondary amenorrhea. PCOS may also be a cause of primary amenorrhea if androgen access is present prior to menarche. Although multiple cysts on the ovary are characteristic of the syndrome, this has not been noted to be a cause of the disease. Low body weight Women who perform extraneous exercise on a regular basis or lose a significant amount of weight are at risk of developing hypothalamic amenorrhoea. Functional hypothalamic amenorrhoea (FHA) can be caused by stress, weight loss, or excessive exercise. Many women who diet or who exercise at a high level do not take in enough calories to maintain their normal menstrual cycles. The threshold of developing amenorrhoea appears to be dependent on low energy availability rather than absolute weight because a critical minimum amount of stored, easily mobilized energy is necessary to maintain regular menstrual cycles. Amenorrhoea is often associated with anorexia nervosa and other eating disorders. The female athlete triad is when a woman experiences amenorrhoea, disordered eating, and osteoporosis.Energy imbalance and weight loss can disrupt menstrual cycles through several hormonal mechanisms. Weight loss can cause elevations in the hormone ghrelin which inhibits the hypothalamic-pituitary-ovarial axis. Elevated concentrations of ghrelin alter the amplitude of GnRH pulses, which causes diminished pituitary release of LH and follicle-stimulating hormone (FSH). Low levels of the hormone leptin are also seen in females with low body weight. Like ghrelin, leptin signals energy balance and fat stores to the reproductive axis. Decreased levels of leptin are closely related to low levels of body fat, and correlate with a slowing of GnRH pulsing. Drug-induced Certain medications, particularly contraceptive medications, can induce amenorrhoea in a healthy woman. The lack of menstruation usually begins shortly after beginning the medication and can take up to a year to resume after stopping its use. Hormonal contraceptives that contain only progestogen, like the oral contraceptive Micronor, and especially higher-dose formulations, such as the injectable Depo-Provera, commonly induce this side effect. Extended cycle use of combined hormonal contraceptives also allow suppression of menstruation. Patients who stop using combined oral contraceptive pills (COCP) may experience secondary amenorrhoea as a withdrawal symptom. The link is not well understood, as studies have found no difference in hormone levels between women who develop amenorrhoea as a withdrawal symptom following the cessation of COCP use and women who experience secondary amenorrhoea because of other reasons. New contraceptive pills which do not have the normal seven days of placebo pills in each cycle, have been shown to increase rates of amenorrhoea in women. Studies show that women are most likely to experience amenorrhoea after one year of treatment with continuous OCP use.The use of opiates (such as heroin) on a regular basis has also been known to cause amenorrhoea in longer term users.Anti-psychotic drugs, which are commonly used to treat schizophrenia, have been known to cause amenorrhoea as well. Research suggests that anti-psychotic medications effect levels of prolactin, insulin, FSH, LH, and testosterone. Recent research suggests that adding a dosage of Metformin to an anti-psychotic drug regimen can restore menstruation. Metformin has been shown to decrease resistance to the hormone insulin, as well as levels of prolactin, testosterone, and luteinizing hormone (LH). Primary ovarian insufficiency Primary ovarian insufficiency (POI) affects 1% of females and is defined as the loss of ovarian function before the age of 40. Although the cause of POI can vary, it has been linked to chromosomal abnormalities, chemotherapy, and autoimmune conditions. Hormone levels in POI are similar to menopause and are categorized by low estradiol and high levels of gonadotropins. Since the pathogenesis of POI involves the depletion of ovarian reserve, restoration of menstrual cycles typically does not occur in this form of secondary amenorrhea. Diagnosis Primary amenorrhoea Primary amenorrhoea can be diagnosed in female children by age 14 if no secondary sex characteristics, such as enlarged breasts and body hair, are present. In the absence of secondary sex characteristics, the most common cause of amenorrhoea is low levels of FSH and LH caused by a delay in puberty. Gonadal dysgenesis, often associated with Turner syndrome, or premature ovarian failure may also be to blame. If secondary sex characteristics are present, but menstruation is not, primary amenorrhoea can be diagnosed by age 16.Evaluation of primary amenorrhea begins with a pregnancy test, prolactin, FSH, LH, and TSH levels. Abnormal TSH levels prompt evaluation for hyper- and hypo-thyroidism with additional thyroid function tests. Elevated prolactin levels prompt evaluation of the pituitary with an MRI to assess for any masses or malignancies. A pelvic ultrasound can also be obtained in the initial evaluation. If a uterus is not present on ultrasound, karyotype analysis and testosterone levels are obtained to assess for MRKH or androgen insensitivity syndrome. If a uterus is present, LH and FSH levels are used to make a diagnosis. Low levels of LH and FSH suggest delayed puberty or functional hypothalamic amenorrhea. Elevated levels of FSH and LH suggest primary ovarian insufficiency, typically due to Turner syndrome. Normal levels of FSH and LH can suggest an anatomical outflow obstruction. Secondary amenorrhea Secondary amenorrheas most common and most easily diagnosable causes are pregnancy, thyroid disease, and hyperprolactinemia. A pregnancy test is a common first step for diagnosis.Similar to primary amenorrhea, evaluation of secondary amenorrhea also begins with a pregnancy test, prolactin, FSH, LH, and TSH levels. A pelvic ultrasound is also obtained. Abnormal TSH should prompt a thyroid workup with a full thyroid function test panel. Elevated prolactin should be followed with an MRI to look for masses. If LH and FSH are elevated, menopause or primary ovarian insufficiency should be considered. Normal or low levels of FSH and LH prompts further evaluation with patient history and the physical exam. Testosterone, DHEA-S, and 17-hydroxyprogesterone levels should be obtained if there is evidence of excess androgens, such as hirsutism or acne. 17-hydroxyprogesterone is elevated in congenital adrenal hyperplasia. Elevated testosterone and amenorrhea can suggest PCOS. Elevated androgens can also be present in ovarian or adrenal tumors, so additional imaging may also be needed. History of disordered eating or excessive exercise should raise concern for hypothalamic amenorrhea. Headache, vomiting, and vision changes can be signs of a tumor and needs evaluation with MRI. Finally, a history of gynecologic procedures should lead to evaluation of Asherman syndrome with a hysteroscopy or progesterone withdrawal bleeding test. Treatment Treatment for amenorrhea varies based on the underlying condition. Treatment not only focuses on restoring menstruation, if possible, but also preventing additional complications associated with the underlying cause of amenorrhea. Primary amenorrhea In primary amenorrhea, the goal is to continue pubertal development, if possible. For example, most patients with Turner syndrome will be infertile due to gonadal dysgenesis. However, patients are frequently prescribed growth hormone therapy and estrogen supplementation to achieve taller stature and prevent osteoporosis. In other cases, such as MRKH, hormones do not need to be prescribed since the ovaries are able to function normally. Patients with constitutional delay of puberty may be monitored by an endocrinologist, but definitive treatment may not be needed as there will eventually be progression to normal puberty. Secondary amenorrhea Treatment for secondary amenorrhea varies greatly based on the root cause. Functional hypothalamic amenorrhoea is typically treated by weight gain through increased calorie intake and decreased expenditure. Multidisciplinary treatment with monitoring from a physician, dietitian, and mental health counselor is recommended, along with support from family, friends, and coaches. Although oral contraceptives can cause menses to return, oral contraceptives should not be the initial treatment as they can mask the underlying problem and allow other effects of the eating disorder, like osteoporosis, continue to develop.Patients with hyperprolactinemia are often treated with dopamine agonists to reduce the levels of prolactin and restore menstruation. Surgery and radiation may also be considered if dopamine agonists, such as cabergoline and bromocriptine are ineffective. Once prolactin levels are lowered, the resulting secondary amenorrhea is typically resolved. Similarly, treatment of thyroid abnormalities often resolves the associated amenorrhea. For example, administration of thyroxine in patients with low thyroid levels restored normal menstruation in a majority of patients.Although there is currently no definitive treatment for PCOS, various interventions are used to restore more frequent ovulation in patients. Weight loss and exercise have been associated with a return of ovulation in patients with PCOS due to normalization of androgen levels. Metformin has also been recently studied to regularize menstrual cycles in patients with PCOS. Although the exact mechanism still remains unknown, it is hypothesized that this is due to metformins ability to increase the bodys sensitivity to insulin. Anti-androgen medications, such as spironolactone, can also be used to lower body androgen levels and restore menstruation. Oral contraceptive pills are also often prescribed to patients with secondary amenorrhea due to PCOS in order to regularize the menstrual cycle, although this is due to the suppression of ovulation. References External links Disability Onlines amenorrhoea page Disability Onlines athletic amenorrhoea page Amenorrhea

Could you describe Hypocalcemia, to me Aarogya

Hypocalcemia

Hypocalcemia is a medical condition characterized by low calcium levels in the blood serum. The normal range of blood calcium is typically between 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L) while levels less than 2.1 mmol/L are defined as hypocalcemic. Mildly low levels that develop slowly often have no symptoms. Otherwise symptoms may include numbness, muscle spasms, seizures, confusion, or cardiac arrest.The most common cause for hypocalcemia is iatrogenic hypoparathyroidism. Other causes include other forms of hypoparathyroidism, vitamin D deficiency, kidney failure, pancreatitis, calcium channel blocker overdose, rhabdomyolysis, tumor lysis syndrome, and medications such as bisphosphonates or denosumab. Diagnosis should generally be confirmed with a corrected calcium or ionized calcium level. Specific changes may be seen on an electrocardiogram (ECG).Initial treatment for severe disease is with intravenous calcium chloride and possibly magnesium sulfate. Other treatments may include vitamin D, magnesium, and calcium supplements. If due to hypoparathyroidism, hydrochlorothiazide, phosphate binders, and a low salt diet may also be recommended. About 18% of people who are being treated in hospital have hypocalcemia. Signs and symptoms The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect (i.e. increased responsiveness) due to the decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, reduced calcium lowers the threshold for depolarization. The symptoms can be recalled by the mnemonic "CATs go numb" - convulsions, arrhythmias, tetany, and numbness in the hands and feet and around the mouth. Causes Hypoparathyroidism is a common cause of hypocalcemia. Calcium is tightly regulated by the parathyroid hormone (PTH). In response to low calcium levels, PTH levels rise, and conversely if there are high calcium levels then PTH secretion declines. However, in the setting of absent, decreased, or ineffective PTH hormone, the body loses this regulatory function, and hypocalcemia ensues. Hypoparathyroidism is commonly due to surgical destruction of the parathyroid glands. Hypoparathyroidism may also be due to autoimmune problem. Some causes of hypocalcaemia are as follows: Mechanism Physiologically, blood calcium is tightly regulated within a narrow range for proper cellular processes. Calcium in the blood exists in three primary states: bound to proteins (mainly albumin), bound to anions such as phosphate and citrate, and as free (unbound) ionized calcium; all of these forms are ionised. Only the unbound calcium is physiologically active. Normal blood calcium level is between 8.5 and 10.5 mg/dL (2.12 to 2.62 mmol/L) and that of unbound calcium is 4.65 to 5.25 mg/dL (1.16 to 1.31 mmol/L). Diagnosis Because a significant portion of calcium is bound to albumin, any alteration in the level of albumin will affect the measured level of calcium. A corrected calcium level based on the albumin level is: Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 * (4.0 - serum albumin [g/dL]). Since calcium is also bound to small anions, it may be more useful to correct total calcium for both albumin and the anion gap. Management Management of this condition includes: Intravenous calcium gluconate 10% can be administered, or if the hypocalcaemia is severe, calcium chloride is given instead. This is only appropriate if the hypocalcemia is acute and has occurred over a relatively short time frame. But if the hypocalcemia has been severe and chronic, then this regimen can be fatal, because there is a degree of acclimatization that occurs. The neuromuscular excitability, cardiac electrical instability, and associated symptoms are then not cured or relieved by prompt administration of corrective doses of calcium, but rather exacerbated. Such rapid administration of calcium would result in effective over correction – symptoms of hypercalcemia would follow. However, in either circumstance, maintenance doses of both calcium and vitamin-D (often as 1,25-(OH)2-D3, i.e. calcitriol) are often necessary to prevent further decline See also Milk fever (hypocalcemia in animals) Calcium deficiency (plant disorder) Hypomagnesemia with secondary hypocalcemia References == External links ==

Aarogya, share information about a health condition involving Carpal tunnel syndrome

Carpal tunnel syndrome

Carpal tunnel syndrome (CTS) is the collection of symptoms and signs associated with median neuropathy at the carpal tunnel. Most CTS is related to idiopathic compression of the median nerve as it travels through the wrist at the carpal tunnel (IMNCT). Idiopathic means that there is no other disease process contributing to pressure on the nerve. As with most structural issues, it occurs in both hands, and the strongest risk factor is genetics.Other conditions can cause CTS such as wrist fracture or rheumatoid arthritis. After fracture, swelling, bleeding, and deformity compress the median nerve. With rheumatoid arthritis, the enlarged synovial lining of the tendons causes compression. The main symptoms are numbness and tingling in the thumb, index finger, middle finger and the thumb side of the ring finger. People often report pain, but pain without tingling is not characteristic of IMNCT. Rather, the numbness can be so intense that it is described as painful. Symptoms are typically most troublesome at night. Untreated, and over years to decades, IMNCT causes loss of sensibility and weakness and shrinkage (atrophy) of the muscles at the base of the thumb. Work-related factors such as vibration, wrist extension or flexion, hand force, and repetition increase the risk of developing CTS. The only certain risk factor for IMNCT is genetics. All other risk factors are open to debate. It is important to consider IMNCT separately from CTS in diseases such as rheumatoid arthritis.Diagnosis of IMNCT can be made with a high probability based on characteristic symptoms and signs. IMNCT can be measured with electrodiagnostic tests.People wake less often at night if they wear a wrist splint. Injection of corticosteroids may or may not alleviate better than simulated (placebo) injections. There is no evidence that corticosteroid injection alters the natural history of the disease, which seems to be a gradual progression of neuropathy. Surgery to cut the transverse carpal ligament is the only known disease modifying treatment. Anatomy The carpal tunnel is an anatomical compartment located at the base of the palm. Nine flexor tendons and the median nerve pass through the carpal tunnel that is surrounded on three sides by the carpal bones that form an arch. The median nerve provides feeling or sensation to the thumb, index finger, long finger, and half of the ring finger. At the level of the wrist, the median nerve supplies the muscles at the base of the thumb that allow it to abduct, move away from the other four fingers, as well as move out of the plane of the palm. The carpal tunnel is located at the middle third of the base of the palm, bounded by the bony prominence of the scaphoid tubercle and trapezium at the base of the thumb, and the hamate hook that can be palpated along the axis of the ring finger. From the anatomical position, the carpal tunnel is bordered on the anterior surface by the transverse carpal ligament, also known as the flexor retinaculum. The flexor retinaculum is a strong, fibrous band that attaches to the pisiform and the hamulus of the hamate. The proximal boundary is the distal wrist skin crease, and the distal boundary is approximated by a line known as Kaplans cardinal line. This line uses surface landmarks, and is drawn between the apex of the skin fold between the thumb and index finger to the palpated hamate hook. Pathophysiology The median nerve can be compressed by a decrease in the size of the canal, an increase in the size of the contents (such as the swelling of tissue around the flexor tendons), or both. When the pressure builds up inside the tunnel, it damages the median nerve (median neuropathy). As the median neuropathy gets worse, there is loss of sensibility in the thumb, index, middle, and thumb side of the ring finger. As the neuropathy progresses, there may be first weakness, then to atrophy of the muscles of thenar eminence (the flexor pollicis brevis, opponens pollicis, and abductor pollicis brevis). The sensibility of the palm remains normal because the superficial sensory branch of the median nerve branches proximal to the TCL and travels superficial to it.The role of nerve adherence is speculative. Epidemiology IMNCT is estimated to affect one out of ten people during their lifetime and is the most common nerve compression syndrome. There is notable variation in such estimates based on how one defines the problem, in particular whether one studies people presenting with symptoms vs. measurable median neuropathy (IMNCT) whether or not people are seeking care. It accounts for about 90% of all nerve compression syndromes. The best data regarding IMNCT and CTS comes from population-based studies, which demonstrate no relationship to gender, and increasing prevalence (accumulation) with age. Symptoms The characteristic symptom of CTS is numbness, tingling, or burning sensations in the thumb, index, middle, and radial half of the ring finger. These areas process sensation through the median nerve. Numbness or tingling is usually worse with sleep. People tend to sleep with their wrists flexed, which increases pressure on the nerve. Ache and discomfort may be reported in the forearm or even the upper arm, but its relationship to IMNCT is uncertain. Symptoms that are not characteristic of CTS include pain in the wrists or hands, loss of grip strength, minor loss of sleep, and loss of manual dexterity.Median nerve symptoms may arise from compression at the level of the thoracic outlet or the area where the median nerve passes between the two heads of the pronator teres in the forearm, although this is debated. Signs Severe IMNCT is associated with measurable loss of sensibility. Diminished threshold sensibility (the ability to distinguish different amounts of pressure) can be measured using Semmes-Weinstein monofilament testing. Diminished discriminant sensibility can be measured by testing two-point discrimination: the number of millimeters two points of contact need to be separated before you can distinguish them.A person with idiopathic median neuropathy at the carpal tunnel will not have any sensory loss over the thenar eminence (bulge of muscles in the palm of hand and at the base of the thumb). This is because the palmar branch of the median nerve, which innervates that area of the palm, separates from the median nerve and passes over the carpal tunnel.Severe IMNCT is also associated with weakness and atrophy of the muscles at the base of the thumb. People may lose the ability to palmarly abduct the thumb. IMNCT can be detected on examination using one of several maneuvers to provoke paresthesia (a sensation of tingling or "pins and needles" in the median nerve distribution). These so-called provocative signs include: Phalens maneuver. Performed by fully flexing the wrist, then holding this position and awaiting symptoms. A positive test is one that results in paresthesia in the median nerve distribution within sixty seconds. Tinels sign is performed by lightly tapping the median nerve just proximal to flexor retinaculum to elicit paresthesia. Durkan test, carpal compression test, or applying firm pressure to the palm over the nerve for up to 30 seconds to elicit paresthesia. Hand elevation test The hand elevation test is performed by lifting both hands above the head. Paresthesia in the median nerve distribution within 2 minutes is considered positive.Diagnostic performance characteristics such as sensitivity and specificity are reported, but difficult to interpret because of the lack of a consensus reference standard for CTS or IMNCT. Causes Idiopathic Median Neuropathy at the Carpal Tunnel Genetic factors are believed to be the most important determinants of who develops carpal tunnel syndrome due to IMNCT. In other words, your wrist structure seems programmed at birth to develop IMNCT later in life. A genome-wide association study (GWAS) of carpal tunnel syndrome identified 16 genomic loci significantly associated with the disease, including several loci previously known to be associated with human height.Factors that may contribute to symptoms, but have not been experimentally associated with neuropathy include obesity, and Diabetes mellitus . One case-control study noted that individuals classified as obese (BMI > 29) are 2.5 times more likely than slender individuals (BMI < 20) to be diagnosed with CTS. Its not clear whether this association is due to an alteration of pathophysiology, a variation in symptoms, or a variation in care-seeking. Discrete Pathophysiology and Carpal Tunnel Syndrome Hereditary neuropathy with susceptibility to pressure palsies is a genetic condition that appears to increase the probability of developing MNCT. Heterozygous mutations in the gene SH3TC2, associated with Charcot-Marie-Tooth, may confer susceptibility to neuropathy, including CTS.Association between common benign tumors such as lipomas, ganglion, and vascular malformation should be handled with care. Such tumors are very common and overlap with IMNCT is more likely than pressure on the median nerve. Similarly, the degree to which transthyretin amyloidosis-associated polyneuropathy and carpal tunnel syndrome is under investigation. Prior carpal tunnel release is often noted in individuals who later present with transthyretin amyloid-associated cardiomyopathy. There is consideration that bilateral carpal tunnel syndrome could be a reason to consider amyloidosis, timely diagnosis of which could improve heart health. Amyloidosis is rare, even among people with carpal tunnel syndrome (0.55% incidence within 10 years of carpal tunnel release). In the absence of other factors associated with a notable probability of amyloidosis, its not clear that biopsy at the time of carpal tunnel release has a suitable balance between potential harms and potential benefits.Other specific pathophysiologies that can cause median neuropathy via pressure include: Rheumatoid arthritis and other diseases that cause inflammation of the flexor tendons. With severe untreated hypothyroidism, generalized myxedema causes deposition of mucopolysaccharides within both the perineurium of the median nerve, as well as the tendons passing through the carpal tunnel. Association of CTS and IMNCT with lesser degrees of hypothyroidism is questioned. Pregnancy may bring out symptoms in genetically predisposed individuals. Perhaps the changes in hormones and fluid increase pressure temporarily in the carpal tunnel. High progesterone levels and water retention may increase the size of the synovium. Bleeding and swelling from a fracture or dislocation. This is referred to as acute carpal tunnel syndrome. Acromegaly causes excessive secretion of growth hormones. This causes the soft tissues and bones around the carpal tunnel to grow and compress the median nerve.Other considerations Double-crush syndrome is a debated hypothesis that compression or irritation of nerve branches contributing to the median nerve in the neck, or anywhere above the wrist, increases sensitivity of the nerve to compression in the wrist. There is little evidence to support this theory and some concern that it may be used to justify more surgery. Median Neuropathy and Activity Work-related factors that increase risk of CTS include vibration (5.4 effect ratio), hand force (4.2), and repetition (2.3). Exposure to wrist extension or flexion at work increases the risk of CTS by two times. The balance of evidence suggests that keyboard and computer use does not cause CTS.The international debate regarding the relationship between CTS and repetitive hand use (at work in particular) is ongoing. The Occupational Safety and Health Administration (OSHA) has adopted rules and regulations regarding so-called "cumulative trauma disorders" based concerns regarding potential harm from exposure to repetitive tasks, force, posture, and vibration.A review of available scientific data by the National Institute for Occupational Safety and Health (NIOSH) indicated that job tasks that involve highly repetitive manual acts or specific wrist postures were associated with symptoms of CTS, but there was not a clear distinction of paresthesia (appropriate) from pain (inappropriate) and causation was not established. The distinction from work-related arm pains that are not carpal tunnel syndrome was unclear. It is proposed that repetitive use of the arm can affect the biomechanics of the upper limb or cause damage to tissues. It is proposed that postural and spinal assessment along with ergonomic assessments should be considered, based on observation that addressing these factors has been found to improve comfort in some studies although experimental data are lacking and the perceived benefits may not be specific to those interventions. A 2010 survey by NIOSH showed that 2/3 of the 5 million carpal tunnel diagnosed in the US that year were related to work. Women are more likely to be diagnosed with work-related carpal tunnel syndrome than men. Associated conditions A variety of patient factors can lead to CTS, including heredity, size of the carpal tunnel, associated local and systematic diseases, and certain habits. Non-traumatic causes generally happen over a period of time, and are not triggered by one certain event. Many of these factors are manifestations of physiologic aging. Diagnosis There is no consensus reference standard for the diagnosis of carpal tunnel syndrome. A combination of characteristic symptoms (how it feels) and signs (what the clinician finds on exam) are associated with a high probability of IMNCT without electrophysiological testing. Electrodiagnostic testing (electromyography and nerve conduction velocity) can objectively measure and verify median neuropathy.Ultrasound can image and measure the cross sectional diameter of the median nerve, which has some correlation with idiopathic median neuropathy at the carpal tunnel (IMNCT). The role of ultrasound in diagnosis--just as for electrodiagnostic testing--is a matter of debate. EDX cannot fully exclude the diagnosis of CTS due to the lack of sensitivity. A joint report published by the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM), the American Academy of Physical Medicine and Rehabilitation (AAPM&R), and the American Academy of Neurology defines practice parameters, standards, and guidelines for EDX studies of CTS based on an extensive critical literature review. This joint review concluded median and sensory nerve conduction studies are valid and reproducible in a clinical laboratory setting and a clinical diagnosis of CTS can be made with a sensitivity greater than 85% and specificity greater than 95%. Given the key role of electrodiagnostic testing in the diagnosis of CTS, The AANEM has issued evidence-based practice guidelines, both for the diagnosis of carpal tunnel syndrome. Electrodiagnostic testing (electromyography and nerve conduction velocity) can objectively verify the median nerve dysfunction. Normal nerve conduction studies, however, do not exclude the diagnosis of CTS. Clinical assessment by history taking and physical examination can support a diagnosis of CTS. If clinical suspicion of CTS is high, treatment should be initiated despite normal electrodiagnostic testing. The role of confirmatory electrodiagnostic testing is debated. The goal of electrodiagnostic testing is to compare the speed of conduction in the median nerve with conduction in other nerves supplying the hand. When the median nerve is compressed, as in IMNCT, it will conduct more slowly than normal and more slowly than other nerves. Compression results in damage to the myelin sheath and manifests as delayed latencies and slowed conduction velocities. There are many electrodiagnostic tests used to make a diagnosis of CTS, but the most sensitive, specific, and reliable test is the Combined Sensory Index (also known as the Robinson index). Electrodiagnosis rests upon demonstrating impaired median nerve conduction across the carpal tunnel in context of normal conduction elsewhere. It is often stated that normal electrodiagnostic studies do not preclude the diagnosis of carpal tunnel syndrome. The rational for this is that a threshold of neuropathy must be reached before study results become abnormal and also that threshold values for abnormality vary. Others contend that idiopathic median neuropathy at the carpal tunnel with normal electrodiagnostic tests would represent very, very mild neuropathy that would be best managed as a normal median nerve. Even more important, notable symptoms with mild disease is strongly associated with unhelpful thoughts and symptoms of worry and despair. Notable CTS with unmeasurable IMNCT should remind clinicians to always consider the whole person, including their mindset and circumstances, in strategies to help people get and stay healthy. Imaging The role of MRI or ultrasound imaging in the diagnosis of idiopathic median neuropathy at the carpal tunnel (IMNCT) is unclear. Their routine use is not recommended. MRI has high sensitivity but low specificity for IMNCT. High signal intensity may suggest accumulation of axonal transportation, myelin sheath degeneration or oedema. Differential diagnosis There are few disorders on the differential diagnosis for carpal tunnel syndrome. Cervical radiculopathy can also cause paresthesia abnormal sensibility in the hands and wrist. The distribution usually follows the nerve root, and the paresthesia may be provoked by neck movement. Electromyography and imaging of the cervical spine can help to differentiate cervical radiculopathy from carpal tunnel syndrome if the diagnosis is unclear. Carpal tunnel syndrome is sometimes applied as a label to anyone with pain, numbness, swelling, or burning in the radial side of the hands or wrists. When pain is the primary symptom, carpal tunnel syndrome is unlikely to be the source of the symptoms.When the symptoms and signs point to atrophy and muscle weakness more than numbness, consider neurodegenerative disorders such as Amyotrophic Lateral Sclerosis or Charcot-Marie Tooth. Prevention There is little or no data to support the concept that activity adjustment prevents carpal tunnel syndrome. The evidence for wrist rest is debated. There is also little research supporting that ergonomics is related to carpal tunnel syndrome. Due to risk factors for hand and wrist dysfunction being multifactorial and very complex it is difficult to assess the true physical factors of carpal tunnel syndrome.Biological factors such as genetic predisposition and anthropometric features are more strongly associated with idiopathic carpal tunnel syndrome than occupational/environmental factors such as hand use. Treatment CTS related to another pathophysiology is addressed by treating that pathology. For instance, disease-modifying medications for rheumatoid arthritis or surgery for traumatic acute carpal tunnel syndrome.Generally accepted treatments include: physiotherapy, steroids either orally or injected locally, splinting, and surgical release of the transverse carpal ligament. Limited evidence suggests that gabapentin is no more effective than placebo for CTS treatment. There is insufficient evidence to recommend therapeutic ultrasound, yoga, acupuncture, low level laser therapy, vitamin B6, myofascial release, and any form of stretch or exercise. Change in activity may include avoiding activities that worsen symptoms.The American Academy of Orthopedic Surgeons recommends proceeding conservatively with a course of nonsurgical therapies tried before release surgery is considered. A different treatment should be tried if the current treatment fails to resolve the symptoms within 2 to 7 weeks. Early surgery with carpal tunnel release is indicated where there is evidence of median nerve denervation or a person elects to proceed directly to surgical treatment. Recommendations may differ when carpal tunnel syndrome is found in association with the following conditions: diabetes mellitus, coexistent cervical radiculopathy, hypothyroidism, polyneuropathy, pregnancy, rheumatoid arthritis, and carpal tunnel syndrome in the workplace. Splint Immobilizations The importance of wrist braces and splints in the carpal tunnel syndrome therapy is known, but many people are unwilling to use braces. In 1993, The American Academy of Neurology recommended a non-invasive treatment for the CTS at the beginning (except for sensitive or motor deficit or grave report at EMG/ENG): a therapy using splints was indicated for light and moderate pathology. Current recommendations generally dont suggest immobilizing braces, but instead activity modification and non-steroidal anti-inflammatory drugs as initial therapy, followed by more aggressive options or specialist referral if symptoms do not improve.Many health professionals suggest that, for the best results, one should wear braces at night. When possible, braces can be worn during the activity primarily causing stress on the wrists. The brace should not generally be used during the day as wrist activity is needed to keep the wrist from becoming stiff and to prevent muscles from weakening. Corticosteroids Corticosteroid injections may provide temporary alleviation of symptoms although they are not clearly better than placebo. This form of treatment is thought to reduce discomfort in those with CTS due to its ability to decrease median nerve swelling. The use of ultrasound while performing the injection is more expensive but leads to faster resolution of CTS symptoms. The injections are done under local anesthesia. This treatment is not appropriate for extended periods, however. In general, local steroid injections are only used until more definitive treatment options can be used. Corticosteroid injections do not appear to slow disease progression. Surgery Release of the transverse carpal ligament is known as "carpal tunnel release" surgery. It is recommended when there is static (constant, not just intermittent) numbness, muscle weakness, or atrophy, and when night-splinting or other palliative interventions no longer alleviate intermittent symptoms. The surgery may be done with local or regional anesthesia with or without sedation, or under general anesthesia. In general, milder cases can be controlled for months to years, but severe cases are unrelenting symptomatically and are likely to result in surgical treatment.Surgery is more beneficial in the short term to alleviate symptoms (up to six months) than wearing an orthosis for a minimum of six weeks. However, surgery and wearing a brace resulted in similar symptom relief in the long term (12–18 month outcomes). Physical therapy An evidence-based guideline produced by the American Academy of Orthopedic Surgeons assigned various grades of recommendation to physical therapy and other nonsurgical treatments. One of the primary issues with physiotherapy is that it attempts to reverse (often) years of pathology inside the carpal tunnel. Self-myofascial ligament stretching can be an easy, do-at-home, treatment to help alleviate symptoms. Self-myofascial stretching involves stretching the carpal ligament for 30 seconds, 6 times a day for about 6 weeks. Many patients report improvements in symptoms such as pain, function, and nerve conduction. Practitioners caution that any physiotherapy such as myofascial release may take weeks of persistent application to effectively manage carpal tunnel syndrome.Again, some claim that pro-active ways to reduce stress on the wrists, which alleviates wrist pain and strain, involve adopting a more ergonomic work and life environment. For example, some have claimed that switching from a QWERTY computer keyboard layout to a more optimised ergonomic layout such as Dvorak was commonly cited as beneficial in early CTS studies; however, some meta-analyses of these studies claim that the evidence that they present is limited.Tendon and nerve gliding exercises appear to be useful in carpal tunnel syndrome.A randomized control trial published in 2017 sought to examine the efficacy of manual therapy techniques for the treatment of carpal tunnel syndrome. The study included a total of 140 individuals diagnosed with carpal tunnel syndrome and the patients were divided into two groups. One group received treatment that consisted of manual therapy. Manual therapy included the incorporation of specified neurodynamic techniques, functional massage, and carpal bone mobilizations. Another group only received treatment through electrophysical modalities. The duration of the study was over the course of 20 physical therapy sessions for both groups. Results of this study showed that the group being treated through manual techniques and mobilizations yielded a 290% reduction in overall pain when compared to reports of pain prior to conducting the study. Total function improved by 47%. Conversely, the group being treated with electrophysical modalities reported a 47% reduction in overall pain with a 9% increase in function. Alternative medicine A 2018 Cochrane review on acupuncture and related interventions for the treatment of carpal tunnel syndrome concluded that, "Acupuncture and laser acupuncture may have little or no effect in the short term on symptoms of carpal tunnel syndrome (CTS) in comparison with placebo or sham acupuncture." It was also noted that all studies had an unclear or high overall risk of bias and that all evidence was of low or very low quality. Prognosis Most people relieved of their carpal tunnel symptoms with conservative or surgical management find minimal residual or "nerve damage". Long-term chronic carpal tunnel syndrome (typically seen in the elderly) can result in permanent "nerve damage", i.e. irreversible numbness, muscle wasting, and weakness. Those that undergo a carpal tunnel release are nearly twice as likely as those not having surgery to develop trigger thumb in the months following the procedure.While outcomes are generally good, certain factors can contribute to poorer results that have little to do with nerves, anatomy, or surgery type. One study showed that mental status parameters or alcohol use yields much poorer overall results of treatment.Recurrence of carpal tunnel syndrome after successful surgery is rare. History The condition known as carpal tunnel syndrome had major appearances throughout the years but it was most commonly heard of in the years following World War II. Individuals who had had this condition have been depicted in surgical literature for the mid-19th century. In 1854, Sir James Paget was the first to report median nerve compression at the wrist in two cases.The first to notice the association between the carpal ligament pathology and median nerve compression appear to have been Pierre Marie and Charles Foix in 1913. They described the results of a postmortem of an 80-year-old man with bilateral carpal tunnel syndrome. They suggested that division of the carpal ligament would be curative in such cases. Putman had previously described a series of 37 patients and suggested a vasomotor origin. The association between the thenar muscle atrophy and compression was noted in 1914. The name "carpal tunnel syndrome" appears to have been coined by Moersch in 1938.In the early 20th century there were various cases of median nerve compression underneath the transverse carpal ligament. Physician George S. Phalen of the Cleveland Clinic identified the pathology after working with a group of patients in the 1950s and 1960s. TreatmentPaget described two cases of carpal tunnel syndrome. The first was due to an injury where a cord had been wrapped around a mans wrist. The second was due to a distal radial fracture. For the first case, Paget performed an amputation of the hand. For the second case Paget recommended a wrist splint – a treatment that is still in use today. Surgery for this condition initially involved the removal of cervical ribs despite Marie and Foixs suggested treatment. In 1933 Sir James Learmonth outlined a method of decompression of the nerve at the wrist. This procedure appears to have been pioneered by the Canadian surgeons Herbert Galloway and Andrew MacKinnon in 1924 in Winnipeg but was not published. Endoscopic release was described in 1988. See also Repetitive strain injury Tarsal tunnel syndrome Ulnar nerve entrapment References External links Carpal Tunnel Syndrome Fact Sheet (National Institute of Neurological Disorders and Stroke) Archived 2016-03-03 at the Wayback Machine NHS website carpal-tunnel.net provides a free to use, validated, online self diagnosis questionnaire for CTS "Carpal Tunnel Syndrome". MedlinePlus. U.S. National Library of Medicine.

Hi Aarogya, explain a situation where Wrist drop occurs

Wrist drop

Wrist drop is a medical condition in which the wrist and the fingers cannot extend at the metacarpophalangeal joints. The wrist remains partially flexed due to an opposing action of flexor muscles of the forearm. As a result, the extensor muscles in the posterior compartment remain paralyzed. Forearm anatomy The forearm is the part of the body that extends from the elbow to the wrist and is not to be confused with the arm, which extends from the shoulder to the elbow. The extensor muscles in the forearm are the extensor carpi ulnaris, extensor digiti minimi, extensor digitorum, extensor indicis, extensor carpi radialis brevis, and extensor carpi radialis longus. These extensor muscles are supplied by the posterior interosseous nerve, a branch of the radial nerve. Other muscles in the forearm that are innervated by this nerve are the supinator, extensor pollicis brevis, extensor pollicis longus and abductor pollicis longus. All of these muscles are situated in the posterior half of the forearm (posterior is when it is in its standard anatomical position). Also, the brachioradialis, anconeus, triceps brachii and extensor carpi radialis longus are all innervated by muscular branches of the radial nerve in the arm. Causes Wrist extension is achieved by muscles in the forearm contracting, pulling on tendons that attach distal to (beyond) the wrist. If the tendons, muscles, or nerves supplying these muscles are damaged or otherwise not working as they should be, wrist drop may occur. The following situations may result in wrist drop: Stab wounds to the chest at or below the clavicle–The radial nerve is the terminal branch of the posterior cord of the brachial plexus. A stab wound may damage the posterior cord and result in neurological deficits, including an inability to abduct the shoulder beyond the first 15 degrees, an inability to extend the forearm, reduced ability to supinate the hand, reduced ability to abduct the thumb and sensory loss to the posterior surface of the arm and hand. Broken humerus–The radial nerve can be damaged if the humerus (the bone of the arm) is broken because it runs through the radial groove on the lateral border of this bone along with the deep brachial artery. Lead poisoning–Wrist drop is associated with lead poisoning due to the effect of lead on the radial nerve. Persistent injury–Persistent injury to the nerve is a common cause through either repetitive motion or by applying pressure externally along the route of the radial nerve as in the prolonged use of crutches, extended leaning on the elbows, or regular upper body rope suspension. The colloquial terms for radial nerve palsy are derived from this cause. Correcting dislocated shoulders–Radial nerve palsy can result from the now discredited practice of correcting a dislocated shoulder by putting a foot in the persons armpit and pulling on the arm in attempts to slide the humerus back into the glenoid cavity of the scapula. Neuropathy in the hands and/or arms in patients with rheumatoid arthritis may in rare cases cause wrist drop. "When a joint swells, it can pinch the nerves of sensation that pass next to it. If the swelling irritates the nerve, either because of the inflammation or simply because of pressure, the nerve can send sensations of pain, numbness, and/or tingling to the brain. This is called nerve entrapment. Nerve entrapment most frequently occurs at the wrist (carpal tunnel syndrome) and elbow (ulnar nerve entrapment). A rare form of nerve disease in patients with rheumatoid arthritis that causes numbness and/or tingling is neuropathy. Neuropathy is nerve damage that in people with rheumatoid arthritis can result from inflammation of blood vessels (vasculitis)." Types Types of wrist drop are distinguished by the nerves affected: Weakness of brachioradialis, wrist extension and finger flexion = radial nerve lesion Weakness of finger extension and radial deviation of the wrist on extension = posterior interosseous nerve lesion Weakness of triceps, finger extensors and flexors = c7,8 lesion General weakness of upper limb marked in deltoid, triceps, wrist extension and finger extension = corticospinal lesion Diagnosis The workup for wrist drop frequently includes nerve conduction velocity studies to isolate and confirm the radial nerve as the source of the problem. Other screening tests include the inability to extend the thumb into a "hitchhikers sign". Plain films can help identify bone spurs and fractures that may have injured the nerve. Sometimes MRI imaging is required to differentiate subtle causes. Treatment Initial treatment includes splinting of the wrist for support, along with osteopathic medicine, physiotherapy and occupational therapy. In some cases, surgical removal of bone spurs or other anatomical defects that may be impinging on the nerve might be warranted. If the injury was the result of pressure from prolonged use of improperly fitted crutches or other similar mechanisms of injury, then the symptoms of wrist drop will most likely resolve spontaneously within 8–12 weeks. See also Radial neuropathy References External links clinicalconsiderations at The Anatomy Lesson by Wesley Norman (Georgetown University) William C. Shiel Jr., MD, FACP, FACR. "Rheumatoid Arthritis: 17 Warning Signs of Serious Complications".{{cite web}}: CS1 maint: multiple names: authors list (link)

Aarogya , Do you know what is Autumn,

Autumn

Autumn, also known as fall in American English and Canadian English, is one of the four temperate seasons on Earth. Outside the tropics, autumn marks the transition from summer to winter, in September (Northern Hemisphere) or March (Southern Hemisphere). Autumn is the season when the duration of daylight becomes noticeably shorter and the temperature cools considerably. Day length decreases and night length increases as the season progresses until the Winter Solstice in December (Northern Hemisphere) and June (Southern Hemisphere). One of its main features in temperate climates is the striking change in colour for the leaves of deciduous trees as they prepare to shed. Date definitions Some cultures regard the autumnal equinox as "mid-autumn", while others with a longer temperature lag treat the equinox as the start of autumn. In the English-speaking world of high latitude countries, autumn traditionally began with Lammas Day and ended around Halloween, the approximate mid-points between midsummer, the autumnal equinox, and midwinter. Meteorologists (and Australia and most of the temperate countries in the southern hemisphere) use a definition based on Gregorian calendar months, with autumn being September, October, and November in the northern hemisphere, and March, April, and May in the southern hemisphere. In the higher latitude countries in the Northern Hemisphere, autumn traditionally starts with the September equinox (21 to 24 September) and ends with the winter solstice (21 or 22 December). Popular culture in the United States associates Labor Day, the first Monday in September, as the end of summer and the start of autumn; certain summer traditions, such as wearing white, are discouraged after that date. As daytime and nighttime temperatures decrease, trees change colour and then shed their leaves.Under the traditional East Asian solar term system, autumn starts on or around 8 August and ends on or about 7 November. In Ireland, the autumn months according to the national meteorological service, Met Éireann, are September, October, and November. However, according to the Irish Calendar, which is based on ancient Gaelic traditions, autumn lasts throughout the months of August, September, and October, or possibly a few days later, depending on tradition. In the Irish language, September is known as Meán Fómhair ("middle of autumn") and October as Deireadh Fómhair ("end of autumn"). Persians celebrate the beginning of the autumn as Mehregan to honor Mithra (Mehr). Etymology The word autumn () is derived from Latin autumnus, archaic auctumnus, possibly from the ancient Etruscan root autu- and has within it connotations of the passing of the year. Alternative etymologies include Proto-Indo-European *h₃ewǵ- ("cold") or *h₂sows- ("dry").After the Greek era, the word continued to be used as the Old French word autompne (automne in modern French) or autumpne in Middle English, and was later normalised to the original Latin. In the Medieval period, there are rare examples of its use as early as the 12th century, but by the 16th century, it was in common use. Before the 16th century, harvest was the term usually used to refer to the season, as it is common in other West Germanic languages to this day (cf. Dutch herfst, German Herbst, and Scots hairst). However, as more people gradually moved from working the land to living in towns, the word harvest lost its reference to the time of year and came to refer only to the actual activity of reaping, and autumn, as well as fall, began to replace it as a reference to the season.The alternative word fall for the season traces its origins to old Germanic languages. The exact derivation is unclear, with the Old English fiæll or feallan and the Old Norse fall all being possible candidates. However, these words all have the meaning "to fall from a height" and are clearly derived either from a common root or from each other. The term came to denote the season in 16th-century England, a contraction of Middle English expressions like "fall of the leaf" and "fall of the year". Compare the origin of spring from "spring of the leaf" and "spring of the year".During the 17th century, Englishmen began emigrating to the new North American colonies, and the settlers took the English language with them. While the term fall gradually became nearly obsolete in Britain, it became the more common term in North America.The name backend, a once common name for the season in Northern England, has today been largely replaced by the name autumn. Associations Harvest Association with the transition from warm to cold weather, and its related status as the season of the primary harvest, has dominated its themes and popular images. In Western cultures, personifications of autumn are usually pretty, well-fed females adorned with fruits, vegetables and grains that ripen at this time. Many cultures feature autumnal harvest festivals, often the most important on their calendars. Still-extant echoes of these celebrations are found in the autumn Thanksgiving holiday of the United States and Canada, and the Jewish Sukkot holiday with its roots as a full-moon harvest festival of "tabernacles" (living in outdoor huts around the time of harvest). There are also the many festivals celebrated by indigenous peoples of the Americas tied to the harvest of ripe foods gathered in the wild, the Chinese Mid-Autumn or Moon festival, and many others. The predominant mood of these autumnal celebrations is a gladness for the fruits of the earth mixed with a certain melancholy linked to the imminent arrival of harsh weather. This view is presented in English poet John Keats poem To Autumn, where he describes the season as a time of bounteous fecundity, a time of mellow fruitfulness. In North America, while most foods are harvested during the autumn, foods usually associated with the season include pumpkins (which are integral parts of both Thanksgiving and Halloween) and apples, which are used to make the seasonal beverage apple cider. Melancholia Autumn, especially in poetry, has often been associated with melancholia. The possibilities and opportunities of summer are gone, and the chill of winter is on the horizon. Skies turn grey, the amount of usable daylight drops rapidly, and many people turn inward, both physically and mentally. It has been referred to as an unhealthy season.Similar examples may be found in Irish poet W.B. Yeats poem The Wild Swans at Coole where the maturing season that the poet observes symbolically represents his own ageing self. Like the natural world that he observes, he too has reached his prime and now must look forward to the inevitability of old age and death. French poet Paul Verlaines "Chanson dautomne" ("Autumn Song") is likewise characterised by strong, painful feelings of sorrow. Keats To Autumn, written in September 1819, echoes this sense of melancholic reflection but also emphasises the lush abundance of the season. The song "Autumn Leaves", based on the French song "Les Feuilles mortes", uses the melancholic atmosphere of the season and the end of summer as a metaphor for the mood of being separated from a loved one. Halloween Autumn is associated with Halloween (influenced by Samhain, a Celtic autumn festival), and with it a widespread marketing campaign that promotes it. The Celtic people also used this time to celebrate the harvest with a time of feasting. At the same time though, it was a celebration of death as well. Crops were harvested, livestock were butchered, and Winter was coming.Halloween, 31 October, is in autumn in the northern hemisphere. Television, film, book, costume, home decoration, and confectionery businesses use this time of year to promote products closely associated with such a holiday, with promotions going from late August or early September to 31 October, since their themes rapidly lose strength once the holiday ends, and advertising starts concentrating on Christmas. Other associations In some parts of the northern hemisphere, autumn has a strong association with the end of summer holiday and the start of a new school year, particularly for children in primary and secondary education. "Back to School" advertising and preparations usually occurs in the weeks leading to the beginning of autumn. Thanksgiving Day is a national holiday celebrated in Canada, in the United States, in some of the Caribbean islands and in Liberia. Thanksgiving is celebrated on the second Monday of October in Canada, on the fourth Thursday of November in the United States (where it is commonly regarded as the start of the Christmas and holiday season), and around the same part of the year in other places. Similarly named festival holidays occur in Germany and Japan. Television stations and networks, particularly in North America, traditionally begin their regular seasons in their autumn, with new series and new episodes of existing series debuting mostly during late September or early October (series that debut outside the autumn season are usually known as mid-season replacements). A sweeps period takes place in November to measure Nielsen Ratings. American football is played almost exclusively in the autumn months; at the high school level, seasons run from late August through early November, with some playoff games and holiday rivalry contests being played as late as Thanksgiving. In many American states, the championship games take place in early December. College footballs regular season runs from September through November, while the main professional circuit, the National Football League, plays from September through to early January. Summer sports, such as association football (in Northern America, East Asia, Argentina, and South Africa), Canadian football, stock car racing, tennis, golf, cricket, and professional baseball, wrap up their seasons in early to late autumn; Major League Baseballs championship World Series is popularly known as the "Fall Classic". (Amateur baseball is usually finished by August.) Likewise, professional winter sports, such as ice hockey and basketball, and most leagues of association football in Europe, are in the early stages of their seasons during autumn; American college basketball and college ice hockey play teams outside their athletic conferences during the late autumn before their in-conference schedules begin in winter. The Christian religious holidays of All Saints Day and All Souls Day are observed in autumn in the Northern hemisphere. Easter falls in autumn in the southern hemisphere. The secular celebration of International Workers Day also falls in autumn in the southern hemisphere. Since 1997, Autumn has been one of the top 100 names for girls in the United States.In Indian mythology, autumn is considered to be the preferred season for the goddess of learning Saraswati, who is also known by the name of "goddess of autumn" (Sharada). In Asian mysticism, Autumn is associated with the element of metal, and subsequently with the colour white, the White Tiger of the West, and death and mourning. Tourism Although colour change in leaves occurs wherever deciduous trees are found, coloured autumn foliage is noted in various regions of the world: most of North America, Eastern Asia (including China, Korea, and Japan), Europe, southeast, south, and part of the midwest of Brazil, the forest of Patagonia, eastern Australia and New Zealands South Island. Eastern Canada and New England are famous for their autumnal foliage, and this attracts major tourism (worth billions of US dollars) for the regions. Views of autumn Allegories of autumn in art See also Autumn in New England Diwali References == External links ==

Give me a short description about Thoracic aortic aneurysm , Aarogya

Thoracic aortic aneurysm

A thoracic aortic aneurysm is an aortic aneurysm that presents primarily in the thorax. A thoracic aortic aneurysm is the "ballooning" of the upper aspect of the aorta, above the diaphragm. Untreated or unrecognized they can be fatal due to dissection or "popping" of the aneurysm leading to nearly instant death. Thoracic aneurysms are less common than an abdominal aortic aneurysm. However, a syphilitic aneurysm is more likely to be a thoracic aortic aneurysm than an abdominal aortic aneurysm. This condition is commonly treated via a specialized multidisciplinary approach with both vascular surgeons and cardiac surgeons. Presentation Complications The principal causes of death due to thoracic aneurysmal disease are dissection and rupture. Once rupture occurs, the mortality rate is 50–80%. Most deaths in patients with Marfan syndrome are the result of aortic disease. Causes There are a number of causes, Aneurysms in patients younger than 40 usually involve the ascending aorta due to a weakening of the aortic wall associated with connective tissue disorders like the Marfan and Ehler-Danlos syndromes or congenital bicuspid aortic valve. Younger patients may develop aortic aneurysms of the thoracoabdominal aorta after an aortic dissection. It can also be caused by blunt injury. Atherosclerosis is the principal cause of descending aortic aneurysms, while aneurysms of the aortic arch may be due to dissection, atherosclerosis, or inflammation. Age The diagnosis of thoracic aortic aneurysm usually involves patients in their 60s and 70s. Risk factors Hypertension and cigarette smoking are the most important risk factors, though the importance of genetic factors has been increasingly recognized. Approximately 10 percent of patients may have other family members who have aortic aneurysms. It is also important to note that individuals with a history of aneurysms in other parts of the body have a higher chance of developing a thoracic aortic aneurysm. Diagnosis Thoracic aortic aneurysm is defined as a cross-sectional diameter exceeding the following cutoff: 4.5 cm in the United States 4.0 cm in South KoreaA diameter of 3.5 cm is generally considered dilated. However, average values vary with age and size of the reference population, as well as different segments of the aorta. Screening Guidelines were issued in March 2010 for early detection of thoracic aortic disease, by the American College of Cardiology, the American Heart Association, and other groups. Among the recommendations: First-degree relatives of people with thoracic aortic aneurysm or dissection should have aortic imaging to identify asymptomatic disease. People with symptoms suggestive of thoracic aortic dissection should be routinely evaluated "to establish a pretest risk of disease that can then be used to guide diagnostic decisions." People diagnosed with Marfan syndrome should immediately have an echocardiogram to measure the aorta and followed up six months later to check for aortic enlargement. Treatment The size cut off for aortic aneurysm is crucial to its treatment. A thoracic aorta greater than 4.5 cm is generally defined as aneurysmal, while a size greater than 6 cm is the distinction for treatment, which can be either endovascular or surgical, with the former reserved for pathology at the descending aorta.Indication for surgery may depend upon the size of the aneurysm. Aneurysms in the ascending aorta may require surgery at a smaller size than aneurysms in the descending aorta.Treatment may be via open or via endovascular means. Epidemiology Each year in the United States, some 45,000 people die from diseases of the aorta and its branches. Acute aortic dissection, a life-threatening event due to a tear in the aortic wall, affects 5 to 10 patients per million population each year, most often men between the ages of 50 and 70; of those that occur in women younger than 40, nearly half arise during pregnancy. The majority of these deaths occur as a result of complications of thoracic aneurysmal disease References == External links ==

Aarogya, can you share information about a health condition involving Esophageal candidiasis

Esophageal candidiasis

Esophageal candidiasis is an opportunistic infection of the esophagus by Candida albicans. The disease usually occurs in patients in immunocompromised states, including post-chemotherapy and in AIDS. However, it can also occur in patients with no predisposing risk factors, and is more likely to be asymptomatic in those patients. It is also known as candidal esophagitis or monilial esophagitis. Signs and symptoms People with esophageal candidiasis typically present with difficult or painful swallowing. Longstanding esophageal candidiasis can result in weight loss. There is often concomitant thrush in the mouth. Some patients present with esophageal candidiasis as a first presentation of systemic candidiasis. Diagnosis In most cases, the diagnosis is established based on response to therapy. Patients in whom esophageal candidiasis is suspected should receive a brief course of antifungal therapy with fluconazole. If the infection resolves after treatment with fluconazole, then the diagnosis of esophageal candidiasis is made and no further investigation is needed. However, if the infection persists or if there are other factors involved which may warrant further investigation, then patient will undergo an esophagogastroduodenoscopy if it is safe to do so. Endoscopy often reveals classic diffuse raised plaques that characteristically can be removed from the mucosa by the endoscope. Brushing or biopsy of the plaques shows yeast and pseudohyphae by histology that are characteristic of Candida species. Treatment The current first-line treatment is fluconazole, 200 mg. on the first day, followed by daily dosing of 100 mg. for at least 21 days total. Treatment should continue for 14 days after relief of symptoms. Other therapy options include: Nystatin is an effective treatment for mild esophageal candidiasis. It can be used as (swish, do not swallow) treatment for oral candidiasis that occurs with the use of asthma pumps. Oral fluconazole can be used for moderate to severe esophageal candidiasis (and oropharyngeal candidiasis). Other oral triazoles, such as itraconazole Caspofungin, used in refractory or systemic cases Amphotericin, used in refractory or systemic cases Mimidis, K; Papadopoulos, V; Margaritis, V; Thomopoulos, K; Gatopoulou, A; Nikolopoulou, V; Kartalis, G (February 2005). "Predisposing factors and clinical symptoms in HIV-negative patients with Candida oesophagitis: are they always present?". International Journal of Clinical Practice. 59 (2): 210–3. doi:10.1111/j.1742-1241.2004.00249.x. PMID 15854199. References == External links ==

Aarogya, Please give me a short description about Monocytic leukemia

Monocytic leukemia

Monocytic leukemia is a type of myeloid leukemia characterized by a dominance of monocytes in the marrow. When the monocytic cells are predominantly monoblasts, it can be subclassified into acute monoblastic leukemia. Monocytic leukemia is almost always broken down into "acute" and "chronic": acute monocytic leukemia chronic myelomonocytic leukemia References == External links ==

Can you describe Organ donation, to me Aarogya

Organ donation

Organ donation is the process when a person allows an organ of their own to be removed and transplanted to another person, legally, either by consent while the donor is alive or dead with the assent of the next of kin. Donation may be for research or, more commonly, healthy transplantable organs and tissues may be donated to be transplanted into another person.Common transplantations include kidneys, heart, liver, pancreas, intestines, lungs, bones, bone marrow, skin, and corneas. Some organs and tissues can be donated by living donors, such as a kidney or part of the liver, part of the pancreas, part of the lungs or part of the intestines, but most donations occur after the donor has died.In 2019, Spain had the highest donor rate in the world at 46.91 per million people, followed by the US (36.88 per million), Croatia (34.63 per million), Portugal (33.8 per million), and France (33.25 per million).As of February 2, 2019, there were 120,000 people waiting for life-saving organ transplants in the US. Of these, 74,897 people were active candidates waiting for a donor. While views of organ donation are positive, there is a large gap between the numbers of registered donors compared to those awaiting organ donations on a global level.To increase the number of organ donors, especially among underrepresented populations, current approaches include the use of optimized social network interventions, exposing tailored educational content about organ donation to target social media users. Every year August 13 is observed as World Organ Donation Day to raising awareness about the importance of organ donation. Process in the United States Organ donors are usually dead at the time of donation, but may be living. For living donors, organ donation typically involves extensive testing before the donation, including psychological evaluation to determine whether the would-be donor understands and consents to the donation. On the day of the donation, the donor and the recipient arrive at the hospital, just like they would for any other major surgery.For dead donors, the process begins with verifying that the person is undoubtedly deceased, determining whether any organs could be donated, and obtaining consent for the donation of any usable organs. Normally, nothing is done until the person has already died, although if death is inevitable, it is possible to check for consent and to do some simple medical tests shortly beforehand, to help find a matching recipient.The verification of death is normally done by a neurologist (a physician specializing in brain function) that is not involved in the previous attempts to save the patients life. This physician has nothing to do with the transplantation process. Verification of death is often done multiple times, to prevent doctors from overlooking any remaining sign of life, however small. After death, the hospital may keep the body on a mechanical ventilator and use other methods to keep the organs in good condition. The donors estate and their families are not charged for any expenses related to the donation. The surgical process depends upon which organs are being donated. The body is normally restored to as normal an appearance as possible, so that the family can proceed with funeral rites and either cremation or burial. The lungs are highly vulnerable to injury and thus the most difficult to preserve, with only 15–25% of donated organs utilized. History The first living organ donor in a successful transplant was Ronald Lee Herrick (1931–2010), who donated a kidney to his identical twin brother in 1954. The lead surgeon, Joseph Murray, and the Nephrologist, John Merril won the Nobel Prize in Physiology or Medicine in 1990 for advances in organ transplantation. The youngest organ donor was a baby with anencephaly, born in 2014, who lived for only 100 minutes and donated his kidneys to an adult with renal failure. The oldest known cornea donor was a 107-year-old Scottish woman, whose corneas were donated after her death in 2016. The oldest known organ donor for an internal organ was a 95-year-old West Virginia man, who donated his liver after he died.The oldest altruistic living organ donor was an 85-year-old woman in Britain, who donated a kidney to a stranger in 2014 after hearing how many people needed to receive a transplant.Researchers were able to develop a novel way to transplant human fetal kidneys into anephric rats to overcome a significant obstacle in impeding human fetal organ transplantations. The human fetal kidneys demonstrated both growth and function within the rats. Brain donation Donated brain tissue is a valuable resource for research into brain function, neurodiversity, neuropathology and possible treatments. Both divergent and healthy control brains are needed for comparison. Brain banks typically source tissue from donors that had directly registered with them before their passing, since organ donor registries focus on tissue meant for transplantation. In the United States the nonprofit Brain Donor Project facilitates this process. Legislation and global perspectives The laws of different countries allow potential donors to permit or refuse donation, or give this choice to relatives. The frequency of donations varies among countries. Consent process The term consent is typically defined as a subject adhering to an agreement of principles and regulations; however, the definition becomes difficult to execute concerning the topic of organ donation, mainly because the subject is incapable of consent due to death or mental impairment. There are two types of consent being reviewed; explicit consent and presumed consent. Explicit consent consists of the donor giving direct consent through proper registration depending on the country. The second consent process is presumed consent, which does not need direct consent from the donor or the next of kin. Presumed consent assumes that donation would have been permitted by the potential donor if permission was pursued. Of possible donors an estimated twenty-five percent of families refuse to donate a loved ones organs. Opt-in versus opt-out As medical science advances, the number of people who could be helped by organ donors increases continuously. As opportunities to save lives increase with new technologies and procedures, the demand for organ donors rises faster than the actual number of donors. In order to respect individual autonomy, voluntary consent must be determined for the individuals disposition of their remains following death. There are two main methods for determining voluntary consent: "opt in" (only those who have given explicit consent are donors) and "opt out" (anyone who has not refused consent to donate is a donor). In terms of an opt-out or presumed consent system, it is assumed that individuals do intend to donate their organs to medical use when they expire. Opt-out legislative systems dramatically increase effective rates of consent for donation as a consequence of the default effect. For example, Germany, which uses an opt-in system, has an organ donation consent rate of 12% among its population, while Austria, a country with a very similar culture and economic development, but which uses an opt-out system, has a consent rate of 99.98%.Opt-out consent, otherwise known as "deemed" consent, support refers to the notion that the majority of people support organ donation, but only a small percentage of the population are actually registered, because they fail to go through the actual step of registration, even if they want to donate their organs at the time of death. This could be resolved with an opt-out system, where many more people would be registered as donors when only those who object consent to donation have to register to be on the non-donation list.For these reasons, countries, such as Wales, have adopted a "soft opt-out" consent, meaning if a citizen has not clearly made a decision to register, then they will be treated as a registered citizen and participate in the organ donation process. Likewise, opt-in consent refers to the consent process of only those who are registered to participate in organ donation. Currently, the United States has an opt-in system, but studies show that countries with an opt-out system save more lives due to more availability of donated organs. The current opt-in consent policy assumes that individuals are not willing to become organ donors at the time of their death, unless they have documented otherwise through organ donation registration.Registering to become an organ donor heavily depends on the attitude of the individual; those with a positive outlook might feel a sense of altruism towards organ donation, while others may have a more negative perspective, such as not trusting doctors to work as hard to save the lives of registered organ donors. Some common concerns regarding a presumed consent ("opt-out") system are sociologic fears of a new system, moral objection, sentimentality, and worries of the management of the objection registry for those who do decide to opt-out of donation. Additional concerns exist with views of compromising the freedom of choice to donate, conflicts with extant religious beliefs and the possibility of posthumous violations of bodily integrity. Even though concerns exist, the United States still has a 95 percent organ donation approval rate. This level of nationwide acceptance may foster an environment where moving to a policy of presumed consent may help solve some of the organ shortage problem, where individuals are assumed to be willing organ donors unless they document a desire to "opt-out", which must be respected.Because of public policies, cultural, infrastructural and other factors, presumed consent or opt-out models do not always translate directly into increased effective rates of donation. The United Kingdom has several different laws and policies for the organ donation process, such as consent of a witness or guardian must be provided to participate in organ donation. This policy is currently being consulted on by Department of Health and Social Care.In terms of effective organ donations, in some systems like Australia (14.9 donors per million, 337 donors in 2011), family members are required to give consent or refusal, or may veto a potential recovery even if the donor has consented. Some countries with an opt-out system like Spain (40.2 donors per million inhabitants), Croatia (40.2 donors/million) or Belgium (31.6 donors/million) have high donor rates, however some countries such as Greece (6 donors/million) maintain low donor rates even with this system. The president of the Spanish National Transplant Organisation has acknowledged Spains legislative approach is likely not the primary reason for the countrys success in increasing the donor rates, starting in the 1990s.Looking to the example of Spain, which has successfully adopted the presumed consent donation system, intensive care units (ICUs) must be equipped with enough doctors to maximize the recognition of potential donors and maintain organs while families are consulted for donation. The characteristic that enables the Spanish presumed consent model to be successful is the resource of transplant coordinators; it is recommended to have at least one at each hospital where opt-out donation is practiced to authorize organ procurement efficiently.Public views are crucial to the success of opt-out or presumed consent donation systems. In a study done to determine if health policy change to a presumed consent or opt-out system would help to increase donors, an increase of 20 to 30 percent was seen among countries who changed their policies from some type of opt-in system to an opt-out system. Of course, this increase must have a great deal to do with the health policy change, but also may be influenced by other factors that could have impacted donor increases.Transplant Priority for Willing Donors, also known as the "donor-priority rule", is a newer method and the first to incorporate a "non-medical" criteria into the priority system to encourage higher donation rates in the opt-in system. Initially implemented in Israel, it allows an individual in need of an organ to move up the recipient list. Moving up the list is contingent on the individual opting-in prior to their need for an organ donation. The policy applies nonmedical criteria when allowing the individual who has previously registered as an organ donor, or family has previously donated an organ, priority over another possible recipient. It must be determined that both recipients have identical medical needs prior to moving a recipient up the list. While incentives like this in the opt-in system do help raise donation rates, they are not as successful in doing so as the opt-out, presumed consent default policies for donation. Argentina On November 30, 2005, the Congress introduced an opt-out policy on organ donation, where all people over 18 years of age will be organ donors unless they or their family state otherwise. The law was promulgated on December 22, 2005, as "Law 26,066".On July 4, 2018, the Congress passed a law removing the family requirement, making the organ donor the only person that can block donation. It was promulgated on July 4, 2018, as Law Justina or "Law 27,447". Brazil A campaign by Sport Club Recife has led to waiting lists for organs in north-east Brazil to drop almost to zero; while according to the Brazilian law the family has the ultimate authority, the issuance of the organ donation card and the ensuing discussions have however eased the process. Canada In 2001, the Government of Canada announced the formation of the Canadian Council for Donation and Transplantation, whose purpose would be to advise the Conference of Deputy Ministers of Health on activities relating to organ donation and transplantation. The deputy ministers of health for all provinces and territories with the exception of Québec decided to transfer the responsibilities of the Canadian Council for Donation and Transplantation to Canadian Blood Services.In Québec, an organization called Transplant Québec is responsible for managing all organ donation; Héma-Québec is responsible for tissue donation. Consent for organ donation by an individual is given by either registering with the organ donation registry established by the Chambre des notaires du Québec, signing and affixing the sticker to the back of ones health insurance card, or registering with either Régie de lassurance maladie du Québec or Registre des consentements au don dorganes et de tissus. In 2017, the majority of transplants completed were kidney transplants. Canadian Blood Services has a program called the kidney paired donation, where transplant candidates are matched with compatible living donors from all over Canada. It also gives individuals an opportunity to be a living donor for an anonymous patient waiting for a transplant. As of December 31, 2017, there were 4,333 patients on the transplant waitlist. In 2017, there were a total of 2,979 transplants, including multi-organ transplants; 242 patients died while on the waitlist. 250 Canadians die on average waiting for transplant organs every year.Each province has different methods and registries for intent to donate organs or tissues as a deceased donor. In some provinces, such as Newfoundland and Labrador and New Brunswick organ donation registration is completed by completing the "Intent to donate" section when applying or renewing ones provincial medical care. In Ontario, one must be 16 years of age to register as an organ and tissue donor and register with ServiceOntario. Alberta requires that a person must be 18 years of age or older and register with the Alberta Organ and Tissue Donation Registry. Opt-out donation in Canada Nova Scotia, Canada, is the first jurisdiction in North America that will be introducing an automatic organ donation program unless residents opt out; this is known as presumed consent. The Human Organ and Tissue Act was introduced on April 2, 2019. When the new legislation is in effect, all people who have been Nova Scotia residents for a minimum of 12 consecutive months, with appropriate decision-making capacity and are over 19 years of age are considered potential donors and will be automatically referred to donation programs if they are determined to be good candidates. In the case of persons under 19 years of age and people without appropriate decision-making capacity, they will only be considered as organ donors if their parent, guardian or decision-maker opts them into the program. The new legislation is scheduled to take effect in mid to late 2020, and will not be applicable to tourists visiting Nova Scotia or post-secondary students from other provinces or countries Chile On January 6, 2010, the "Law 20,413" was promulgated, introducing an opt-out policy on organ donation, where all people over 18 years of age will be organ donors unless they state their negative. Colombia On August 4, 2016, the Congress passed the "Law 1805", which introduced an opt-out policy on organ donation where all people will be organ donors unless they state their negative. The law came into force on February 4, 2017. Europe Within the European Union, organ donation is regulated by member states. As of 2010, 24 European countries have some form of presumed consent (opt-out) system, with the most prominent and limited opt-out systems in Spain, Austria, and Belgium yielding high donor rates. Spain had the highest donor rate in the world, 46.9 per million people in the population, in 2017. This is attributed to multiple factors in the Spanish medical system, including identification and early referral of possible donors, expanding criteria for donors and standardised frameworks for transplantation after circulatory death.In England organ donation is voluntary and no consent is presumed. Individuals who wish to donate their organs after death can use the Organ Donation Register, a national database. The government of Wales became the first constituent country in the UK to adopt presumed consent in July 2013. The opt-out organ donation scheme in Wales went live on December 1, 2015, and is expected to increase the number of donors by 25%. In 2008, the UK discussed whether to switch to an opt-out system in light of the success in other countries and a severe British organ donor shortfall. In Italy if the deceased neither allowed nor refused donation while alive, relatives will pick the decision on his or her behalf despite a 1999 act that provided for a proper opt-out system. In 2008, the European Parliament overwhelmingly voted for an initiative to introduce an EU organ donor card in order to foster organ donation in Europe.Landstuhl Regional Medical Center (LRMC) has become one of the most active organ donor hospitals in all of Germany, which otherwise has one of the lowest organ donation participation rates in the Eurotransplant organ network. LRMC, the largest U.S. military hospital outside the United States, is one of the top hospitals for organ donation in the Rhineland-Palatinate state of Germany, even though it has relatively few beds compared to many German hospitals. According to the German organ transplantation organization, Deutsche Stiftung Organtransplantation (DSO), 34 American military service members who died at LRMC (roughly half of the total number who died there) donated a total of 142 organs between 2005 and 2010. In 2010 alone, 10 of the 12 American service members who died at LRMC were donors, donating a total of 45 organs. Of the 205 hospitals in the DSOs central region—which includes the large cities of Frankfurt and Mainz—only six had more organ donors than LRMC in 2010.Scotland conforms to the Human Tissue Authority Code of Practice, which grants authority to donate organs, instead of consent of the individual. This helps to avoid conflict of implications and contains several requirements. In order to participate in organ donation, one must be listed on the Organ Donor Registry (ODR). If the subject is incapable of providing consent, and is not on the ODR, then an acting representative, such as a legal guardian or family member can give legal consent for organ donation of the subject, along with a presiding witness, according to the Human Tissue Authority Code of Practice. Consent or refusal from a spouse, family member, or relative is necessary for a subject is incapable. Austria participates in the "opt-out" consent process, and have laws that make organ donation the default option at the time of death. In this case, citizens must explicitly "opt out" of organ donation. Yet in countries such as U.S.A. and Germany, people must explicitly "opt in" if they want to donate their organs when they die. In Germany and Switzerland there are Organ Donor Cards available.In May 2017, Ireland began the process of introducing an "opt-out" system for organ donation. Minister for Health, Simon Harris, outlined his expectations to have the Human Tissue Bill passed by the end of 2017. This bill would put in place the system of "presumed consent".The Mental Capacity Act is another legal policy in place for organ donation in the UK. The act is used by medical professionals to declare a patients mental capacity. The act claims that medical professionals are to "act in a patients best interest", when the patient is unable to do so. India India has a fairly well developed corneal donation programme; however, donation after brain death has been relatively slow to take off. Most of the transplants done in India are living related or unrelated transplants. To curb organ commerce and promote donation after brain death the government enacted a law called "The Transplantation of Human Organs Act" in 1994 that brought about a significant change in the organ donation and transplantation scene in India. Many Indian states have adopted the law and in 2011 further amendment of the law took place. Despite the law there have been stray instances of organ trade in India and these have been widely reported in the press. This resulted in the amendment of the law further in 2011. Deceased donation after brain death have slowly started happening in India and 2012 was the best year for the programme. Source the Indian Transplant News Letter of the MOHAN FoundationThe year 2013 has been the best yet for deceased organ donation in India. A total of 845 organs were retrieved from 310 multi-organ donors resulting in a national organ donation rate of 0.26 per million population(Table 2). * ODR (pmp) – Organ Donation Rate (per million population) In the year 2000 through the efforts of an NGO called MOHAN Foundation state of Tamil Nadu started an organ sharing network between a few hospitals. This NGO also set up similar sharing network in the state of Andhra Pradesh and these two states were at the forefront of deceased donation and transplantation programme for many years. As a result, retrieval of 1,033 organs and tissues were facilitated in these two states by the NGO.Similar sharing networks came up in the states of Maharashtra and Karnataka; however, the numbers of deceased donation happening in these states were not sufficient to make much impact. In 2008, the Government of Tamil Nadu put together government orders laying down procedures and guidelines for deceased organ donation and transplantation in the state. These brought in almost thirty hospitals in the programme and has resulted in significant increase in the donation rate in the state. With an organ donation rate of 1.15 per million population, Tamil Nadu is the leader in deceased organ donation in the country. The small success of Tamil Nadu model has been possible due to the coming together of both government and private hospitals, NGOs and the State Health department. Most of the deceased donation programmes have been developed in southern states of India. The various such programmes are as follows: In the year 2012 besides Tamil Nadu other southern states too did deceased donation transplants more frequently. An online organ sharing registry for deceased donation and transplantation is used by the states of Tamil Nadu and Kerala. Both these registries have been developed, implemented and maintained by MOHAN Foundation. However. National Organ and Tissue Transplant Organization (NOTTO) is a National level organization set up under Directorate General of Health Services, Ministry of Health and Family Welfare, Government of India and only official organization. Organ selling is legally banned in Asia. Numerous studies have documented that organ vendors have a poor quality of life (QOL) following kidney donation. However, a study done by Vemuru reddy et al shows a significant improvement in Quality of life contrary to the earlier belief. Live related renal donors have a significant improvement in the QOL following renal donation using the WHO QOL BREF in a study done at the All India Institute of Medical Sciences from 2006 to 2008. The quality of life of the donor was poor when the graft was lost or the recipient died.In India, there are six types of life saving organs that can be donated to save the life of a patient. These include Kidneys, Liver, Heart, Lungs, Pancreas and Intestine. Off late, uterus transplant has also been started in India. However, uterus is not a life saving organ as per the Transplantation of Human Organs Act (2011). Recently a scoring system, Seth-Donation of Organs and Tissues (S-DOT) score, has been developed to assess hospitals for best practices in tissue donation and organ donation after brain death. Iran Only one country, Iran has eliminated the shortage of transplant organs—and only Iran has a working and legal payment system for organ donation. It is also the only country where organ trade is legal. The way their system works is, if a patient does not have a living relative or who are not assigned an organ from a deceased donor, apply to the nonprofit Dialysis and Transplant Patients Association (Datpa). The association establishes potential donors, those donors are assessed by transplant doctors who are not affiliated with the Datpa association. The government gives a compensation of $1,200 to the donors and aid them a year of limited health-insurance. Additionally, working through Datpa, kidney recipients pay donors between $2,300 and $4,500. Importantly, it is illegal for the medical and surgical teams involved or any middleman to receive payment. Charity donations are made to those donors whose recipients are unable to pay. The Iranian system began in 1988 and eliminated the shortage of kidneys by 1999. Within the first year of the establishment of this system, the number of transplants had almost doubled; nearly four-fifths were from living unrelated sources.[55] Nobel Laureate economist Gary Becker and Julio Elias estimated that a payment of $15,000 for living donors would alleviate the shortage of kidneys in the U.S. Israel Since 2008, signing an organ donor card in Israel has provided a potential medical benefit to the signer. If two patients require an organ donation and have the same medical need, preference will be given to the one that had signed an organ donation card. (This policy was nicknamed "Dont give, dont get".) Organ donation in Israel increased after 2008. Japan The rate of organ donation in Japan is significantly lower than in Western countries. This is attributed to cultural reasons, some distrust of western medicine, and a controversial organ transplantation in 1968 that provoked a ban on cadaveric organ donation that would last thirty years. Organ donation in Japan is regulated by a 1997 organ transplant law, which defines "brain death" and legalized organ procurement from brain dead donors. Netherlands The Netherlands sends everyone living in the country a postcard when they turn 18 (and everyone living in the country when the 2020 law came into effect), and one reminder if they do not reply. They may choose to donate, not to donate, to delegate the choice to family, or to name a specific person. If they do not reply to either notice, they are considered a donor by default. A family cannot object unless there is reason to show the person would not have wanted to donate. If a person cannot be found in the national donor registry, because they are travelling from another country or because they are undocumented, their organs are not harvested without family consent. Organs are not harvested from people who die an unnatural death without the approval of the local attorney general. New Zealand New Zealand law allows live donors to participate in altruistic organ donation only. In the five years to 2018, there were 16 cases of liver donation by live donors and 381 cases of kidney donation by live donors. New Zealand has low rates of live donation, which could be due to the fact that it is illegal to pay someone for their organs. The Human Tissue Act 2008 states that trading in human tissue is prohibited, and is punishable by a fine of up to $50,000 or a prison term of up to 1 year. The Compensation for Live Organ Donors Act 2016, which came into force in December 2017, allows live organ donors to be compensated for lost income for up to 12 weeks post-donation.New Zealand law also allows for organ donation from deceased individuals. In the five years to 2018, organs were taken from 295 deceased individuals. Everyone who applies for a drivers licence in New Zealand indicates whether or not they wish to be a donor if they die in circumstances that would allow for donation. The question is required to be answered for the application to be processed, meaning that the individual must answer yes or no, and does not have the option of leaving it unanswered. However, the answer given on the drivers license does not constitute informed consent, because at the time of drivers license application not all individuals are equipped to make an informed decision regarding whether to be a donor, and it is therefore not the deciding factor in whether donation is carried out or not. It is there to simply give indication of the persons wishes. Family must agree to the procedure for donation to take place.A 2006 bill proposed setting up an organ donation register where people can give informed consent to organ donations and clearly state their legally binding wishes. However, the bill did not pass, and there was condemnation of the bill from some doctors, who said that even if a person had given express consent for organ donation to take place, they would not carry out the procedure in the presence of any disagreement from grieving family members.The indigenous population of New Zealand also have strong views regarding organ donation. Many Maori people believe organ donation is morally unacceptable due to the cultural need for a dead body to remain fully intact. However, because there is not a universally recognised cultural authority, no one view on organ donation is universally accepted in the Maori population. They are, however, less likely to accept a kidney transplant than other New Zealanders, despite being overrepresented in the population receiving dialysis. South Korea In South Korea, the 2006 provision of the Organ Transplant Act introduced a monetary incentive equivalent to US$4,500 to the surviving family of brain-death donors; the reward is intended as consolation and compensation for funeral expenses and hospital fees. Sri Lanka Organ donation in Sri Lanka was ratified by the Human Tissue Transplantation Act No. 48 of 1987. Sri Lanka Eye Donation Society, a non-governmental organization established in 1961 has provided over 60,000 corneas for corneal transplantation, for patients in 57 countries. It is one of the major suppliers of human eyes to the world, with a supply of approximately 3,000 corneas per year. United Kingdom Wales Since December 2015, Human Transplantation (Wales) Act 2013 passed by the Welsh Government has enabled an opt-out organ donation register, the first country in the UK to do so. The legislation is deemed consent, whereby all citizens are considered to have no objection to becoming a donor, unless they have opted out on this register. England and Scotland Englands Organ Donation Act, also known as Max and Keiras law, came into effect in May 2020. It means adults in England will be automatically be considered potential donors unless they chose to opt out or are excluded. As of March 2021 Scotland also has an opt-out system. Dependencies The British Crown dependency of Jersey moved to an opt-out register on July 1, 2019. United States Over 121,000 people in need of an organ are on the U.S. government waiting list. This crisis within the United States is growing rapidly because on average there are only 30,000 transplants performed each year. More than 8,000 people die each year from lack of a donor organ, an average of 22 people a day. Between the years 1988 and 2006 the number of transplants doubled, but the number of patients waiting for an organ grew six times as large.In the past presumed consent was urged to try to decrease the need for organs. The Uniform Anatomical Gift Act of 1987 was adopted in several states, and allowed medical examiners to determine if organs and tissues of cadavers could be donated. By the 1980s, several states adopted different laws that allowed only certain tissues or organs to be retrieved and donated, some allowed all, and some did not allow any without consent of the family. In 2006 when the UAGA was revised, the idea of presumed consent was abandoned. In the United States today, organ donation is done only with consent of the family or donator themselves.According to economist Alex Tabarrok, the shortage of organs has increased the use of so-called expanded criteria organs, or organs that used to be considered unsuitable for transplant. Five patients that received kidney transplants at the University of Maryland School of Medicine developed cancerous or benign tumors which had to be removed. The head surgeon, Dr. Michael Phelan, explained that "the ongoing shortage of organs from deceased donors, and the high risk of dying while waiting for a transplant, prompted five donors and recipients to push ahead with the surgery." Several organizations such as the American Kidney Fund are pushing for opt-out organ donation in the United States. Donor Leave Laws In addition to their sick and annual leave, federal executive agency employees are entitled to 30 days paid leave for organ donation. Thirty-two states (excluding only Alabama, Connecticut, Florida, Kentucky, Maine, Michigan, Montana, Nebraska, Nevada, New Hampshire, New Jersey, North Carolina, Pennsylvania, Rhode Island, South Dakota, Tennessee, Vermont, and Wyoming) and the District of Columbia also offer paid leave for state employees. Five states (California, Hawaii, Louisiana, Minnesota, and Oregon) require certain private employers to provide paid leave for employees for organ or bone marrow donation, and seven others (Arkansas, Connecticut, Maine, Nebraska, New York, South Carolina, and West Virginia) either require employers to provide unpaid leave, or encourage employers to provide leave, for organ or bone marrow donation.A bill in the US House of Representatives, the Living Donor Protection Act (introduced in 2016, then reintroduced in 2017), would amend the Family and Medical Leave Act of 1993 to provide leave under the act for an organ donor. If successful, this new law would permit "eligible employee" organ donors to receive up to 12 work weeks of leave in a 12-month period. Tax incentives Nineteen US states and the District of Columbia provide tax incentives for organ donation. The most generous state tax incentive is Utahs tax credit, which covers up to $10,000 of unreimbursed expenses (travel, lodging, lost wages, and medical expenses) associated with organ or tissue donation. Idaho (up to $5,000 of unreimbursed expenses) and Louisiana (up to $7,500 of 72% of unreimbursed expenses) also provide donor tax credits. Arkansas, the District of Columbia, Louisiana and Pennsylvania provide tax credits to employers for wages paid to employees on leave for organ donation. Thirteen states (Arkansas, Georgia, Iowa, Massachusetts, Mississippi, New Mexico, New York, North Dakota, Ohio, Oklahoma, Rhode Island and Wisconsin) have a tax deduction for up to $10,000 of unreimbursed costs, and Kansas and Virginia offer a tax deduction for up to $5,000 of unreimbursed costs.States have focused their tax incentives on unreimbursed costs associated with organ donation to ensure compliance with the National Organ Transplant Act of 1984. NOTA prohibits, "any person to knowingly acquire, receive, or otherwise transfer any human organ for valuable consideration for use in human transplantation." However, NOTA exempts, "the expenses of travel, housing, and lost wages incurred by the donor of a human organ in connection with the donation of the organ," from its definition of "valuable consideration".While offering income tax deductions has been the preferred method of providing tax incentives, some commentators have expressed concern that these incentives provide disproportionate benefits to wealthier donors. Tax credits, on the other hand, are perceived as more equitable since the after tax benefit of the incentive is not tied to the marginal tax rate of the donor.Additional tax favored approaches have been proposed for organ donation, including providing: tax credits to the families of deceased donors (seeking to encourage consent), refundable tax credits (similar to the earned income credit) to provide greater tax equity among potential donors, and charitable deductions for the donation of blood or organs. Other financial incentives As stated above, under the National Organ Transplant Act of 1984, granting monetary incentives for organ donation is illegal in the United States. However, there has been some discussion about providing fixed payment for potential live donors. In 1988, regulated paid organ donation was instituted in Iran and, as a result, the renal transplant waiting list was eliminated. Critics of paid organ donation argue that the poor and vulnerable become susceptible to transplant tourism. Travel for transplantation becomes transplant tourism if the movement of organs, donors, recipients or transplant professionals occurs across borders and involves organ trafficking or transplant commercialism. Poor and underserved populations in underdeveloped countries are especially vulnerable to the negative consequences of transplant tourism because they have become a major source of organs for the transplant tourists that can afford to travel and purchase organs.In 1994 a law was passed in Pennsylvania which proposed to pay $300 for room and board and $3,000 for funeral expenses to an organ donors family. Developing the program was an eight-year process; it is the first of its kind. Procurement directors and surgeons across the nation await the outcomes of Pennsylvanias program. There have been at least nineteen families that have signed up for the benefit. Due to investigation of the program, however, there has been some concern whether the money collected is being used to assist families. Nevertheless, funeral aids to induce post-mortem organ donation have also received support from experts and the general public, as they present more ethical values, such as honoring the deceased donor, and potentially increase donation willingness.Some organizations, such as the National Kidney Foundation, oppose financial incentives associated with organ donation claiming, "Offering direct or indirect economic benefits in exchange for organ donation is inconsistent with our values as a society." One argument is it will disproportionately affect the poor. The $300–3,000 reward may act as an incentive for poorer individuals, as opposed to the wealthy who may not find the offered incentives significant. The National Kidney Foundation has noted that financial incentives, such as this Pennsylvania statute, diminish human dignity. Bioethical issues Deontological Deontological issues are issues about whether a person has an ethical duty or responsibility to take an action. Nearly all scholars and societies around the world agree that voluntarily donating organs to sick people is ethically permissible. Although nearly all scholars encourage organ donation, fewer scholars believe that all people are ethically required to donate their organs after death. Similarly, nearly all religions support voluntary organ donation as a charitable act of great benefit to the community. Certain small faiths such as Jehovah Witnesses and Shinto are opposed to organ donation based upon religious teachings; for Jehovah Witnesses this opposition is absolute whereas there exists increasing flexibility amongst Shinto scholars. The Roma People, are also often opposed to organ donation based on prevailing spiritual beliefs and not religious views per se. Issues surrounding patient autonomy, living wills, and guardianship make it nearly impossible for involuntary organ donation to occur. From the standpoint of deontological ethics, the primary issues surrounding the morality of organ donation are semantic in nature. The debate over the definitions of life, death, human, and body is ongoing. For example, whether or not a brain-dead patient ought to be kept artificially animate in order to preserve organs for donation is an ongoing problem in clinical bioethics. In addition, some have argued that organ donation constitutes an act of self-harm, even when an organ is donated willingly.Further, the use of cloning to produce organs with a genotype identical to the recipient is a controversial topic, especially considering the possibility for an entire person to be brought into being for the express purpose of being destroyed for organ procurement. While the benefit of such a cloned organ would be a zero-percent chance of transplant rejection, the ethical issues involved with creating and killing a clone may outweigh these benefits. However, it may be possible in the future to use cloned stem-cells to grow a new organ without creating a new human being. A relatively new field of transplantation has reinvigorated the debate. Xenotransplantation, or the transfer of animal (usually pig) organs into human bodies, promises to eliminate many of the ethical issues, while creating many of its own. While xenotransplantation promises to increase the supply of organs considerably, the threat of organ transplant rejection and the risk of xenozoonosis, coupled with general anathema to the idea, decreases the functionality of the technique. Some animal rights groups oppose the sacrifice of an animal for organ donation and have launched campaigns to ban them. Teleological On teleological or utilitarian grounds, the moral status of "black market organ donation" relies upon the ends, rather than the means. In so far as those who donate organs are often impoverished and those who can afford black market organs are typically well-off, it would appear that there is an imbalance in the trade. In many cases, those in need of organs are put on waiting lists for legal organs for indeterminate lengths of time—many die while still on a waiting list. Organ donation is fast becoming an important bioethical issue from a social perspective as well. While most first-world nations have a legal system of oversight for organ transplantation, the fact remains that demand far outstrips supply. Consequently, there has arisen a black market trend often referred to as transplant tourism. The issues are weighty and controversial. On the one hand are those who contend that those who can afford to buy organs are exploiting those who are desperate enough to sell their organs. Many suggest this results in a growing inequality of status between the rich and the poor. On the other hand, are those who contend that the desperate should be allowed to sell their organs and that preventing them from doing so is merely contributing to their status as impoverished. Further, those in favor of the trade hold that exploitation is morally preferable to death, and in so far as the choice lies between abstract notions of justice on the one hand and a dying person whose life could be saved on the other hand, the organ trade should be legalized. Conversely, surveys conducted among living donors postoperatively and in a period of five years following the procedure have shown extreme regret in a majority of the donors, who said that given the chance to repeat the procedure, they would not. Additionally, many study participants reported a decided worsening of economic condition following the procedure. These studies looked only at people who sold a kidney in countries where organ sales are already legal. A consequence of the black market for organs has been a number of cases and suspected cases of organ theft, including murder for the purposes of organ theft. Proponents of a legal market for organs say that the black-market nature of the current trade allows such tragedies and that regulation of the market could prevent them. Opponents say that such a market would encourage criminals by making it easier for them to claim that their stolen organs were legal. Legalization of the organ trade carries with it its own sense of justice as well. Continuing black-market trade creates further disparity on the demand side: only the rich can afford such organs. Legalization of the international organ trade could lead to increased supply, lowering prices so that persons outside the wealthiest segments could afford such organs as well. Exploitation arguments generally come from two main areas: Physical exploitation suggests that the operations in question are quite risky, and, taking place in third-world hospitals or "back-alleys", even more risky. Yet, if the operations in question can be made safe, there is little threat to the donor. Financial exploitation suggests that the donor (especially in the Indian subcontinent and Africa) are not paid enough. Commonly, accounts from persons who have sold organs in both legal and black market circumstances put the prices at between $150 and $5,000, depending on the local laws, supply of ready donors and scope of the transplant operation. In Chennai, India, where one of the largest black markets for organs is known to exist, studies have placed the average sale price at little over $1,000. Many accounts also exist of donors being postoperatively denied their promised pay.The New Cannibalism is a phrase coined by anthropologist Nancy Scheper-Hughes in 1998 for an article written for The New Internationalist. Her argument was that the actual exploitation is an ethical failing, a human exploitation; a perception of the poor as organ sources which may be used to extend the lives of the wealthy.Economic drivers leading to increased donation are not limited to areas such as India and Africa, but also are emerging in the United States. Increasing funeral expenses combined with decreasing real value of investments such as homes and retirement savings which took place in the 2000s have purportedly led to an increase in citizens taking advantage of arrangements where funeral costs are reduced or eliminated. Brain death versus cardiac death Brain death may result in legal death, but still with the heart beating and with mechanical ventilation, keeping all other vital organs alive and functional for a certain period of time. Given long enough, patients who do not fully die in the complete biological sense, but who are declared brain dead, will usually start to build up toxins and wastes in the body. In this way, the organs can eventually dysfunction due to coagulopathy, fluid or electrolyte and nutrient imbalances, or even fail. Thus, the organs will usually only be sustainable and viable for acceptable use up until a certain length of time. This may depend on factors such as how well the patient is maintained, any comorbidities, the skill of the healthcare teams and the quality their facilities. A major point of contention is whether transplantation should be allowed at all if the patient is not yet fully biologically dead, and if brain death is acceptable, whether the persons whole brain needs to have died, or if the death of a certain part of the brain is enough for legal and ethical and moral purposes. Most organ donation for organ transplantation is done in the setting of brain death. However, in Japan this is a fraught point, and prospective donors may designate either brain death or cardiac death – see organ transplantation in Japan. In some nations such as Belgium, France, Netherlands, New Zealand, Poland, Portugal, Singapore and Spain, everyone is automatically an organ donor unless they opt out of the system. Elsewhere, consent from family members or next-of-kin is required for organ donation. The non-living donor is kept on ventilator support until the organs have been surgically removed. If a brain-dead individual is not an organ donor, ventilator and drug support is discontinued and cardiac death is allowed to occur. In the United States, where since the 1980s the Uniform Determination of Death Act has defined death as the irreversible cessation of the function of either the brain or the heart and lungs, the 21st century has seen an order-of-magnitude increase of donation following cardiac death. In 1995, only one out of 100 dead donors in the nation gave their organs following the declaration of cardiac death. That figure grew to almost 11 percent in 2008, according to the Scientific Registry of Transplant Recipients. That increase has provoked ethical concerns about the interpretation of "irreversible" since "patients may still be alive five or even 10 minutes after cardiac arrest because, theoretically, their hearts could be restarted, [and thus are] clearly not dead because their condition was reversible." Gender inequality The majority of organ donors are women. For example, in the United States, 62% of kidney donors and 53% of liver donors are women. In India, women constitute 74% of kidney donors and 60.5% of liver donors. Additionally, the number of female organ recipients is conspicuously lower than that of male recipients. In the U.S., 35% of liver recipients and 39% of kidney recipients are women. In India, the figures are 24% and 19% respectively. Political issues There are also controversial issues regarding how organs are allocated to recipients. For example, some believe that livers should not be given to alcoholics in danger of reversion, while others view alcoholism as a medical condition like diabetes. Faith in the medical system is important to the success of organ donation. Brazil switched to an opt-out system and ultimately had to withdraw it because it further alienated patients who already distrusted the countrys medical system. Adequate funding, strong political will to see transplant outcomes improve, and the existence of specialized training, care and facilities also increase donation rates. Expansive legal definitions of death, such as Spain uses, also increase the pool of eligible donors by allowing physicians to declare a patient to be dead at an earlier stage, when the organs are still in good physical condition. Allowing or forbidding payment for organs affects the availability of organs. Generally, where organs cannot be bought or sold, quality and safety are high, but supply is not adequate to the demand. Where organs can be purchased, the supply increases. Iran adopted a system of paying kidney donors in 1988 and within 11 years it became the only country in the world to clear its waiting list for transplants. Healthy humans have two kidneys, a redundancy that enables living donors (inter vivos) to give a kidney to someone who needs it. The most common transplants are to close relatives, but people have given kidneys to other friends. The rarest type of donation is the undirected donation whereby a donor gives a kidney to a stranger. Less than a few hundred of such kidney donations have been performed. In recent years, searching for altruistic donors via the internet has also become a way to find life saving organs. However, internet advertising for organs is a highly controversial practice, as some scholars believe it undermines the traditional list-based allocation system.The National Transplant Organization of Spain is one of the most successful in the world (Spain has been the world leader in organ donation for decades), but it still cannot meet the demand, as 10% of those needing a transplant die while still on the transplant list. Donations from corpses are anonymous, and a network for communication and transport allows fast extraction and transplant across the country. Under Spanish law, every corpse can provide organs unless the deceased person had expressly rejected it. Because family members still can forbid the donation, carefully trained doctors ask the family for permission, making it very similar in practice to the United States system.In the overwhelming majority of cases, organ donation is not possible for reasons of recipient safety, match failures, or organ condition. Even in Spain, which has the highest organ donation rate in the world, there are only 35.1 actual donors per million people, and there are hundreds of patients on the waiting list. This rate compares to 24.8 per million in Austria, where families are rarely asked to donate organs, and 22.2 per million in France, which—like Spain—has a presumed-consent system. Prison inmates In the United States, prisoners are not discriminated against as organ recipients and are equally eligible for organ transplants along with the general population. A 1976 U.S. Supreme Court case ruled that withholding health care from prisoners constituted "cruel and unusual punishment". United Network for Organ Sharing, the organization that coordinates available organs with recipients, does not factor a patients prison status when determining suitability for a transplant. An organ transplant and follow-up care can cost the prison system up to one million dollars. If a prisoner qualifies, a state may allow compassionate early release to avoid high costs associated with organ transplants. However, an organ transplant may save the prison system substantial costs associated with dialysis and other life-extending treatments required by the prisoner with the failing organ. For example, the estimated cost of a kidney transplant is about $111,000. A prisoners dialysis treatments are estimated to cost a prison $120,000 per year.Because donor organs are in short supply, there are more people waiting for a transplant than available organs. When a prisoner receives an organ, there is a high probability that someone else will die waiting for the next available organ. A response to this ethical dilemma states that felons who have a history of violent crime, who have violated others basic rights, have lost the right to receive an organ transplant, though it is noted that it would be necessary "to reform our justice system to minimize the chance of an innocent person being wrongly convicted of a violent crime and thus being denied an organ transplant".Prisons typically do not allow inmates to donate organs to anyone but immediate family members. There is no law against prisoner organ donation; however, the transplant community has discouraged use of prisoners organs since the early 1990s due to concern over prisons high-risk environment for infectious diseases. Physicians and ethicists also criticize the idea because a prisoner is not able to consent to the procedure in a free and non-coercive environment, especially if given inducements to participate. However, with modern testing advances to more safely rule out infectious disease and by ensuring that there are no incentives offered to participate, some have argued that prisoners can now voluntarily consent to organ donation just as they can now consent to medical procedures in general. With careful safeguards, and with over 2 million prisoners in the U.S., they reason that prisoners can provide a solution for reducing organ shortages in the U.S.While some have argued that prisoner participation would likely be too low to make a difference, one Arizona program started by former Maricopa County Sheriff Joe Arpaio encourages inmates to voluntarily sign up to donate their heart and other organs. As of 2015, there have been over 16,500 participants. Similar initiatives have been started in other US states. In 2013, Utah became the first state to allow prisoners to sign up for organ donation upon death. Religious viewpoints There are several different religions that have different perspectives. Islam has a conflicting view regarding the issue, with half believing that it is against the religion. Muslims are commanded to seek medical attention when in need and saving life is a very important factor of the Islamic religion. Christianity is lenient on the topic of organ donation, and believe it is a service of life.All major religions accept organ donation in at least some form on either utilitarian grounds (i.e., because of its life-saving capabilities) or deontological grounds (e.g., the right of an individual believer to make his or her own decision). Most religions, among them the Roman Catholic Church, support organ donation on the grounds that it constitutes an act of charity and provides a means of saving a life. One religious group, The Jesus Christians, became known as "The Kidney Cult" because more than half its members had donated their kidneys altruistically. Jesus Christians claim altruistic kidney donation is a great way to "Do unto others what they would want you to do unto them." Some religions impose certain restrictions on the types of organs that may be donated and/or on the means by which organs may be harvested and/or transplanted. For example, Jehovahs Witnesses require that organs be drained of any blood due to their interpretation of the Hebrew Bible/Christian Old Testament as prohibiting blood transfusion, and Muslims require that the donor have provided written consent in advance. A few groups disfavor organ transplantation or donation; notably, these include Shinto and the Romani.Orthodox Judaism considers organ donation obligatory if it will save a life, as long as the donor is considered dead as defined by Jewish law. In both Orthodox Judaism and non-Orthodox Judaism, the majority view holds that organ donation is permitted in the case of irreversible cardiac rhythm cessation. In some cases, rabbinic authorities believe that organ donation may be mandatory, whereas a minority opinion considers any donation of a live organ as forbidden. Organ shortfall The demand for organs significantly surpasses the number of donors everywhere in the world. There are more potential recipients on organ donation waiting lists than organ donors. In particular, due to significant advances in dialysis techniques, patients with end-stage renal disease (ESRD) can survive longer than ever before. Because these patients do not die as quickly as they used to, and as kidney failure increases with the rising age and prevalence of high blood pressure and diabetes in a society, the need especially for kidneys rises every year.As of March 2014, about 121,600 people in the United States are on the waiting list, although about a third of those patients are inactive and could not receive a donated organ. Wait times and success rates for organs differ significantly between organs due to demand and procedure difficulty. As of 2007, three-quarters of patients in need of an organ transplant were waiting for a kidney, and as such kidneys have much longer waiting times. As stated by the Gift of Life Donor Program website, the median patient who ultimately received an organ waited 4 months for a heart or lung—but 18 months for a kidney, and 18–24 months for a pancreas because demand for these organs substantially outstrips supply. An increased prevalence of self-driving cars could exacerbate this problem: In the US, 13% of organ donations come from car crash victims, and autonomous vehicles are projected to reduce the frequency of car crashes.In Australia, there are 10.8 transplants per million people, about a third of the Spanish rate. The Lions Eye Institute, in Western Australia, houses the Lions Eye Bank. The Bank was established in 1986 and coordinates the collection, processing and distribution of eye tissue for transplantation. The Lions Eye Bank also maintains a waitlist of patients who require corneal graft operations. About 100 corneas are provided by the Bank for transplant each year, but there is still a waiting list for corneas. "To an economist, this is a basic supply-and-demand gap with tragic consequences." Approaches to addressing this shortfall include: Donor registries and "primary consent" laws, to remove the burden of the donation decision from the legal next-of-kin. Illinois adopted a policy of "mandated choice" in 2006, which requires drivers license registrants to answer the question "Do you want to be an organ donor?" Illinois has a registration rate of 60 percent compared to 38 percent nationally. The added cost of adding a question to the registration form is minimal. Monetary incentives for signing up to be a donor. Some economists have advocated going as far as allowing the sale of organs. The New York Times reported that "Gary Becker and Julio Jorge Elias argued in a recent paper that monetary incentives would increase the supply of organs for transplant sufficiently to eliminate the very large queues in organ markets, and the suffering and deaths of many of those waiting, without increasing the total cost of transplant surgery by more than 12 percent." Iran allows the sale of kidneys and has no waiting list. Organ futures have been proposed to incentivise donation through direct or indirect compensation. The primary argument against such proposals is a moral one; as the article notes, many find such a suggestion repugnant. As the National Kidney Foundation puts it, "Offering direct or indirect economic benefits in exchange for organ donation is inconsistent with our values as a society. Any attempt to assign a monetary value to the human body, or body parts, either arbitrarily, or through market forces, diminishes human dignity." An opt-out system ("dissent solution"), in which a potential donor or his/her relatives must take specific action to be excluded from organ donation, rather than specific action to be included. This model is used in several European countries, such as Austria, which has a registration rate eight times that of Germany, which uses an opt-in system. Social incentive programs, wherein members sign a legal agreement to direct their organs first to other members who are on the transplant waiting list. One historical example of a private organization using this model is LifeSharers, which is free to join and whose members agree to sign a document giving preferred access to their organs. "The proposal [for an organ mutual insurance pool] can be easily summarized: An individual would receive priority for any needed transplant if that individual agrees that his or her organs will be available to other members of the insurance pool in the event of his or her death. … The main purpose [of this proposal] is to increase the supply of transplantable organs in order to save or improve more lives." Technical advances allows the use of donors that were previously rejected. For example, hepatitis C can be knowingly transplanted and treated in the organ recipient.In hospitals, organ network representatives routinely screen patient records to identify potential donors shortly in advance of their deaths. In many cases, organ-procurement representatives will request screening tests (such as blood typing) or organ-preserving drugs (such as blood pressure drugs) to keep potential donors organs viable until their suitability for transplants can be determined and family consent (if needed) can be obtained. This practice increases transplant efficiency, as potential donors who are unsuitable due to infection or other causes are removed from consideration before their deaths, and decreases the avoidable loss of organs. It may also benefit families indirectly, as the families of unsuitable donors are not approached to discuss organ donation. Distribution The United States has two agencies that govern organ procurement and distribution within the country. The United Network for Organ Sharing and the Organ Procurement and Transplant Network (OPTN) regulate Organ Procurement Organizations (OPO) with regard to procurement and distribution ethics and standards. OPOs are non-profit organizations charged with the evaluation, procurement and allocation of organs within their Designated Service Area (DSA). Once a donor has been evaluated and consent obtained, provisional allocation of organs commences. UNOS developed a computer program that automatically generates donor specific match lists for suitable recipients based on the criteria that the patient was listed with. OPO coordinators enter donor information into the program and run the respective lists. Organ offers to potential recipients are made to transplant centers to make them aware of a potential organ. The surgeon will evaluate the donor information and make a provisional determination of medical suitability to their recipient. Distribution varies slightly between different organs but is essentially very similar. When lists are generated many factors are taken into consideration; these factors include: distance of transplant center from the donor hospital, blood type, medical urgency, wait time, donor size and tissue typing. For heart recipients medical urgency is denoted by a recipients "Status" (Status 1A, 1B and status 2). Lungs are allocated based on a recipients Lung Allocation Score (LAS) that is determined based on the urgency of clinical need as well as the likelihood of benefit from the transplant. Livers are allocated using both a status system and MELD/PELD score (Model for End-stage Liver Disease/Pediatric End-stage Liver Disease). Kidney and pancreas lists are based on location, blood type, Human Leukocyte Antigen (HLA) typing and wait time. When a recipient for a kidney or pancreas has no direct antibodies to the donor HLA the match is said to be a 0 ABDR mismatch or zero antigen mismatch. A zero mismatch organ has a low rate of rejection and allows a recipient to be on lower doses of immunosuppressive drugs. Since zero mismatches have such high graft survival these recipients are afforded priority regardless of location and wait time. UNOS has in place a "Payback" system to balance organs that are sent out of a DSA because of a zero mismatch. Location of a transplant center with respect to a donor hospital is given priority due to the effects of Cold Ischemic Time (CIT). Once the organ is removed from the donor, blood no longer perfuses through the vessels and begins to starve the cells of oxygen (ischemia). Each organ tolerates different ischemic times. Hearts and lungs need to be transplanted within 4–6 hours from recovery, liver about 8–10 hours and pancreas about 15 hours; kidneys are the most resilient to ischemia. Kidneys packaged on ice can be successfully transplanted 24–36 hours after recovery. Developments in kidney preservation have yielded a device that pumps cold preservation solution through the kidneys vessels to prevent Delayed Graft Function (DGF) due to ischemia. Perfusion devices, often called kidney pumps, can extend graft survival to 36–48 hours post recovery for kidneys. Recently similar devices have been developed for the heart and lungs, in an effort to increase distances procurement teams may travel to recover an organ. Suicide People committing suicide have a higher rate of donating organs than average. One reason is lower negative response or refusal rate by the family and relatives, but the explanation for this remains to be clarified. In addition, donation consent is higher than average from people committing suicide.Attempted suicide is a common cause of brain death (3.8%), mainly among young men. Organ donation is more common in this group compared to other causes of death. Brain death may result in legal death, but still with the heart beating, and with mechanical ventilation all other vital organs may be kept completely alive and functional, providing optimal opportunities for organ transplantation. Controversies In 2008, California transplant surgeon Hootan Roozrokh was charged with dependent adult abuse for prescribing what prosecutors alleged were excessive doses of morphine and sedatives to hasten the death of a man with adrenal leukodystrophy and irreversible brain damage, in order to procure his organs for transplant. The case brought against Roozrokh was the first criminal case against a transplant surgeon in the US, and resulted in his acquittal. Further, Dr. Roozrokh successfully sued for defamation stemming from the incident.At Californias Emanuel Medical Center, neurologist Narges Pazouki, MD, said an organ-procurement organization representative pressed her to declare a patient brain-dead before the appropriate tests had been done. In September 1999, eBay blocked an auction for "one functional human kidney" which had reached a highest bid of $5.7 million. Under United States federal laws, eBay was obligated to dismiss the auction for the selling of human organs which is punishable by up to five years in prison and a $50,000 fine.On June 27, 2008, Indonesian Sulaiman Damanik, 26, pled guilty in a Singapore court for sale of his kidney to CK Tangs executive chair, Mr. Tang Wee Sung, 55, for 150 million rupiah (US$17,000). The Transplant Ethics Committee must approve living donor kidney transplants. Organ trading is banned in Singapore and in many other countries to prevent the exploitation of "poor and socially disadvantaged donors who are unable to make informed choices and suffer potential medical risks." Toni, 27, the other accused, donated a kidney to an Indonesian patient in March, alleging he was the patients adopted son, and was paid 186 million rupiah (US$21,000). Public service announcements Marketing for organ donation must walk a fine line between stressing the need for organ donation and not being too forceful. If the marketing agent is too forceful, then the target of the message will react defensively to the request. According to psychological reactance theory, a person will perceive their freedom threatened and will react to restore the freedom. According to Ashley Anker, the use of transportation theory has a positive effect on target reactions by marketing attempts. When public service announcements use recipient-focused messages, targets were more transported. Individuals who watched recipient-focused messages were more transported because potential donors experience empathy for the potential recipient. Future public service announcements should use recipient-focused stories to elicit relationship formation between potential donors and recipients. Awareness about organ donation leads to greater social support for organ donation, in turn leading to greater registration. By starting with promoting college students awareness of organ donation and moving to increasing social support for organ donation, the more likely people will be to register as organ donors.The United States Department of Health funded a study by the University of Wisconsin Hospital to increase efforts to increase awareness and the number of registered donors by pursuing members of the university and their family and friends through social media. The results of the study showed a 20% increase in organ donation by creating support and awareness through social media. See also References External links National Institute of Healths MedLine on Organ Donation Organ Donation India NHS Organ Transplant (UK) OrganDonor.gov (US) Portal for Organ Donation After Execution Portal for The National Network of Organ Donors Human Tissue Donation – NPR News Investigation Organ and Tissue Donation What Every Nurse Needs to Know course on www.RN.org

Hello Aarogya, what is Combined immunodeficiencies

Combined immunodeficiencies

Combined immunodeficiencies (or combined immunity deficiency) are immunodeficiency disorders that involve multiple components of the immune system, including both humoral immunity and cell-mediated immunity. This category includes conditions such as bare lymphocyte syndrome, as well as severe combined immunodeficiency. Combined immunodeficiencies are commonly distinguished from SCID by low but not absent T-cell function.ICD-9 divides immune deficiencies into three categories: humoral (279.0), cell-mediated (279.1), and combined (279.2). However, ICD-10 does not include a category for cell-mediated immune dysfunction (antibody is D80, and combined is D81), thus grouping T-cell mediated conditions with combined conditions. References == External links ==

Hi Aarogya , Do you know what is Oligomenorrhea,

Oligomenorrhea

Oligomenorrhea is infrequent (or, in occasional usage, very light) menstruation. More strictly, it is menstrual periods occurring at intervals of greater than 35 days, with only four to nine periods in a year. Menstrual periods should have been regularly established before the development of infrequent flow. The duration of such events may vary. Causes Oligomenorrhea can be a result of prolactinomas (adenomas of the anterior pituitary). It may be caused by thyrotoxicosis, hormonal changes in perimenopause, Prader–Willi syndrome, and Graves disease. Endurance exercises such as running or swimming can affect the reproductive physiology of female athletes. Female runners, swimmers and ballet dancers either menstruate infrequently in comparison to non-athletic females of comparable age or exhibit amenorrhea. A more recent study shows that athletes competing in sports that emphasise thinness or a specific weight exhibit a higher rate of menstrual dysfunction than either athletes competing in sports with less focus on these or control subjects.Breastfeeding has been linked to irregularity of menstrual cycles due to hormones that delay ovulation. People with polycystic ovary syndrome (PCOS) are also likely to have oligomenorrhea. PCOS is a condition in which excessive androgens (male sex hormones) are released by the ovaries. People with PCOS show menstrual irregularities that range from oligomenorrhea and amenorrhea, to very heavy, irregular periods. The condition affects about 6% of premenopausal females. Eating disorders can result in oligomenorrhea. Although menstrual disorders are most strongly associated with anorexia nervosa, bulimia nervosa may also result in oligomenorrhea or amenorrhea. There is some controversy regarding the mechanism for the menstrual dysregulation, since amenorrhea may sometimes precede substantial weight loss in some anorexics. See also Amenorrhea: a total cessation of the menstrual period Menorrhagia: unusually heavy periods References == External links ==

Aarogya what is Allergic rhinitis

Allergic rhinitis

Allergic rhinitis, of which the seasonal type is called hay fever, is a type of inflammation in the nose that occurs when the immune system overreacts to allergens in the air. Signs and symptoms include a runny or stuffy nose, sneezing, red, itchy, and watery eyes, and swelling around the eyes. The fluid from the nose is usually clear. Symptom onset is often within minutes following allergen exposure, and can affect sleep and the ability to work or study. Some people may develop symptoms only during specific times of the year, often as a result of pollen exposure. Many people with allergic rhinitis also have asthma, allergic conjunctivitis, or atopic dermatitis.Allergic rhinitis is typically triggered by environmental allergens such as pollen, pet hair, dust, or mold. Inherited genetics and environmental exposures contribute to the development of allergies. Growing up on a farm and having multiple siblings decreases this risk. The underlying mechanism involves IgE antibodies that attach to an allergen, and subsequently result in the release of inflammatory chemicals such as histamine from mast cells. It causes mucous membranes in the nose, eyes and throat to become inflamed and itchy as they work to eject the allergen. Diagnosis is typically based on a combination of symptoms and a skin prick test or blood tests for allergen-specific IgE antibodies. These tests, however, can be falsely positive. The symptoms of allergies resemble those of the common cold; however, they often last for more than two weeks and, despite the common name, typically do not include a fever.Exposure to animals early in life might reduce the risk of developing these specific allergies. Several different types of medications reduce allergic symptoms, including nasal steroids, antihistamines, such as diphenhydramine, cromolyn sodium, and leukotriene receptor antagonists such as montelukast. Oftentimes, medications do not completely control symptoms, and they may also have side effects. Exposing people to larger and larger amounts of allergen, known as allergen immunotherapy (AIT), is often effective. The allergen can be given as an injection under the skin or as a tablet under the tongue. Treatment typically lasts three to five years, after which benefits may be prolonged.Allergic rhinitis is the type of allergy that affects the greatest number of people. In Western countries, between 10 and 30% of people are affected in a given year. It is most common between the ages of twenty and forty. The first accurate description is from the 10th-century physician Abu Bakr al-Razi. In 1859, Charles Blackley identified pollen as the cause. In 1906, the mechanism was determined by Clemens von Pirquet. The link with hay came about due to an early (and incorrect) theory that the symptoms were brought about by the smell of new hay. Although the scent per se is irrelevant, the correlation with hay remains more than random, as peak hay-harvesting season overlaps with peak pollen season, and hay-harvesting work puts people in close contact with seasonal allergens. Signs and symptoms The characteristic symptoms of allergic rhinitis are: rhinorrhea (excess nasal secretion), itching, sneezing fits, and nasal congestion and obstruction. Characteristic physical findings include conjunctival swelling and erythema, eyelid swelling with Dennie–Morgan folds, lower eyelid venous stasis (rings under the eyes known as "allergic shiners"), swollen nasal turbinates, and middle ear effusion.There can also be behavioral signs; in order to relieve the irritation or flow of mucus, people may wipe or rub their nose with the palm of their hand in an upward motion: an action known as the "nasal salute" or the "allergic salute". This may result in a crease running across the nose (or above each nostril if only one side of the nose is wiped at a time), commonly referred to as the "transverse nasal crease", and can lead to permanent physical deformity if repeated enough.People might also find that cross-reactivity occurs. For example, people allergic to birch pollen may also find that they have an allergic reaction to the skin of apples or potatoes. A clear sign of this is the occurrence of an itchy throat after eating an apple or sneezing when peeling potatoes or apples. This occurs because of similarities in the proteins of the pollen and the food. There are many cross-reacting substances. Hay fever is not a true fever, meaning it does not cause a core body temperature in the fever over 37.5–38.3 °C (99.5–100.9 °F). Cause Pollen is often considered as a cause of allergic rhinitis, hence called hay fever (See sub-section below). Predisposing factors to allergic rhinitis include eczema (atopic dermatitis) and asthma. These three conditions can often occur together which is referred to as the atopic triad. Additionally, environmental exposures such as air pollution and maternal tobacco smoking can increase an individuals chances of developing allergies. Pollen-related causes Allergic rhinitis triggered by the pollens of specific seasonal plants is commonly known as "hay fever", because it is most prevalent during haying season. However, it is possible to have allergic rhinitis throughout the year. The pollen that causes hay fever varies between individuals and from region to region; in general, the tiny, hardly visible pollens of wind-pollinated plants are the predominant cause. Pollens of insect-pollinated plants are too large to remain airborne and pose no risk. Examples of plants commonly responsible for hay fever include: Trees: such as pine (Pinus), mulberry (Morus), birch (Betula), alder (Alnus), cedar (Cedrus), hazel (Corylus), hornbeam (Carpinus), horse chestnut (Aesculus), willow (Salix), poplar (Populus), plane (Platanus), linden/lime (Tilia), and olive (Olea). In northern latitudes, birch is considered to be the most common allergenic tree pollen, with an estimated 15–20% of people with hay fever sensitive to birch pollen grains. A major antigen in these is a protein called Bet V I. Olive pollen is most predominant in Mediterranean regions. Hay fever in Japan is caused primarily by sugi (Cryptomeria japonica) and hinoki (Chamaecyparis obtusa) tree pollen. "Allergy friendly" trees include: female ash, red maple, yellow poplar, dogwood, magnolia, double-flowered cherry, fir, spruce, and flowering plum. Grasses (Family Poaceae): especially ryegrass (Lolium sp.) and timothy (Phleum pratense). An estimated 90% of people with hay fever are allergic to grass pollen. Weeds: ragweed (Ambrosia), plantain (Plantago), nettle/parietaria (Urticaceae), mugwort (Artemisia Vulgaris), Fat hen (Chenopodium), and sorrel/dock (Rumex)Allergic rhinitis may also be caused by allergy to Balsam of Peru, which is in various fragrances and other products. Genetic factors The causes and pathogenesis of allergic rhinitis are hypothesized to be affected by both genetic and environmental factors, with many recent studies focusing on specific loci that could be potential therapeutic targets for the disease. Genome-wide association studies (GWAS) have identified a number of different loci and genetic pathways that seem to mediate the bodys response to allergens and promote the development of allergic rhinitis, with some of the most promising results coming from studies involving single-nucleotide polymorphisms (SNPs) in the interleukin-33 (IL-33) gene. The IL-33 protein that is encoded by the IL-33 gene is part of the interleukin family of cytokines that interact with T-helper 2 (Th2) cells, a specific type of T cell. Th2 cells contribute to the bodys inflammatory response to allergens, and specific ST2 receptors, also known as IL1RL1, on these cells bind to the ligand IL-33 protein. This IL-33/ST2 signaling pathway has been found to be one of the main genetic determinants in bronchial asthma pathogenesis, and because of the pathological linkage between asthma and rhinitis, the experimental focus of IL-33 has now turned to its role in the development of allergic rhinitis in humans and mouse models. Recently, it was found that allergic rhinitis patients expressed higher levels of IL-33 in their nasal epithelium and had a higher concentration of ST2 serum in nasal passageways following their exposure to pollen and other allergens, indicating that this gene and its associated receptor are expressed at a higher rate in allergic rhinitis patients. In a 2020 study on polymorphisms of the IL-33 gene and their link to allergic rhinitis within the Han Chinese population, researchers found that five SNPs specifically contributed to the pathogenesis of allergic rhinitis, with three of those five SNPs previously identified as genetic determinants for asthma.Another study focusing on Han Chinese children found that certain SNPs in the protein tyrosine phosphatase non-receptor 22 (PTPN22) gene and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) gene can be associated with childhood allergic rhinitis and allergic asthma. The encoded PTPN22 protein, which is found primarily in lymphoid tissue, acts as a post-translational regulator by removing phosphate groups from targeted proteins. Importantly, PTPN22 can affect the phosphorylation of T cell responses, and thus the subsequent proliferation of the T cells. As mentioned earlier, T cells contribute to the bodys inflammatory response in a variety of ways, so any changes to the cells structure and function can have potentially deleterious effects on the bodys inflammatory response to allergens. To date, one SNP in the PTPN22 gene has been found to be significantly associated with allergic rhinitis onset in children. On the other hand, CTLA-4 is an immune-checkpoint protein that helps mediate and control the bodys immune response to prevent overactivation. It is expressed only in T cells as a glycoprotein for the Immunoglobulin (Ig) protein family, also known as antibodies. There have been two SNPs in CTLA-4 that were found to be significantly associated with childhood allergic rhinitis. Both SNPs most likely affect the associated proteins shape and function, causing the body to exhibit an overactive immune response to the posed allergen. The polymorphisms in both genes are only beginning to be examined, therefore more research is needed to determine the severity of the impact of polymorphisms in the respective genes.Finally, epigenetic alterations and associations are of particular interest to the study and ultimate treatment of allergic rhinitis. Specifically, microRNAs (miRNA) are hypothesized to be imperative to the pathogenesis of allergic rhinitis due to the post-transcriptional regulation and repression of translation in their mRNA complement. Both miRNAs and their common carrier vessel exosomes have been found to play a role in the bodys immune and inflammatory responses to allergens. miRNAs are housed and packaged inside of exosomes until they are ready to be released into the section of the cell that they are coded to reside and act. Repressing the translation of proteins can ultimately repress parts of the bodys immune and inflammatory responses, thus contributing to the pathogenesis of allergic rhinitis and other autoimmune disorders. There are many miRNAs that have been deemed potential therapeutic targets for the treatment of allergic rhinitis by many different researchers, with the most widely studied being miR-133, miR-155, miR-205, miR-498, and let-7e. Diagnosis Allergy testing may reveal the specific allergens to which an individual is sensitive. Skin testing is the most common method of allergy testing. This may include a patch test to determine if a particular substance is causing the rhinitis, or an intradermal, scratch, or other test. Less commonly, the suspected allergen is dissolved and dropped onto the lower eyelid as a means of testing for allergies. This test should be done only by a physician, since it can be harmful if done improperly. In some individuals not able to undergo skin testing (as determined by the doctor), the RAST blood test may be helpful in determining specific allergen sensitivity. Peripheral eosinophilia can be seen in differential leukocyte count.Allergy testing is not definitive. At times, these tests can reveal positive results for certain allergens that are not actually causing symptoms, and can also not pick up allergens that do cause an individuals symptoms. The intradermal allergy test is more sensitive than the skin prick test, but is also more often positive in people that do not have symptoms to that allergen.Even if a person has negative skin-prick, intradermal and blood tests for allergies, they may still have allergic rhinitis, from a local allergy in the nose. This is called local allergic rhinitis. Specialized testing is necessary to diagnose local allergic rhinitis. Classification Seasonal allergic rhinitis (hay fever): Caused by seasonal peaks in the airborne load of pollens. Perennial allergic rhinitis (nonseasonal allergic rhinitis; atopic rhinitis): Caused by allergens present throughout the year (e.g., dander).Allergic rhinitis may be seasonal, perennial, or episodic. Seasonal allergic rhinitis occurs in particular during pollen seasons. It does not usually develop until after 6 years of age. Perennial allergic rhinitis occurs throughout the year. This type of allergic rhinitis is commonly seen in younger children.Allergic rhinitis may also be classified as mild-intermittent, moderate-severe intermittent, mild-persistent, and moderate-severe persistent. Intermittent is when the symptoms occur <4 days per week or <4 consecutive weeks. Persistent is when symptoms occur >4 days/week and >4 consecutive weeks. The symptoms are considered mild with normal sleep, no impairment of daily activities, no impairment of work or school, and if symptoms are not troublesome. Severe symptoms result in sleep disturbance, impairment of daily activities, and impairment of school or work. Local allergic rhinitis Local allergic rhinitis is an allergic reaction in the nose to an allergen, without systemic allergies. So skin-prick and blood tests for allergy are negative, but there are IgE antibodies produced in the nose that react to a specific allergen. Intradermal skin testing may also be negative.The symptoms of local allergic rhinitis are the same as the symptoms of allergic rhinitis, including symptoms in the eyes. Just as with allergic rhinitis, people can have either seasonal or perennial local allergic rhinitis. The symptoms of local allergic rhinitis can be mild, moderate, or severe. Local allergic rhinitis is associated with conjunctivitis and asthma.In one study, about 25% of people with rhinitis had local allergic rhinitis. In several studies, over 40% of people having been diagnosed with nonallergic rhinitis were found to actually have local allergic rhinitis. Steroid nasal sprays and oral antihistamines have been found to be effective for local allergic rhinitis.As of 2014, local allergenic rhinitis had mostly been investigated in Europe; in the United States, the nasal provocation testing necessary to diagnose the condition was not widely available.: 617 Prevention Prevention often focuses on avoiding specific allergens that cause an individuals symptoms. These methods include not having pets, not having carpets or upholstered furniture in the home, and keeping the home dry. Specific anti-allergy zippered covers on household items like pillows and mattresses have also proven to be effective in preventing dust mite allergies.Studies have shown that growing up on a farm and having many older siblings can decrease an individuals risk for developing allergic rhinitis.Studies in young children have shown that there is higher risk of allergic rhinitis in those who have early exposure to foods or formula or heavy exposure to cigarette smoking within the first year of life. Treatment The goal of rhinitis treatment is to prevent or reduce the symptoms caused by the inflammation of affected tissues. Measures that are effective include avoiding the allergen. Intranasal corticosteroids are the preferred medical treatment for persistent symptoms, with other options if this is not effective. Second line therapies include antihistamines, decongestants, cromolyn, leukotriene receptor antagonists, and nasal irrigation. Antihistamines by mouth are suitable for occasional use with mild intermittent symptoms. Mite-proof covers, air filters, and withholding certain foods in childhood do not have evidence supporting their effectiveness. Antihistamines Antihistamine drugs can be taken orally and nasally to control symptoms such as sneezing, rhinorrhea, itching, and conjunctivitis.It is best to take oral antihistamine medication before exposure, especially for seasonal allergic rhinitis. In the case of nasal antihistamines like azelastine antihistamine nasal spray, relief from symptoms is experienced within 15 minutes allowing for a more immediate as-needed approach to dosage. There is not enough evidence of antihistamine efficacy as an add-on therapy with nasal steroids in the management of intermittent or persistent allergic rhinitis in children, so its adverse effects and additional costs must be considered.Ophthalmic antihistamines (such as azelastine in eye drop form and ketotifen) are used for conjunctivitis, while intranasal forms are used mainly for sneezing, rhinorrhea, and nasal pruritus.Antihistamine drugs can have undesirable side-effects, the most notable one being drowsiness in the case of oral antihistamine tablets. First-generation antihistamine drugs such as diphenhydramine cause drowsiness, while second- and third-generation antihistamines such as cetirizine and loratadine are less likely to.Pseudoephedrine is also indicated for vasomotor rhinitis. It is used only when nasal congestion is present and can be used with antihistamines. In the United States, oral decongestants containing pseudoephedrine must be purchased behind the pharmacy counter in an effort to prevent the manufacturing of methamphetamine. Desloratadine/pseudoephedrine can also be used for this condition Steroids Intranasal corticosteroids are used to control symptoms associated with sneezing, rhinorrhea, itching, and nasal congestion. Steroid nasal sprays are effective and safe, and may be effective without oral antihistamines. They take several days to act and so must be taken continually for several weeks, as their therapeutic effect builds up with time.In 2013, a study compared the efficacy of mometasone furoate nasal spray to betamethasone oral tablets for the treatment of people with seasonal allergic rhinitis and found that the two have virtually equivalent effects on nasal symptoms in people.Systemic steroids such as prednisone tablets and intramuscular triamcinolone acetonide or glucocorticoid (such as betamethasone) injection are effective at reducing nasal inflammation, but their use is limited by their short duration of effect and the side-effects of prolonged steroid therapy. Other Other measures that may be used second line include: decongestants, cromolyn, leukotriene receptor antagonists, and nonpharmacologic therapies such as nasal irrigation.Topical decongestants may also be helpful in reducing symptoms such as nasal congestion, but should not be used for long periods, as stopping them after protracted use can lead to a rebound nasal congestion called rhinitis medicamentosa.For nocturnal symptoms, intranasal corticosteroids can be combined with nightly oxymetazoline, an adrenergic alpha-agonist, or an antihistamine nasal spray without risk of rhinitis medicamentosa.Nasal saline irrigation (a practice where salt water is poured into the nostrils), may have benefits in both adults and children in relieving the symptoms of allergic rhinitis and it is unlikely to be associated with adverse effects. Allergen immunotherapy Allergen immunotherapy (AIT, also termed desensitization) treatment involves administering doses of allergens to accustom the body to substances that are generally harmless (pollen, house dust mites), thereby inducing specific long-term tolerance. Allergen immunotherapy is the only treatment that alters the disease mechanism. Immunotherapy can be administered orally (as sublingual tablets or sublingual drops), or by injections under the skin (subcutaneous). Subcutaneous immunotherapy is the most common form and has the largest body of evidence supporting its effectiveness. Alternative medicine There are no forms of complementary or alternative medicine that are evidence-based for allergic rhinitis. Therapeutic efficacy of alternative treatments such as acupuncture and homeopathy is not supported by available evidence. While some evidence shows that acupuncture is effective for rhinitis, specifically targeting the sphenopalatine ganglion acupoint, these trials are still limited. Overall, the quality of evidence for complementary-alternative medicine is not strong enough to be recommended by the American Academy of Allergy, Asthma and Immunology. Epidemiology Allergic rhinitis is the type of allergy that affects the greatest number of people. In Western countries, between 10 and 30 percent of people are affected in a given year. It is most common between the ages of twenty and forty. History The first accurate description is from the 10th century physician Rhazes. Pollen was identified as the cause in 1859 by Charles Blackley. In 1906 the mechanism was determined by Clemens von Pirquet. The link with hay came about due to an early (and incorrect) theory that the symptoms were brought about by the smell of new hay. References Further reading External links Allergic rhinitis at Curlie Types of Pollen Allergies

Please give me a short description about Organ (biology) , Aarogya

Organ (biology)

In biology, an organ is a collection of tissues joined in a structural unit to serve a common function. In the hierarchy of life, an organ lies between tissue and an organ system. Tissues are formed from same type cells to act together in a function. Tissues of different types combine to form an organ which has a specific function. The intestinal wall for example is formed by epithelial tissue and smooth muscle tissue. Two or more organs working together in the execution of a specific body function form an organ system, also called a biological system or body system. An organs tissues can be broadly categorized as parenchyma, the functional tissue, and stroma, the structural tissue with supportive, connective, or ancillary functions. For example, the glands tissue that makes the hormones is the parenchyma, whereas the stroma includes the nerves that innervate the parenchyma, the blood vessels that oxygenate and nourish it and carry away its metabolic wastes, and the connective tissues that provide a suitable place for it to be situated and anchored. The main tissues that make up an organ tend to have common embryologic origins, such as arising from the same germ layer. Organs exist in most multicellular organisms. In single-celled organisms such as bacteria, the functional analogue of an organ is known as an organelle. In plants, there are three main organs.In the study of anatomy, viscera (singular viscus) refers to the internal organs of the abdominal, thoracic, and pelvic cavities. The abdominal organs may be classified as solid organs, or hollow organs. The solid organs are the liver, pancreas, spleen, kidneys, and adrenal glands. The hollow organs of the abdomen are the stomach, intestines, gallbladder, bladder, and rectum. In the thoracic cavity the heart is a hollow, muscular organ.The number of organs in any organism depends on the definition used. By one widely adopted definition, 79 organs have been identified in the human body. Animals Except for placozoans, multicellular animals including humans have a variety of organ systems. These specific systems are widely studied in human anatomy. The functions of these organ systems often share significant overlap. For instance, the nervous and endocrine system both operate via a shared organ, the hypothalamus. For this reason, the two systems are combined and studied as the neuroendocrine system. The same is true for the musculoskeletal system because of the relationship between the muscular and skeletal systems. Cardiovascular system: pumping and channeling blood to and from the body and lungs with heart, blood and blood vessels. Digestive system: digestion and processing food with salivary glands, esophagus, stomach, liver, gallbladder, pancreas, intestines, colon, rectum and anus. Endocrine system: communication within the body using hormones made by endocrine glands such as the hypothalamus, pituitary gland, pineal body or pineal gland, thyroid, parathyroids and adrenals, i.e., adrenal glands. Excretory system: kidneys, ureters, bladder and urethra involved in fluid balance, electrolyte balance and excretion of urine. Lymphatic system: structures involved in the transfer of lymph between tissues and the blood stream, the lymph and the nodes and vessels that transport it including the immune system: defending against disease-causing agents with leukocytes, tonsils, adenoids, thymus and spleen. Integumentary system: skin, hair and nails of mammals. Also scales of fish, reptiles, and birds, and feathers of birds. Muscular system: movement with muscles. Nervous system: collecting, transferring and processing information with brain, spinal cord and nerves. Reproductive system: the sex organs, such as ovaries, fallopian tubes, uterus, vulva, vagina, testes, vas deferens, seminal vesicles, prostate and penis. Respiratory system: the organs used for breathing, the pharynx, larynx, trachea, bronchi, lungs and diaphragm. Skeletal system: structural support and protection with bones, cartilage, ligaments and tendons. Viscera In the study of anatomy, viscera (singular viscus) refers to the internal organs of the abdominal, thoracic, and pelvic cavities. The abdominal organs may be classed as solid organs, or hollow organs. The solid organs are the liver, pancreas, spleen, kidneys, and adrenal glands. The hollow organs are the stomach, intestines, gallbladder, bladder, and rectum. In the thoracic cavity the heart is a hollow, muscular organ. Splanchnology is the study of the viscera. The term "visceral" is contrasted with the term "parietal", meaning "of or relating to the wall of a body part, organ or cavity" The two terms are often used in describing a membrane or piece of connective tissue, referring to the opposing sides. Origin and evolution The organ level of organisation in animals can be first detected in flatworms and the more derived phyla, i.e. the bilaterians. The less-advanced taxa (i.e. Placozoa, Porifera, Ctenophora and Cnidaria) do not show consolidation of their tissues into organs. More complex animals are composed of different organs, which have evolved over time. For example, the liver and heart evolved in the chordates about 550-500 million years ago, while the gut and brain are even more ancient, arising in the ancestor of vertebrates, insects, molluscs, and worms about 700-650 million years ago. Given the ancient origin of most vertebrate organs, researchers have looked for model systems, where organs have evolved more recently, and ideally have evolved multiple times independently. An outstanding model for this kind of research is the placenta, which has evolved more than 100 times independently in vertebrates, has evolved relatively recently in some lineages, and exists in intermediate forms in extant taxa. Studies on the evolution of the placenta have identified a variety of genetic and physiological processes that contribute to the origin and evolution of organs, these include the re-purposing of existing animal tissues, the acquisition of new functional properties by these tissues, and novel interactions of distinct tissue types. Plants The study of plant organs is covered in plant morphology. Organs of plants can be divided into vegetative and reproductive. Vegetative plant organs include roots, stems, and leaves. The reproductive organs are variable. In flowering plants, they are represented by the flower, seed and fruit. In conifers, the organ that bears the reproductive structures is called a cone. In other divisions (phyla) of plants, the reproductive organs are called strobili, in Lycopodiophyta, or simply gametophores in mosses. Common organ system designations in plants include the differentiation of shoot and root. All parts of the plant above ground (in non-epiphytes), including the functionally distinct leaf and flower organs, may be classified together as the shoot organ system.The vegetative organs are essential for maintaining the life of a plant. While there can be 11 organ systems in animals, there are far fewer in plants, where some perform the vital functions, such as photosynthesis, while the reproductive organs are essential in reproduction. However, if there is asexual vegetative reproduction, the vegetative organs are those that create the new generation of plants (see clonal colony). Society and culture Many societies have a system for organ donation, in which a living or deceased donors organ are transplanted into a person with a failing organ. The transplantation of larger solid organs often requires immunosuppression to prevent organ rejection or graft-versus-host disease. There is considerable interest throughout the world in creating laboratory-grown or artificial organs. Organ transplants Beginning in the 20th century organ transplants began to take place as scientists knew more about the anatomy of organs. These came later in time as procedures were often dangerous and difficult. Both the source and method of obtaining the organ to transplant are major ethical issues to consider, and because organs as resources for transplant are always more limited than demand for them, various notions of justice, including distributive justice, are developed in the ethical analysis. This situation continues as long as transplantation relies upon organ donors rather than technological innovation, testing, and industrial manufacturing. History The English word "organ" dates back to the twelfth century and refers to any musical instrument. By the late 14th century, the musical terms meaning had narrowed to refer specifically to the keyboard-based instrument. At the same time, a second meaning arose, in reference to a "body part adapted to a certain function".Plant organs are made from tissue composed of different types of tissue. The three tissue types are ground, vascular, and dermal. When three or more organs are present, it is called an organ system.The adjective visceral, also splanchnic, is used for anything pertaining to the internal organs. Historically, viscera of animals were examined by Roman pagan priests like the haruspices or the augurs in order to divine the future by their shape, dimensions or other factors. This practice remains an important ritual in some remote, tribal societies. The term "visceral" is contrasted with the term "parietal", meaning "of or relating to the wall of a body part, organ or cavity" The two terms are often used in describing a membrane or piece of connective tissue, referring to the opposing sides. Antiquity Aristotle used the word frequently in his philosophy, both to describe the organs of plants or animals (e.g. the roots of a tree, the heart or liver of an animal), and to describe more abstract "parts" of an interconnected whole (e.g. his logical works, taken as a whole, are referred to as the Organon).Some alchemists (e.g. Paracelsus) adopted the Hermetic Qabalah assignment between the seven vital organs and the seven classical planets as follows: See also Organoid Organ-on-a-chip References External links Media related to Organs (anatomy) at Wikimedia Commons

What does Self-esteem mean Aarogya

Self-esteem

Self-esteem is confidence in ones own worth or abilities. Self-esteem encompasses beliefs about oneself (for example, "I am loved", "I am worthy") as well as emotional states, such as triumph, despair, pride, and shame. Smith and Mackie (2007) defined it by saying "The self-concept is what we think about the self; self-esteem, is the positive or negative evaluations of the self, as in how we feel about it."Self-esteem is an attractive psychological construct because it predicts certain outcomes, such as academic achievement, happiness, satisfaction in marriage and relationships, and criminal behavior. Self-esteem can apply to a specific attribute or globally. Psychologists usually regard self-esteem as an enduring personality characteristic (trait self-esteem), though normal, short-term variations (state self-esteem) also exist. Synonyms or near-synonyms of self-esteem include: self-worth, self-regard, self-respect, and self-integrity. History The concept of self-esteem has its origins in the 18th century, first expressed in the writings of the Scottish enlightenment thinker David Hume. Hume posits that it is important to value and think well of oneself because it serves a motivational function that enables people to explore their full potential.The identification of self-esteem as a distinct psychological construct has its origins in the work of philosopher, psychologist, geologist, and anthropologist William James (1892). James identified multiple dimensions of the self, with two levels of hierarchy: processes of knowing (called the "I-self") and the resulting knowledge about the self (the "Me-self"). The observation about the self and storage of those observations by the I-self creates three types of knowledge, which collectively account for the Me-self, according to James. These are the material self, social self, and spiritual self. The social self comes closest to self-esteem, comprising all characteristics recognized by others. The material self consists of representations of the body and possessions and the spiritual self of descriptive representations and evaluative dispositions regarding the self. This view of self-esteem as the collection of an individuals attitudes toward itself remains today.In the mid-1960s, social psychologist Morris Rosenberg defined self-esteem as a feeling of self-worth and developed the Rosenberg self-esteem scale (RSES), which became the most-widely used scale to measure self-esteem in the social sciences.In the early 20th century, the behaviorist movement minimized introspective study of mental processes, emotions, and feelings, replacing introspection with objective study through experiments on behaviors observed in relation with the environment. Behaviorism viewed the human being as an animal subject to reinforcements, and suggested placing psychology as an experimental science, similar to chemistry or biology. As a consequence, clinical trials on self-esteem were overlooked, since behaviorists considered the idea less liable to rigorous measurement. In the mid-20th century, the rise of phenomenology and humanistic psychology led to renewed interest in self-esteem. Self-esteem then took a central role in personal self-actualization and in the treatment of psychic disorders. Psychologists started to consider the relationship between psychotherapy and the personal satisfaction of people with high self-esteem as useful to the field. This led to new elements being introduced to the concept of self-esteem, including the reasons why people tend to feel less worthy and why people become discouraged or unable to meet challenges by themselves.In 1992 the political scientist Francis Fukuyama associated self-esteem with what Plato called thymos – the "spiritedness" part of the Platonic soul.From 1997, the core self-evaluations approach included self-esteem as one of four dimensions that comprise ones fundamental appraisal of oneself – along with locus of control, neuroticism, and self-efficacy. The concept of core self-evaluations as first examined by Judge, Locke, and Durham (1997), has since proven to have the ability to predict job satisfaction and job performance. Self-esteem may be essential to self-evaluation. In public policy The importance of self-esteem gained endorsement from some government and non-government groups starting around the 1970s, such that one can speak of a self-esteem movement. This movement can be used as an example of promising evidence that psychological research can have an effect on forming public policy. The underlying idea of the movement was that low self-esteem was the root of problems for individuals, making it the root of societal problems and dysfunctions. A leading figure of the movement, psychologist Nathaniel Branden, stated: "[I] cannot think of a single psychological problem – from anxiety and depression, to fear of intimacy or of success, to spouse battery or child molestation – that is not traced back to the problem of low self-esteem".: 3 Self-esteem was believed to be a cultural phenomenon of Western individualistic societies since low self-esteem was not found in collectivist countries such as Japan. Concern about low self-esteem and its many presumed negative consequences led California assemblyman John Vasconcellos to work to set up and fund the Task Force on Self-Esteem and Personal and Social Responsibility, in California, in 1986. Vasconcellos argued that this task force could combat many of the states problems – from crime and teen pregnancy to school underachievement and pollution. He compared increasing self-esteem to giving out a vaccine for a disease: it could help protect people from being overwhelmed by lifes challenges. The task force set up committees in many California counties and formed a committee of scholars to review the available literature on self-esteem. This committee found very small associations between low self-esteem and its assumed consequences, ultimately showing that low self-esteem was not the root of all societal problems and not as important as the committee had originally thought. However, the authors of the paper that summarized the review of the literature still believed that self-esteem is an independent variable that affects major social problems. The task force disbanded in 1995, and the National Council for Self-Esteem and later the National Association for Self-Esteem (NASE) was established, taking on the task forces mission. Vasconcellos and Jack Canfield were members of its advisory board in 2003, and members of its masters coalition included Anthony Robbins, Bernie Siegel, and Gloria Steinem. Theories Many early theories suggested that self-esteem is a basic human need or motivation. American psychologist Abraham Maslow included self-esteem in his hierarchy of human needs. He described two different forms of "esteem": the need for respect from others in the form of recognition, success, and admiration, and the need for self-respect in the form of self-love, self-confidence, skill, or aptitude. Respect from others was believed to be more fragile and easily lost than inner self-esteem. According to Maslow, without the fulfillment of the self-esteem need, individuals will be driven to seek it and unable to grow and obtain self-actualization. Maslow also states that the healthiest expression of self-esteem "is the one which manifests in the respect we deserve for others, more than renown, fame, and flattery". Modern theories of self-esteem explore the reasons humans are motivated to maintain a high regard for themselves. Sociometer theory maintains that self-esteem evolved to check ones level of status and acceptance in ones social group. According to Terror Management Theory, self-esteem serves a protective function and reduces anxiety about life and death.Carl Rogers (1902–1987), an advocate of humanistic psychology, theorized the origin of many peoples problems to be that they despise themselves and consider themselves worthless and incapable of being loved. This is why Rogers believed in the importance of giving unconditional acceptance to a client and when this was done it could improve the clients self-esteem. In his therapy sessions with clients, he offered positive regard no matter what. Indeed, the concept of self-esteem is approached since then in humanistic psychology as an inalienable right for every person, summarized in the following sentence: Every human being, with no exception, for the mere fact to be it, is worthy of unconditional respect of everybody else; he deserves to esteem himself and to be esteemed. Measurement Self-esteem is typically assessed using self-report inventories. One of the most widely used instruments, the Rosenberg self-esteem scale (RSES) is a 10-item self-esteem scale score that requires participants to indicate their level of agreement with a series of statements about themselves. An alternative measure, the Coopersmith Inventory uses a 50-question battery over a variety of topics and asks subjects whether they rate someone as similar or dissimilar to themselves. If a subjects answers demonstrate solid self-regard, the scale regards them as well adjusted. If those answers reveal some inner shame, it considers them to be prone to social deviance.Implicit measures of self-esteem began to be used in the 1980s. These rely on indirect measures of cognitive processing thought to be linked to implicit self-esteem, including the name letter task (or initial preference task) and the Implicit Association Task.Such indirect measures are designed to reduce awareness of the process of assessment. When using them to assess implicit self-esteem, psychologists apply self-relevant stimuli to the participant and then measure how quickly a person identifies positive or negative stimuli. For example, if a woman was given the self-relevant stimuli of female and mother, psychologists would measure how quickly she identified the negative word, evil, or the positive word, kind. Development across lifespan Experiences in a persons life are a major source of how self-esteem develops. In the early years of a childs life, parents have a significant influence on self-esteem and can be considered the main source of positive and negative experiences a child will have. Unconditional love from parents helps a child develop a stable sense of being cared for and respected. These feelings translate into later effects on self-esteem as the child grows older. Students in elementary school who have high self-esteem tend to have authoritative parents who are caring, supportive adults who set clear standards for their child and allow them to voice their opinion in decision making. Although studies thus far have reported only a correlation of warm, supportive parenting styles (mainly authoritative and permissive) with children having high self-esteem, these parenting styles could easily be thought of as having some causal effect in self-esteem development. Childhood experiences that contribute to healthy self-esteem include being listened to, being spoken to respectfully, receiving appropriate attention and affection and having accomplishments recognized and mistakes or failures acknowledged and accepted. Experiences that contribute to low self-esteem include being harshly criticized, being physically, sexually or emotionally abused, being ignored, ridiculed or teased or being expected to be "perfect" all the time.During school-aged years, academic achievement is a significant contributor to self-esteem development. Consistently achieving success or consistently failing will have a strong effect on students individual self-esteem. However, students can also experience low self-esteem while in school. For example, they may not have academic achievements, or they live in a troubled environment outside of school. Issues like the ones previously stated, can cause adolescents to doubt themselves. Social experiences are another important contributor to self-esteem. As children go through school, they begin to understand and recognize differences between themselves and their classmates. Using social comparisons, children assess whether they did better or worse than classmates in different activities. These comparisons play an important role in shaping the childs self-esteem and influence the positive or negative feelings they have about themselves. As children go through adolescence, peer influence becomes much more important. Adolescents make appraisals of themselves based on their relationships with close friends. Successful relationships among friends are very important to the development of high self-esteem for children. Social acceptance brings about confidence and produces high self-esteem, whereas rejection from peers and loneliness brings about self-doubts and produces low self-esteem.Adolescence shows an increase in self-esteem that continues to increase in young adulthood and middle age. A decrease is seen from middle age to old age with varying findings on whether it is a small or large decrease. Reasons for the variability could be because of differences in health, cognitive ability, and socioeconomic status in old age. No differences have been found between males and females in their development of self-esteem. Multiple cohort studies show that there is not a difference in the life-span trajectory of self-esteem between generations due to societal changes such as grade inflation in education or the presence of social media.High levels of mastery, low risk taking, and better health are ways to predict higher self-esteem. In terms of personality, emotionally stable, extroverted, and conscientious individuals experience higher self-esteem. These predictors have shown us that self-esteem has trait-like qualities by remaining stable over time like personality and intelligence. However, this does not mean it can not be changed. Hispanic adolescents have a slightly lower self-esteem than their black and white peers, but then slightly higher levels by age 30. African Americans have a sharper increase in self-esteem in adolescence and young adulthood compared to Whites. However, during old age, they experience a more rapid decline in self-esteem. Shame Shame can be a contributor to those with problems of low self-esteem. Feelings of shame usually occur because of a situation where the social self is devalued, such as a socially evaluated poor performance. A poor performance leads to higher responses of psychological states that indicate a threat to the social self namely a decrease in social self-esteem and an increase in shame. This increase in shame can be helped with self-compassion. Real self, ideal self, and dreaded self There are three levels of self-evaluation development in relation to the real self, ideal self, and the dreaded self. The real, ideal, and dreaded selves develop in children in a sequential pattern on cognitive levels. Moral judgment stages: Individuals describe their real, ideal, and dreaded selves with stereotypical labels, such as "nice" or "bad". Individuals describe their ideal and real selves in terms of disposition for actions or as behavioral habits. The dreaded self is often described as being unsuccessful or as having bad habits. Ego development stages: Individuals describe their ideal and real selves in terms of traits that are based on attitudes as well as actions. The dreaded self is often described as having failed to meet social expectations or as self-centered. Self-understanding stages: Individuals describe their ideal and real selves as having unified identities or characters. Descriptions of the dreaded self focus on a failure to live up to ones ideals or role expectations often because of real world problems.This development brings with it increasingly complicated and encompassing moral demands. This level is where individuals self-esteems can suffer because they do not feel as though they are living up to certain expectations. This feeling will moderately affect ones self-esteem with an even larger effect seen when individuals believe they are becoming their dreaded selves. Types High People with a healthy level of self-esteem: Firmly believe in certain values and principles, and are ready to defend them even when finding opposition, feeling secure enough to modify them in light of experience. Are able to act according to what they think to be the best choice, trusting their own judgment, and not feeling guilty when others do not like their choice. Do not lose time worrying excessively about what happened in the past, nor about what could happen in the future. They learn from the past and plan for the future, but live in the present intensely. Fully trust in their capacity to solve problems, not hesitating after failures and difficulties. They ask others for help when they need it. Consider themselves equal in dignity to others, rather than inferior or superior, while accepting differences in certain talents, personal prestige or financial standing. Understand how they are an interesting and valuable person for others, at least for those with whom they have a friendship. Resist manipulation, collaborate with others only if it seems appropriate and convenient. Admit and accept different internal feelings and drives, either positive or negative, revealing those drives to others only when they choose. Are able to enjoy a great variety of activities. Are sensitive to feelings and needs of others; respect generally accepted social rules, and claim no right or desire to prosper at others expense. Can work toward finding solutions and voice discontent without belittling themselves or others when challenges arise. Secure vs. defensive A person can have high self-esteem and hold it confidently where they do not need reassurance from others to maintain their positive self-view, whereas others with defensive high self-esteem may still report positive self-evaluations on the Rosenberg Scale, as all high self-esteem individuals do; however, their positive self-views are fragile and vulnerable to criticism. Defensive high self-esteem individuals internalize subconscious self-doubts and insecurities, causing them to react very negatively to any criticism they may receive. There is a need for constant positive feedback from others for these individuals to maintain their feelings of self-worth. The necessity of repeated praise can be associated with boastful, arrogant behavior or sometimes even aggressive and hostile feelings toward anyone who questions the individuals self-worth, an example of threatened egotism.The Journal of Educational Psychology conducted a study in which they used a sample of 383 Malaysian undergraduates participating in work integrated learning (WIL) programs across five public universities to test the relationship between self-esteem and other psychological attributes such as self-efficacy and self-confidence. The results demonstrated that self-esteem has a positive and significant relationship with self-confidence and self-efficacy since students with higher self-esteem had better performances at university than those with lower self-esteem. It was concluded that higher education institutions and employers should emphasize the importance of undergraduates self-esteem development. Implicit and explicit Implicit self-esteem refers to a persons disposition to evaluate themselves positively or negatively in a spontaneous, automatic, or unconscious manner. It contrasts with explicit self-esteem, which entails more conscious and reflective self-evaluation. Both explicit self-esteem and implicit self-esteem are theoretically subtypes of self-esteem proper. However, the validity of implicit self-esteem as a construct is highly questionable, given not only its weak or nonexistent correlation with explicit self-esteem and informant ratings of self-esteem, but also the failure of multiple measures of implicit self-esteem to correlate with each other.As present, there is little scientific evidence that self-esteem can be reliably or validly measured through implicit means. Narcissism and threatened egotism Narcissism is a disposition people may have that represents an excessive love for ones self. It is characterized by an inflated view of self-worth. Individuals who score high on narcissism measures, Robert Raskins Narcissistic Personality Inventory, would likely select true to such statements as "If I ruled the world, it would be a much better place." There is only a moderate correlation between narcissism and self-esteem; that is to say that an individual can have high self-esteem but low narcissism or can be a conceited, obnoxious person and score high self-esteem and high narcissism. However, when correlation analysis is restricted to the sense of superiority or self-admiration aspects of narcissism, correlations between narcissism and self-esteem become strong (usually at or around r = .50, but sometimes up to β = .86). Moreover, self-esteem is positively correlated with a sense of superiority even when controlling for overall narcissism.In addition to exaggerated regard for oneself, however, narcissism is additionally defined by such characteristics as entitlement, exploitativeness and dominance. Additionally, while positive self-image is a shared characteristic of narcissism and self-esteem, narcissistic self-appraisals are exaggerated and limited to agentic traits (intellect, talent, etc.), whereas in non-narcissistic self-esteem, positive views of the self compared with others are relatively modest and sample equally from the agentic and communal (morality, honesty, etc.) domains. Thus, while sharing positive self-regard as a main feature, and while narcissism is defined by high self-esteem, the two constructs are not interchangeable. Threatened egotism is characterized as a response to criticism that threatens the ego of narcissists; they often react in a hostile and aggressive manner. Low Low self-esteem can result from various factors, including genetic factors, physical appearance or weight, mental health issues, socioeconomic status, significant emotional experiences, social stigma, peer pressure or bullying.A person with low self-esteem may show some of the following characteristics: Heavy self-criticism and dissatisfaction. Hypersensitivity to criticism with resentment against critics and feelings of being attacked. Chronic indecision and an exaggerated fear of mistakes. Excessive will to please and unwillingness to displease any petitioner. Perfectionism, which can lead to frustration when perfection is not achieved. Neurotic guilt, dwelling on or exaggerating the magnitude of past mistakes. Floating hostility and general defensiveness and irritability without any proximate cause. Pessimism and a general negative outlook. Envy, invidiousness, or general resentment. Sees temporary setbacks as permanent, intolerable conditions.Individuals with low self-esteem tend to be critical of themselves. Some depend on the approval and praise of others when evaluating self-worth. Others may measure their likability in terms of successes: others will accept themselves if they succeed but will not if they fail. People with chronic low self esteem are at a higher risk for experiencing psychotic disorders; and this behavior is closely linked to forming psychotic symptoms as well. Treatments Metacognitive therapy, EMDR technique, mindfulness-based cognitive therapy, rational emotive behavior therapy, cognitive behavioral therapy and trait and construct therapies have been shown to improve the patients self-esteem. The three states This classification proposed by Martin Ross distinguishes three states of self-esteem compared to the "feats" (triumphs, honors, virtues) and the "anti-feats" (defeats, embarrassment, shame, etc.) of the individuals. Shattered The individual does not regard themselves as valuable or lovable. They may be overwhelmed by defeat, or shame, or see themselves as such, and they name their "anti-feat". For example, if they consider that being over a certain age is an anti-feat, they define themselves with the name of their anti-feat, and say, "I am old". They express actions and feelings such as pity, insulting themselves, and they may become paralyzed by their sadness. Vulnerable The individual has a generally positive self-image. However, their self-esteem is also vulnerable to the perceived risk of an imminent anti-feat (such as defeat, embarrassment, shame, discredit), consequently, they are often nervous and regularly use defense mechanisms. A typical protection mechanism of those with vulnerable self-esteem may consist in avoiding decision-making. Although such individuals may outwardly exhibit great self-confidence, the underlying reality may be just the opposite: the apparent self-confidence is indicative of their heightened fear of anti-feats and the fragility of their self-esteem. They may also try to blame others to protect their self-image from situations that would threaten it. They may employ defense mechanisms, including attempting to lose at games and other competitions in order to protect their self-image by publicly dissociating themselves from a need to win, and asserting an independence from social acceptance which they may deeply desire. In this deep fear of being unaccepted by an individuals peers, they make poor life choices by making risky decisions. Strong People with strong self-esteem have a positive self-image and enough strength so that anti-feats do not subdue their self-esteem. They have less fear of failure. These individuals appear humble, cheerful, and this shows a certain strength not to boast about feats and not to be afraid of anti-feats. They are capable of fighting with all their might to achieve their goals because, if things go wrong, their self-esteem will not be affected. They can acknowledge their own mistakes precisely because their self-image is strong, and this acknowledgment will not impair or affect their self-image. They live with less fear of losing social prestige, and with more happiness and general well-being. However, no type of self-esteem is indestructible, and due to certain situations or circumstances in life, one can fall from this level into any other state of self-esteem. Contingent vs. non-contingent A distinction is made between contingent (or conditional) and non-contingent (or unconditional) self-esteem. Contingent self-esteem is derived from external sources, such as what others say, ones success or failure, ones competence, or relationship-contingent self-esteem. Therefore, contingent self-esteem is marked by instability, unreliability, and vulnerability. Persons lacking a non-contingent self-esteem are "predisposed to an incessant pursuit of self-value". However, because the pursuit of contingent self-esteem is based on receiving approval, it is doomed to fail, as no one receives constant approval, and disapproval often evokes depression. Furthermore, fear of disapproval inhibits activities in which failure is possible. Non-contingent self-esteem is described as true, stable, and solid. It springs from a belief that one is "acceptable period, acceptable before life itself, ontologically acceptable". Belief that one is "ontologically acceptable" is to believe that ones acceptability is "the way things are without contingency". In this belief, as expounded by theologian Paul Tillich, acceptability is not based on a persons virtue. It is an acceptance given "in spite of our guilt, not because we have no guilt".Psychiatrist Thomas A Harris drew on Tillich for his classic Im OK – Youre OK that addresses non-contingent self-esteem. Harris translated Tillichs "acceptable" by the vernacular OK, a term that means "acceptable". The Christian message, said Harris, is not "YOU CAN BE OK, IF"; it is "YOU ARE ACCEPTED, unconditionally".A secure non-contingent self-esteem springs from the belief that one is ontologically acceptable and accepted. Domain-specific self-esteem Whereas global self-esteem addresses how individuals appraise themselves in their entirety, domain-specific self-esteem facets relate to how they appraise themselves in various pertinent domains of life. Such functionally distinct facets of self-esteem may comprise self-evaluations in social, emotional, body-related, school performance-related, and creative-artistic domains.They have been found to be predictive of outcomes related to psychological functioning, health, education, and work. Low self-esteem in the social domain (i.e., self-perceived social competence), for example, has been repeatedly identified as a risk factor for bullying victimization. Importance Abraham Maslow states that psychological health is not possible unless the essential core of the person is fundamentally accepted, loved and respected by others and by oneself. Self-esteem allows people to face life with more confidence, benevolence, and optimism, and thus easily reach their goals and self-actualize.Self-esteem may make people convinced they deserve happiness. Understanding this is fundamental, and universally beneficial, since the development of positive self-esteem increases the capacity to treat other people with respect, benevolence and goodwill, thus favoring rich interpersonal relationships and avoiding destructive ones. For Erich Fromm, the love of others and love of ourselves are not alternatives. On the contrary, an attitude of love toward themselves will be found in all those who are capable of loving others. Self-esteem allows creativity at the workplace and is a specially critical condition for teaching professions.José-Vicente Bonet claims that the importance of self-esteem is obvious as a lack of self-esteem is, he says, not a loss of esteem from others, but self-rejection. Bonet claims that this corresponds to major depressive disorder. Freud also claimed that the depressive has suffered "an extraordinary diminution in his self-regard, an impoverishment of his ego on a grand scale... He has lost his self-respect".The Yogyakarta Principles, a document on international human rights law, addresses the discriminatory attitude toward LGBT people that makes their self-esteem low to be subject to human rights violation including human trafficking. The World Health Organization recommends in "Preventing Suicide", published in 2000, that strengthening students self-esteem is important to protect children and adolescents against mental distress and despondency, enabling them to cope adequately with difficult and stressful life situations.Other than increased happiness, higher self-esteem is also known to correlate with a better ability to cope with stress and a higher likeliness of taking on difficult tasks relative to those with low self-esteem. Correlations From the late 1970s to the early 1990s many Americans assumed as a matter of course that students self-esteem acted as a critical factor in the grades that they earned in school, in their relationships with their peers, and in their later success in life. Under this assumption, some American groups created programs which aimed to increase the self-esteem of students. Until the 1990s, little peer-reviewed and controlled research took place on this topic. Peer-reviewed research undertaken since then has not validated previous assumptions. Recent research indicates that inflating students self-esteems in and of itself has no positive effect on grades. Roy Baumeister has shown that inflating self-esteem by itself can actually decrease grades. The relationship involving self-esteem and academic results does not signify that high self-esteem contributes to high academic results. It simply means that high self-esteem may be accomplished as a result of high academic performance due to the other variables of social interactions and life events affecting this performance.Attempts by pro-esteem advocates to encourage self-pride in students solely by reason of their uniqueness as human beings will fail if feelings of well-being are not accompanied by well-doing. It is only when students engage in personally meaningful endeavors for which they can be justifiably proud that self-confidence grows, and it is this growing self-assurance that in turn triggers further achievement.High self-esteem has a high correlation to self-reported happiness; whether this is a causal relationship has not been established. The relationship between self-esteem and life satisfaction is stronger in individualistic cultures.Additionally, self-esteem has been found to be related to forgiveness in close relationships, in that people with high self-esteem will be more forgiving than people with low self-esteem.High self-esteem does not prevent children from smoking, drinking, taking drugs, or engaging in early sex. Mental Health Self-esteem has been associated with several mental health conditions, including depression, anxiety, and eating disorders. For example, low self-esteem may increase the likelihood that people who experience dysfunctional thoughts will develop symptoms of depression. In contrast, high self-esteem may protect against the development of mental health conditions, with research finding that high self-esteem reduces the chances of bulimia and anxiety. Neuroscience In research conducted in 2014 by Robert S. Chavez and Todd F. Heatherton, it was found that self-esteem is related to the connectivity of the frontostriatal circuit. The frontostriatal pathway connects the medial prefrontal cortex, which deals with self-knowledge, to the ventral striatum, which deals with feelings of motivation and reward. Stronger anatomical pathways are correlated with higher long-term self-esteem, while stronger functional connectivity is correlated with higher short-term self-esteem. Criticism and controversy The American psychologist Albert Ellis criticized on numerous occasions the concept of self-esteem as essentially self-defeating and ultimately destructive. Although acknowledging the human propensity and tendency to ego rating as innate, he has critiqued the philosophy of self-esteem as unrealistic, illogical and self- and socially destructive – often doing more harm than good. Questioning the foundations and usefulness of generalized ego strength, he has claimed that self-esteem is based on arbitrary definitional premises, and overgeneralized, perfectionistic and grandiose thinking. Acknowledging that rating and valuing behaviors and characteristics is functional and even necessary, he sees rating and valuing human beings totality and total selves as irrational and unethical. The healthier alternative to self-esteem according to him is unconditional self-acceptance and unconditional other-acceptance. Rational Emotive Behavior Therapy is a psychotherapy based on this approach. "There seem to be only two clearly demonstrated benefits of high self-esteem....First, it increases initiative, probably because it lends confidence. People with high self-esteem are more willing to act on their beliefs, to stand up for what they believe in, to approach others, to risk new undertakings. (This unfortunately includes being extra willing to do stupid or destructive things, even when everyone else advises against them.)...It can also lead people to ignore sensible advice as they stubbornly keep wasting time and money on hopeless causes" False attempts For persons with low self-esteem, any positive stimulus will temporarily raise self-esteem. Therefore, possessions, sex, success, or physical appearance will produce the development of self-esteem, but the development is ephemeral at best. Such attempts to raise ones self-esteem by positive stimulus produce a "boom or bust" pattern. "Compliments and positive feedback" produce a boost, but a bust follows a lack of such feedback. For a person whose "self-esteem is contingent", success is "not extra sweet", but "failure is extra bitter". As narcissism Life satisfaction, happiness, healthy behavioral practices, perceived efficacy, and academic success and adjustment have been associated with having high levels of self-esteem (Harter, 1987; Huebner, 1991; Lipschitz-Elhawi & Itzhaky, 2005; Rumberger 1995; Swenson & Prelow, 2005; Yarcheski & Mahon, 1989).: 270  However, a common mistake is to think that loving oneself is necessarily equivalent to narcissism, as opposed for example to what Erik Erikson speaks of as "a post-narcissistic love of the ego". People with a healthy self-esteem accept and love themselves unconditionally, acknowledging both virtues and faults in the self, and yet, in spite of everything, are able to continue to love themselves. In narcissists, by contrast, an " uncertainty about their own worth gives rise to...a self-protective, but often totally spurious, aura of grandiosity" – producing the class "of narcissists, or people with very high, but insecure, self-esteem... fluctuating with each new episode of social praise or rejection.": 479 Narcissism can thus be seen as a symptom of fundamentally low self-esteem, that is, lack of love towards oneself, but often accompanied by "an immense increase in self-esteem" based on "the defense mechanism of denial by overcompensation." "Idealized love of self...rejected the part of him" that he denigrates – "this destructive little child" within. Instead, the narcissist emphasizes their virtues in the presence of others, just to try to convince themself that they are a valuable person and to try to stop feeling ashamed for their faults; such "people with unrealistically inflated self-views, which may be especially unstable and highly vulnerable to negative information,...tend to have poor social skills.": 126 See also References Further reading Baumeister, Roy F. (2001). "Violent Pride: Do people turn violent because of self-hate or self-love?," in Scientific American, 284, No. 4, pp. 96–101; April 2001. Branden, N. (1969). The Psychology of Self-Esteem. New York: Bantam. Branden, N. (2001). The psychology of self-esteem: a revolutionary approach to self-understanding that launched a new era in modern psychology. San Francisco: Jossey-Bass, 2001. ISBN 0787945269 Burke, C. (2008) "Self-esteem: Why?; Why not?," New York: 2008 Crocker J.; Park L. E. (2004). "The costly pursuit of self-esteem". Psychological Bulletin. 130 (3): 392–414. doi:10.1037/0033-2909.130.3.392. PMID 15122925. Franklin, Richard L. (1994). "Overcoming The Myth of Self-Worth: Reason and Fallacy in What You Say to Yourself." ISBN 0963938703 Hill, S.E. & Buss, D.M. (2006). "The Evolution of Self-Esteem." In Michael Kernis, (Ed.), Self Esteem: Issues and Answers: A Sourcebook of Current Perspectives.. Psychology Press:New York. 328–33. Full text Lerner, Barbara (1985). "Self-Esteem and Excellence: The Choice and the Paradox," American Educator, Winter 1985. Mecca, Andrew M., et al., (1989). The Social Importance of Self-esteem University of California Press, 1989. (ed; other editors included Neil J. Smelser and John Vasconcellos) Mruk, C. (2006). Self-Esteem research, theory, and practice: Toward a positive psychology of self-esteem (3rd ed.). New York: Springer. Rodewalt F.; Tragakis M. W. (2003). "Self-esteem and self-regulation: Toward optimal studies of self-esteem". Psychological Inquiry. 14 (1): 66–70. doi:10.1207/s15327965pli1401_02. Ruggiero, Vincent R. (2000). "Bad Attitude: Confronting the Views That Hinder Students Learning" American Educator. Sedikides, C., & Gregg. A. P. (2003). "Portraits of the self." In M. A. Hogg & J. Cooper (Eds.), Sage handbook of social psychology (pp. 110–38). London: Sage Publications. Twenge, Jean M. (2007). Generation Me: Why Todays Young Americans Are More Confident, Assertive, Entitled – and More Miserable Than Ever Before. Free Press. ISBN 978-0743276986

Can you describe Compulsive hoarding, to me Aarogya

Compulsive hoarding

Compulsive hoarding, also known as hoarding disorder, Plyushkins disorder, is a mental disorder characterised by accumulation of possessions due to excessive acquisition of or difficulty discarding them, regardless of their actual value, leading to clinically significant distress or impairment in personal, family, social, educational, occupational or other important areas of functioning. Excessive acquisition is characterized by repetitive urges or behaviours related to amassing or buying items. Difficulty discarding possessions is characterized by a perceived need to save items and distress associated with discarding them. Accumulation of possessions results in living spaces becoming cluttered to the point that their use or safety is compromised. It is recognised by the eleventh revision of the International Classification of Diseases (ICD-11) and the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5). Prevalence rates are estimated at 2% to 5% in adults, though the condition typically manifests in childhood with symptoms worsening in advanced age, at which point collected items have grown excessive and family members who would otherwise help to maintain and control the levels of clutter have either died or moved away.People with hoarding disorder commonly live with other complex and/or psychological disorders such as depression, anxiety, obsessive compulsive disorder (OCD) and attention deficit hyperactivity disorder (ADHD). Other factors often associated with hoarding include alcohol dependence and paranoid, schizotypal and avoidance traits. Differential diagnosis Collecting and hoarding may seem similar, but there are distinct characteristics that set the behaviors apart. Collecting is a hobby often involving the targeted search and acquisition of specific items that form—at least from the perspective of the collector—a greater appreciation, deeper understanding, or increased synergistic value when combined with other similar items. Hoarding, by contrast, typically appears haphazard and involves the overall acquiring of common items that would not be especially meaningful to the person who is gathering such items in large quantities. People who hoard commonly keep items that hold little to no true meaning or value to most others, unlike some collectors, whose items may be of great value to select people. Most hoarders are disorganized, and their living areas are crowded and in disarray. Most collectors can afford to store their items systematically or to have enough room to display their collections. Age, mental state, or finances have caused some collectors to fall into a hoarding state. Clutter Image Rating A UK charity called HoardingUK, has found that people have very different ideas about what it means to have a cluttered home. For some, a small pile of things in the corner of an otherwise well-ordered room constitutes serious clutter. For others, only when the narrow pathways make it hard to get through a room does the clutter register. To ensure an accurate sense of a clutter problem, they created the Clutter Image Rating, a series of pictures of rooms in various stages of clutter – from completely clutter-free to very severely cluttered designed to encourage people to get support. Studies In a 2010 study using data from self-reports of hoarding behavior from 751 participants, it was found most reported the onset of their hoarding symptoms between the ages of 11 and 20 years old, with 70% reporting the behaviors before the age of 21. Fewer than 4% of people reported the onset of their symptoms after the age of 40. The data showed that compulsive hoarding usually begins early, but often does not become more prominent until after age 40. Different reasons have been given for this, such as the effects of family presence earlier in life and limits on hoarding imposed by housing situation and lifestyle. The understanding of early onset hoarding behavior may help in the future to better distinguish hoarding behavior from "normal" childhood collecting behaviors.A second key part of this study was to determine if stressful life events are linked to the onset of hoarding symptoms. Similar to self-harming, traumatized persons may create a problem for themselves in order to avoid their real anxiety or trauma. Facing their real issues may be too difficult for them, so they create an artificial problem (in their case, hoarding) and prefer to battle with it rather than determine, face, or do something about their real anxieties. Hoarders may suppress their psychological pain by hoarding. The study shows that adults who hoard report a greater lifetime incidence of having possessions taken by force, forced sexual activity as either an adult or a child, including forced sexual intercourse, and being physically handled roughly during childhood, thus proving traumatic events are positively correlated with the severity of hoarding. For each five years of life the participant would rate from 1 to 4, 4 being the most severe, the severity of their hoarding symptoms. Of the participants, 548 reported a chronic course, 159 an increasing course and 39 people, a decreasing course of illness. The incidents of increased hoarding behavior were usually correlated to five categories of stressful life events.Although excessive acquiring is not a diagnostic criterion of hoarding, at least two-thirds of individuals with hoarding disorder excessively acquire possessions. Having a more anxiously attached interpersonal style is associated with more compulsive buying and greater acquisition of free items and these relationships are mediated by stronger distress intolerance and greater anthropomorphism. Anthropomorphism has been shown to increase both the sentimental value and perceived utility of items. These findings indicate that individuals may over-value their possessions to compensate for thwarted interpersonal needs. Feeling alone and/or disconnected from others may impair peoples ability to tolerate distress and increase peoples tendencies to see human-like qualities in objects. The humanness of items may increase their perceived value and individuals may acquire these valued objects to alleviate distress. Individuals with hoarding problems have been shown to have greater interpersonal problems than individuals who only excessively acquire possessions, which provides some support for the assumption that individuals with hoarding problems may have a stronger motivation to hang onto possessions for support. As possessions cannot provide support in the way humans can and because saving excessively can frustrate other people due to its impact on their quality of life, individuals with hoarding disorder may be caught in a feedback loop. They may save to alleviate distress, but this saving may cause distress, which may lead them to keep saving to alleviate the distress. Treatment Only 5% of people with hoarding behaviours receive help (Singh, 2012) and the interventions they do receive focus on clearing items, not treating the disorder. Cognitive-behavioral therapy (CBT) is a commonly implemented therapeutic intervention for compulsive hoarding. As part of cognitive behavior therapy, the therapist may help the patient to: Discover why one is compelled to hoard. Learn to organize possessions in order to decide what to discard. Develop decision-making skills. Declutter the home during in-home visits by a therapist or professional organizer. Gain and perform relaxation skills. Attend family and/or group therapy. Be open to trying psychiatric hospitalization if the hoarding is serious. Have periodic visits and consultations to keep a healthy lifestyle.This modality of treatment usually involves exposure and response prevention to situations that cause anxiety and cognitive restructuring of beliefs related to hoarding. Furthermore, research has also shown that certain CBT protocols have been more effective in treatment than others. CBT programs that specifically address the motivation of the affected person, organization, acquiring new clutter, and removing current clutter from the home have shown promising results. This type of treatment typically involves in-home work with a therapist combined with between-session homework, the completion of which is associated with better treatment outcomes. Research on internet-based CBT treatments for the disorder (where participants have access to educational resources, cognitive strategies, and chat groups) has also shown promising results both in terms of short- and long-term recovery.Other therapeutic approaches that have been found to be helpful: Motivational interviewing originated in addiction therapy. This method is significantly helpful when used in hoarding cases in which insight is poor and ambivalence to change is marked. Harm reduction rather than symptom reduction. Also borrowed from addiction therapy. The goal is to decrease the harmful implications of the behavior, rather than the hoarding behaviors. Group psychotherapy reduces social isolation and social anxiety and is cost-effective compared to one-on-one intervention. Group CBT tends to have similar outcomes to individual therapy. Although group treatment often does not include home sessions, experimental research suggests that treatment outcomes may be improved if home sessions are included. Individuals have been shown to discard more possessions when in a cluttered environment compared to a tidy environment. Indeed, a meta-analysis found that a greater number of home sessions improves CBT outcomes.Individuals with hoarding behaviors are often described as having low motivation and poor compliance levels, and as being indecisive and procrastinators, which may frequently lead to premature termination (i.e., dropout) or low response to treatment. Therefore, it was suggested that future treatment approaches, and pharmacotherapy in particular, be directed to address the underlying mechanisms of cognitive impairments demonstrated by individuals with hoarding symptoms. Mental health professionals frequently express frustration regarding hoarding cases, mostly due to premature termination and poor response to treatment. Patients are frequently described as indecisive, procrastinators, recalcitrant, and as having low or no motivation, which can explain why many interventions fail to accomplish significant results. To overcome this obstacle, some clinicians recommend accompanying individual therapy with home visits to help the clinician: Likewise, certain cases are assisted by professional organizers as well. In popular culture Maguire, Emily: Love Objects (2021), Allen & Unwin, ISBN 9781760878337 Hoarders - TV series Hoarding: Buried Alive See also Hoarders Alexander Kennedy Miller, hoarded about 30 Stutz automobiles (1906–1993) Collyer brothers, Homer Collyer (1881–1947) and Langley Collyer (1885–1947) Edmund Trebus (1918–2002), participated in TV documentary References Further reading Frost, Randy O.; Steketee, Gail (2011). Stuff: Compulsive Hoarding and the Meaning of Things. Mariner Books. ISBN 9780547487250. Herring, Scott (2014). The Hoarders: Material Deviance in Modern American Culture. Chicago, IL: University of Chicago Press. ISBN 9780226171715. Mapes, Diane. "Engulfed in clutter, hoarders keep heaping it on". NBC News. Article discussing the disorder and its relationship to OCD. Sholl, Jessie (2010). Dirty Secret: A Daughter Comes Clean About Her Mothers Compulsive Hoarding. New York: Simon & Schuster/Gallery Books. ISBN 9781439192535. External links "Measuring". Squalor Survivors. Non-commercial compulsive hoarding forum HoardingUK

Hey Aarogya!, what is Selective mutism

Selective mutism

Selective mutism (SM) is an anxiety disorder in which a person who is otherwise capable of speech becomes unable to speak when exposed to specific situations, specific places, or to specific people, one or multiple of which serving as triggers. This is caused by the freeze response. Selective mutism usually co-exists with social anxiety disorder. People with selective mutism stay silent even when the consequences of their silence include shame, social ostracism, or punishment. Signs and symptoms Children and adults with selective mutism are fully capable of speech and understanding language but are completely unable to speak in certain situations, though speech is expected of them. The behaviour may be perceived as shyness or rudeness by others. A child with selective mutism may be completely silent at school for years but speak quite freely or even excessively at home. There is a hierarchical variation among people with this disorder: some people participate fully in activities and appear social but do not speak, others will speak only to peers but not to adults, others will speak to adults when asked questions requiring short answers but never to peers, and still others speak to no one and participate in few, if any, activities presented to them. In a severe form known as "progressive mutism", the disorder progresses until the person with this condition no longer speaks to anyone in any situation, even close family members. To meet DSM-5 criteria for selective mutism, one must exhibit the following: Consistent failure to speak in specific social situations (in which there is an expectation for speaking, e.g., at school) despite speaking in other situations. The disturbance interferes with educational or occupational achievement or with social communication. The duration of the disturbance is at least 1 month (not limited to the first month of school). The failure to speak is not due to a lack of knowledge of the spoken language required in the social situation. The disturbance is not better accounted for by a communication disorder (e.g., childhood-onset fluency disorder) and does not occur exclusively in people with autism spectrum disorders or psychotic disorders such as schizophrenia.Selective mutism is strongly associated with other anxiety disorders, particularly social anxiety disorder. In fact, the majority of children diagnosed with selective mutism also have social anxiety disorder (100% of participants in two studies and 97% in another). Some researchers therefore speculate that selective mutism may be an avoidance strategy used by a subgroup of children with social anxiety disorder to reduce their distress in social situations.Particularly in young children, selective mutism can sometimes be confused with an autism spectrum disorder, especially if the child acts particularly withdrawn around their diagnostician, which can lead to incorrect diagnosis and treatment. Although autistic people may also be selectively mute, they often display other behaviors—stimming, repetitive behaviors, social isolation even among family members (not always answering to name, for example)—that set them apart from a child with selective mutism. Some autistic people may be selectively mute due to anxiety in unfamiliar social situations. If mutism is entirely due to autism spectrum disorder, it cannot be diagnosed as selective mutism as stated in the last item on the list above. The former name elective mutism indicates a widespread misconception among psychologists that selective mute people choose to be silent in certain situations, while the truth is that they often wish to speak but are unable to do so. To reflect the involuntary nature of this disorder, the name was changed to selective mutism in 1994. The incidence of selective mutism is not certain. Due to the poor understanding of this condition by the general public, many cases are likely undiagnosed. Based on the number of reported cases, the figure is commonly estimated to be 1 in 1000, 0.1%. However, a 2002 study in The Journal of the American Academy of Child and Adolescent Psychiatry estimated the incidence to be 0.71%. Other symptoms Besides lack of speech, other common behaviors and characteristics displayed by selectively mute people, according to Dr. Elisa Shipon-Blums findings, include: Shyness, social anxiety, fear of social embarrassment or social isolation and withdrawal Difficulty maintaining eye contact Blank expression and reluctance to smile or incessant smiling Difficulty expressing feelings, even to family members Tendency to worry more than most people of the same age Sensitivity to noise and crowdsOn the flip side, there are some positive traits observed in many cases: Above average intelligence, inquisitiveness, or perception A strong sense of right and wrong Creativity Love for the arts Empathy Sensitivity for other people Causes Selective mutism (SM) is an umbrella term for the condition of otherwise well-developed children or adults who cannot speak or communicate under certain settings. The exact causes that affect each person may be different and yet unknown. There have been attempts to categorize, but there are no definitive answers yet due to the under-diagnosis and small/biased sample sizes. Many people are not diagnosed until late in childhood only because they do not speak at school and therefore fail to accomplish assignments requiring public speaking. Their involuntary silence makes the condition harder to understand or test. Parents often are unaware of the condition since the children may be functioning well at home. Teachers and pediatricians also sometimes mistake it for severe shyness or common stage fright.Most children and adults with selective mutism are hypothesized to have an inherited predisposition to anxiety. They often have inhibited temperaments, which is hypothesized to be the result of over-excitability of the area of the brain called the amygdala. This area receives indications of possible threats and sets off the fight-or-flight response. Behavioral inhibitions, or inhibited temperaments, encompass feelings of emotional distress and social withdrawals. In a 2016 study, the relationship between behavioral inhibition and selective mutism was investigated. Children between the ages of three and 19 with lifetime selective mutism, social phobia, internalizing behavior, and healthy controls were assessed using the parent-rated Retrospective Infant Behavioral Inhibition (RIBI) questionnaire, consisting of 20 questions that addressed shyness and fear, as well as other subscales. The results indicated behavioral inhibition does indeed predispose selective mutism. Corresponding with the researchers’ hypothesis, children diagnosed with long-term selective mutism had a higher behavioral inhibition score as an infant. This is indicative of the positive correlation between behavioral inhibition and selective mutism. Given the very high incidence of social anxiety disorder within selective mutism (as high as 100% in some studies), it is possible that social anxiety disorder causes selective mutism. Some children or adults with selective mutism may have trouble processing sensory information. This could cause anxiety and a sense of being overwhelmed in unfamiliar situations, which may cause the child or adult to "shut down" and not be able to speak (something that some autistic people also experience). Many children or adults with selective mutism have some auditory processing difficulties. About 20–30% of children or adults with selective mutism have speech or language disorders that add stress to situations in which the child is expected to speak. Despite the change of name from "elective" to "selective", a common misconception remains that a selectively mute child is defiant or stubborn. In fact, children with selective mutism have a lower rate of oppositional behavior than their peers in a school setting. Some previous studies on the subject of selective mutism have been dismissed as containing serious flaws in their design. According to a more recent systematic study it is believed that children or adults who have selective mutism are not more likely than other children or adults to have a history of early trauma or stressful life events. Many children or adults who have selective mutism almost always speak confidently in some situations. Treatment Contrary to popular belief, people with selective mutism do not necessarily improve with age. Effective treatment is necessary for a child to develop properly. Without treatment, selective mutism can contribute to chronic depression, further anxiety, and other social and emotional problems.Consequently, treatment at an early age is important. If not addressed, selective mutism tends to be self-reinforcing. Others may eventually expect an affected child to not speak and therefore stop attempting to initiate verbal contact. Alternatively, they may pressure the child to talk, increasing their anxiety levels in situations where speech is expected. Due to these problems, a change of environment may be a viable consideration. However, changing school is worth considering only if the alternative environment is highly supportive, otherwise a whole new environment could also be a social shock for the individual or deprive them of any friends or support they have currently. Regardless of the cause, increasing awareness and ensuring an accommodating, supportive environment are the first steps towards effective treatment. Most often affected children do not have to change schools or classes and have no difficulty keeping up except on the communication and social front. Treatment in teenage or adult years can be more difficult because the affected individual has become accustomed to being mute, and lacks social skills to respond to social cues.The exact treatment depends on the persons age, any comorbid mental illnesses, and a number of other factors. For instance, stimulus fading is typically used with younger children because older children and teenagers recognize the situation as an attempt to make them speak, and older people with this condition and people with depression are more likely to need medication.Like other disabilities, adequate accommodations are needed for those with the condition to succeed at school, work, and in the home. Under the U.S. federal law and the Individuals with Disabilities Education Act (IDEA), those with the disorder qualify for services based upon the fact that they have an impairment that hinders their ability to speak, thus disrupting their lives. This assistance is typically documented in the form of an Individualized Education Program (IEP). Post-secondary accommodations are also available for people with disabilities.Under another law, Section 504 of the Rehabilitation Act of 1973, public school districts are required to provide a free, appropriate public education to every "qualified handicapped person" residing within their jurisdiction. If the child is found to have impairments that substantially limit a major life activity (in this case, learning), the education agency has to decide what related aids or services are required to provide equal access to the learning environment.Social Communication Anxiety Treatment (S-CAT) is a common treatment approach by professionals and has proven to be successful. S-CAT integrates components of behavioral-therapy, cognitive-behavioral therapy (CBT), and an insight-oriented approach to increase social communication and promote social confidence. Tactics such as systemic desensitization, modeling, fading, and positive reinforcement enable individuals to develop social engagement skills and begin to progress communicatively in a step-by-step manner. There are many treatment plans that exist and it is recommended for families to do thorough research before deciding on their treatment approach. Self-modeling An affected child is brought into the classroom or the environment where the child will not speak and is videotaped. First, the teacher or another adult prompts the child with questions that likely will not be answered. A parent, or someone the child feels comfortable speaking to, then replaces the prompter and asks the child the same questions, this time eliciting a verbal response. The two videos of the conversations are then edited together to show the child directly answering the questions posed by the teacher or other adult. This video is then shown to the child over a series of several weeks, and every time the child sees themself verbally answering the teacher/other adult, the tape is stopped and the child is given positive reinforcement.Such videos can also be shown to affected childrens classmates to set an expectation in their peers that they can speak. The classmates thereby learn the sound of the childs voice and, albeit through editing, have the opportunity to see the child conversing with the teacher. Mystery motivators Mystery motivation is often paired with self-modeling. An envelope is placed in the childs classroom in a visible place. On the envelope, the childs name is written along with a question mark. Inside is an item that the childs parent has determined to be desirable to the child. The child is told that when they ask for the envelope loudly enough for the teacher and others in the classroom to hear, the child will receive the mystery motivator. The class is also told of the expectation that the child ask for the envelope loudly enough that the class can hear. Stimulus fading Affected subjects can be brought into a controlled environment with someone with whom they are at ease and can communicate. Gradually, another person is introduced into the situation. One example of stimulus fading is the sliding-in technique, where a new person is slowly brought into the talking group. This can take a long time for the first one or two faded-in people but may become faster as the patient gets more comfortable with the technique. As an example, a child may be playing a board game with a family member in a classroom at school. Gradually, the teacher is brought in to play as well. When the child adjusts to the teachers presence, then a peer is brought in to be a part of the game. Each person is only brought in if the child continues to engage verbally and positively. Desensitization The subject communicates indirectly with a person to whom they are afraid to speak through such means as email, instant messaging (text, audio or video), online chat, voice or video recordings, and speaking or whispering to an intermediary in the presence of the target person. This can make the subject more comfortable with the idea of communicating with this person. Shaping The subject is slowly encouraged to speak. The subject is reinforced first for interacting nonverbally, then for saying certain sounds (such as the sound that each letter of the alphabet makes) rather than words, then for whispering, and finally saying a word or more. Spacing Spacing is important to integrate, especially with self-modeling. Repeated and spaced out use of interventions is shown to be the most helpful long-term for learning. Viewing videotapes of self-modeling should be shown over a spaced out period of time of approximately 6 weeks. Drug treatments Some practitioners believe there would be evidence indicating anxiolytics to be helpful in treating children and adults with selective mutism, to decrease anxiety levels and thereby speed the process of therapy. Use of medication may end after nine to twelve months, once the person has learned skills to cope with anxiety and has become more comfortable in social situations. Medication is more often used for older children, teenagers, and adults whose anxiety has led to depression and other problems. Medication, when used, should never be considered the entire treatment for a person with selective mutism. However, the reason why medication needs to be considered as a treatment at all is because selective mutism is still prevalent, despite psychosocial efforts. But while on medication, the person should still be in therapy to help them learn how to handle anxiety and prepare them for life without medication, as medication is typically a short-term solution.Since selective mutism is categorized as an anxiety disorder, using similar medication to treat either makes sense. Antidepressants have been used in addition to self-modeling and mystery motivation to aid in the learning process. Furthermore, SSRIs in particular have been used to treat selective mutism. In a systematic review, ten studies were looked at which involved SSRI medications, and all reported medication was well tolerated. In one of them, Black and Uhde (1994) conducted a double-blind, placebo-controlled study investigating the effects of fluoxetine. By parent report, fluoxetine-treated children showed significantly greater improvement than placebo-treated children. In another, Dummit III et al. (1996) administered fluoxetine to 21 children for nine weeks and found that 76% of the children had reduced or no symptoms by the end of the experiment. This indicates that fluoxetine is an SSRI that is indeed helpful in treating selective mutism. History In 1877, German physician Adolph Kussmaul described children who were able to speak normally but often refused to as having a disorder he named aphasia voluntaria. Although this is now an obsolete term, it was part of an early effort to describe the concept now called selective mutism. In 1980, a study by Torey Hayden identified what she called four "subtypes" of elective mutism (as it was called then), although this set of subtypes is not in current diagnostic use. These subtypes are no longer recognized, though "speech phobia" is sometimes used to describe a selectively mute person who appears not to have any symptoms of social anxiety. The Diagnostic and Statistical Manual of Mental Disorders (DSM), first published in 1952, first included selective mutism in its third edition, published in 1980. Selective mutism was described as "a continuous refusal to speak in almost all social situations" despite normal ability to speak. While "excessive shyness" and other anxiety-related traits were listed as associated features, predisposing factors included "maternal overprotection", "mental retardation", and trauma. Elective mutism in the third edition revised (DSM III-R) is described similarly to the third edition except for specifying that the disorder is not related to social phobia. In 1994, Sue Newman, co-founder of the Selective Mutism Foundation, requested that the fourth edition of the DSM reflect the name change from elective mutism to selective mutism and describe the disorder as a failure to speak. The relation to anxiety disorders was emphasized, particularly in the revised version (DSM IV-TR). As part of the reorganization of the DSM categories, the DSM-5 moved selective mutism from the section "Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence" to the section for anxiety disorders. See also June and Jennifer Gibbons, the Silent Twins Citations == Further reading ==

Hi Aarogya , Do you know what is Sickle cell trait,

Sickle cell trait

Sickle cell trait describes a condition in which a person has one abnormal allele of the hemoglobin beta gene (is heterozygous), but does not display the severe symptoms of sickle cell disease that occur in a person who has two copies of that allele (is homozygous). Those who are heterozygous for the sickle cell allele produce both normal and abnormal hemoglobin (the two alleles are codominant with respect to the actual concentration of hemoglobin in the circulating cells). Sickle cell disease is a blood disorder wherein there is a single amino acid substitution in the hemoglobin protein of the red blood cells, which causes these cells to assume a sickle shape, especially when under low oxygen tension. Sickling and sickle cell disease also confer some resistance to malaria parasitization of red blood cells, so that individuals with sickle-cell trait (heterozygotes) have a selective advantage in environments where malaria is present. Symptoms and signs Sickle cell trait is a hemoglobin genotype AS and is generally regarded as a benign condition. However, individuals with sickle cell trait may have rare complications. For example, in November 2010, Dr. Jeffery K. Taubenberger of the National Institutes of Health discovered the earliest proof of sickle-cell disease while looking for the virus of the 1918 flu during the autopsy of an African-American soldier. Taubenbergers autopsy results showed that the soldier had had a sickle-cell crisis that contributed to his death even though he had only one copy of the gene. There have been calls to reclassify sickle cell trait as a disease state, based on its malignant clinical presentations. Significance may be greater during exercise. Association with other medical conditions Malaria The sickle cell trait provides a survival advantage against malaria fatality over people with normal hemoglobin in regions where malaria is endemic. The trait is known to cause significantly fewer deaths due to malaria, especially when Plasmodium falciparum is the causative organism. This is a prime example of natural selection, evidenced by the fact that the geographical distribution of the gene for hemoglobin S and the distribution of malaria in Africa virtually overlap. Because of the unique survival advantage, people with the trait become increasingly numerous as the number of malaria-infected people increases. Conversely, people who have normal hemoglobin tend to succumb to the complications of malaria.The way in which sickle cell protects against malaria is attributed to several different things. One of the more common explanations is that the sickle hemoglobin inhibits the plasmodium parasite from infecting the red blood cells which reduces the number of malaria parasites to infect the host. Another factor is the production of heme oxygenase-1 (HO-1) enzyme, which is highly present in the sickle hemoglobin. This enzyme produces carbon monoxide which has been proven to protect against cerebral malaria. Established associations Hematuria Hyposthenuria Renal medullary carcinoma, a cancer affecting the kidney, is a very rare complication seen in patients with sickle cell trait. Renal papillary necrosis (only considered "possible" by some sources) Splenic infarcts at high altitude. Surgery may not always be necessary. Sudden deaths during physical exertion in African-American US army recruits, and athletes Urinary tract infection Suggested Probable: complicated hyphema, venous thromboembolic events, fetal loss, neonatal deaths, and preeclampsia Possible: acute chest syndrome, asymptomatic bacteriuria, and anemia in pregnancy Insufficient evidence: retinopathy, cholelithiasis, priapism, leg ulcers, liver necrosis, avascular necrosis of the femoral head, and stroke. An association with complicated migraines has been suggested.There have been reports of pulmonary venous thromboembolism in pregnant women with sickle cell trait, or men during prolonged airflight, and mild strokes and abnormalities on PET scans in children with the trait.Sickle cell trait appears to worsen the complications seen in diabetes mellitus type 2 (retinopathy, nephropathy and proteinuria) and provoke hyperosmolar diabetic coma nephropathy, especially in male patients. Genetics Normally, a person inherits two copies of the gene that produces beta-globin, a protein needed to produce normal hemoglobin (hemoglobin A, genotype AA). A person with sickle cell trait inherits one normal allele and one abnormal allele encoding hemoglobin S (hemoglobin genotype AS).The sickle cell trait can be used to demonstrate the concepts of co-dominance and incomplete dominance. An individual with the sickle cell trait shows incomplete dominance when the shape of the red blood cell is considered. This is because the sickling happens only at low oxygen concentrations. With regards to the actual concentration of hemoglobin in the circulating cells, the alleles demonstrate co-dominance as both normal and mutant forms co-exist in the bloodstream. Thus it is an ambiguous condition showing both incomplete dominance and co-dominance.Unlike the sickle-cell trait, sickle-cell disease is passed on in a recessive manner. Sickle cell anemia affects about 72,000 people in the United States. Most Americans who have sickle cell anemia are of African descent. The disease also affects Americans from the Caribbean, Central America, and parts of South America, Turkey, Greece, Italy, the Middle East and East India. Sickle-cell disease and the associated trait are most prevalent in Africa and Central America, which is attributed to natural selection: the sickle-cell trait confers a survival advantage in areas with a high occurrence of malaria, which has a high death rate among individuals without the trait.There also have been studies that show changes in the globin genes. There have been noted changes in the beta-globin sequence, to what is known as the sickle hemoglobin. The significance of the sickle-cell trait is that it does not show any symptoms, nor does it cause any major difference in blood cell count. The trait confers about 30% protection against malaria and its occurrence appears to have risen tremendously in Africa, India and the Middle East. Some findings also show the reduction of the sickle-cell trait in those who retain much more fetal hemoglobin than usual in adulthood. Fetal hemoglobin likely plays a role in the prevention of sickling. Elevated fetal hemoglobin levels have been observed in populations where sickle-cell disease is prevalent. Whole genome sequence analysis has identified a single origin of the sickle trait, with one haplotype ancestral to all sickle-cell variants. This haplotype is thought to have originated in the Sahara during the Holocene Wet Phase around 7,300 years ago. Sickle cell variants descended from this ancestral haplotype comprise five haplotypes named after toponyms or ethnolinguistic groups (the Arabian/Indian, Benin, Cameroon, Central African Republic/Bantu, and Senegal variants), and another designation earmarked for atypical sickle-cell haplotypes. Their clinical importance is because some are associated with higher HbF levels (e.g., Senegal and Saudi-Asian variants tend to have milder disease). In athletes In some cases, athletes with sickle cell trait do not achieve the same level of performance as elite athletes with normal hemoglobin (AA). Athletes with sickle cell trait and their instructors must be aware of the dangers of the condition during anaerobic exertion especially in hot and dehydrated conditions. In rare cases, exercise-induced dehydration or exhaustion may cause healthy red blood cells to turn sickle-shaped, which can cause death during sporting activities.While more research is necessary on the topic, the correlation found between individuals with sickle cell trait and an increased risk of sudden death appears to be related to microcirculatory disorders, during exercise. In recent years the NCAA has partnered with the ACSM and issued a joint statement, warning athletes about both the prevalence and the potential risk factors of sickle cell trait. The NCAA has also recently encouraged athletes to become aware of their sickle cell trait status, as the trait itself does not typically result in symptoms under normal conditions but can become dangerous during extreme physical activity similar to the daily training that athletes undergo.Normal hemoglobin (and hemoglobin S in the presence of oxygen) contains a deformability characteristic that allows erythrocytes to essentially squeeze their way into smaller vessels, including those involved in microcirculation to the capillaries within muscle tissue as well as blood supply embedded within organ tissues. When hemoglobin S is deprived of oxygen, it can polymerize, which is what is proposed to cause the "sickled" cells. The sickled erythrocytes present a decreased deformability when compared to normal erythrocytes, leading to distress in circulation into the smaller vessels involved in microcirculation, particularly, in this case, the capillaries embedded in muscle tissue.The resulting microvasculatory distress in capillaries specific to muscle tissue can cause acute rhabdomyolysis and necrosis within the muscle cells. The inflammation and leakage of intracellular material resulting from muscle cell necrosis releases a particular protein, myoglobin, into the blood stream. While necessary in muscle tissue to bind iron and oxygen, myoglobin circulating through the bloodstream can break down into smaller compounds that damage kidney cells, leading to various complications, such as those seen in sickle cell trait athletes during high levels of physical exertion.Because of the link between deformability and sickled cells, deformability can be used to evaluate the amount of sickled cells in the blood. Deformability of the erythrocytes that cause the microcirculatory distress can be demonstrated through various other hemorheological characteristics. In order to determine the deformability of erythrocytes multiple factors including blood and plasma viscosity and hematocrit (a calculation of the percent of red blood cells present in the blood) are measured. Alpha-thalassemia Alpha-thalassemia, like sickle cell trait, is typically inherited in areas with increased exposure to malaria. It manifests itself as a decreased expression of alpha-globin chains, causing an imbalance and excess of beta-globin chains, and can occasionally result in anemic symptoms. The abnormal hemoglobin can cause the body to destroy red blood cells, essentially causing anemia.In endurance-trained individuals with sickle cell trait the presence of alpha-thalassemia has been shown to act protectively against microvasculatory distress before, during, and after exercise. Signs, symptoms, and prevention Because of the microcirculatory distress, a telltale sign or symptom of a potential sickling collapse is cramping. Specifically to sickle cell trait, cramping occurs in the lower extremities and back in athletes undergoing intense physical activity or exertion. In comparison to heat cramps, sickling cramps are less intense in terms of pain and have a weakness and fatigue associated with them, as opposed to tightly contracted muscles that lock up during heat cramps.A sickling collapse comes on slowly, following cramps, weakness, general body aches and fatigue. Individuals with known positive sickle cell trait status experiencing significant muscle weakness or fatigue during exercise should take extra time to recover and hydrate before returning to activity in order to prevent further symptoms.A collapse can be prevented by taking steps to ensure sufficient oxygen levels in the blood. Among these preventative measures are proper hydration and gradual acclimation to conditions such as heat, humidity, and decreased air pressure due to higher altitude. Gradual progression of exertion levels also helps athletes bodies adjust and compensate, gaining fitness slowly over the course of several weeks. See also Ryan Clark (American football) References == External links ==

What does Mydriasis mean Aarogya

Mydriasis

Mydriasis is the dilation of the pupil, usually having a non-physiological cause, or sometimes a physiological pupillary response. Non-physiological causes of mydriasis include disease, trauma, or the use of certain types of drugs. Normally, as part of the pupillary light reflex, the pupil dilates in the dark and constricts in the light to respectively improve vividity at night and to protect the retina from sunlight damage during the day. A mydriatic pupil will remain excessively large even in a bright environment. The excitation of the radial fibres of the iris which increases the pupillary aperture is referred to as a mydriasis. More generally, mydriasis also refers to the natural dilation of pupils, for instance in low light conditions or under sympathetic stimulation. Fixed, unilateral mydriasis could be a symptom of raised intracranial pressure. The opposite, constriction of the pupil, is referred to as miosis. Both mydriasis and miosis can be physiological. Anisocoria is the condition of one pupil being more dilated than the other. Causes There are two types of muscle that control the size of the iris: the iris sphincter, composed of circularly arranged muscle fibers, and the iris dilator, composed of radially arranged muscle fibers. The sphincter is controlled by nerves of the parasympathetic nervous system, and the dilator by the sympathetic nervous system. Sympathetic stimulation of the adrenergic receptors causes the contraction of the radial muscle and subsequent dilation of the pupil. Conversely, parasympathetic stimulation causes contraction of the circular muscle and constriction of the pupil. The mechanism of mydriasis depends on the agent being used. It usually involves either a disruption of the parasympathetic nerve supply to the eye (which normally constricts the pupil) or overactivity of the sympathetic nervous system (SNS). Pupil diameter also increases in reaction to cognitive tasks requiring memory and attention, and this phenomenon is used as an indicator of mental activation (‘arousal’) in psychophysiological experiments. Drugs A mydriatic is an agent that induces dilation of the pupil. Drugs such as tropicamide are used in medicine to permit examination of the retina and other deep structures of the eye, and also to reduce painful ciliary muscle spasm (see cycloplegia). One effect of administration of a mydriatic is intolerance to bright light (photophobia). Purposefully-induced mydriasis via mydriatics is also used as a diagnostic test for Horners syndrome. Mydriasis can be induced via modulation of adrenergic or cholinergic signalling. Drugs that can cause mydriasis include: Stimulants (typically monoaminergics) such as amphetamines, cocaine, MDMA, and mephedrone. Anticholinergics such as diphenhydramine, atropine, hyoscyamine, and scopolamine antagonize the muscarinic acetylcholine receptors in the eye. Blocking acetylcholine receptors reduces the pupillary muscles ability to constrict and causes dilation (which is critical in eye surgery procedures such as cataract surgery which require uninterrupted access to the inner eye via the pupillary aperture, thus requiring that the eye be both paralyzed and anesthetized before the procedure can go ahead). The antimuscarinic, tropicamide, may be used as a mydriastic agent during surgery. Serotonergics such as LSD, psilocybin mushrooms, mescaline and 2C-B. These drugs are typically hallucinogens. Similarly, selective serotonin reuptake inhibitors can cause mydriasis. Dissociatives such as dextromethorphan (an SSRI and sigma-1 agonist). Certain GABAergic drugs, such as phenibut and GHB. Adrenergic agonists, such as phenylephrine and cyclomydril. Adrenergic agonists may be used if strong mydriasis is needed in surgery. Norepinephrine is a hormone and neurotransmitter that regulates the involuntary muscles of the autonomic nervous system, including dilation of the pupil aperture via the muscles of the iris. Hence adrenergic agonists mimic the activity of norepinephrine, which is how they induce mydriasis.Natural release of the hormone oxytocin can cause mild to moderate mydriasis.Long term effects of drugs can also cause mydriasis, for example opioid withdrawal. Autonomic neuropathy Parasympathetic fibers travel with cranial nerve III, the oculomotor nerve, to innervate the circular layer of muscle of the eye (sphincter pupillae). Damage to this nerve typically manifests itself as mydriasis, because the sympathetic supply to the pupil, which causes mydriasis, remains unaffected, and therefore unopposed. Multiple central nervous system disorders e.g. epilepsy, stroke, and impending brain herniation are known to lead to temporal mydriasis as well. A brain catastrophe, or a rapidly increasing brain mass, can cause compression of the oculomotor nerve. Trauma In cases of head injury or orbit trauma (eye injury), the iris sphincter (the muscle responsible for closing the pupil) or the nerves controlling it can be damaged, reducing or eliminating the normal pupillary light reflex. References == External links ==

Could you describe Hurler–Scheie syndrome, to me Aarogya

Hurler–Scheie syndrome

Hurler–Scheie syndrome is a genetic disorder caused by the buildup of glycosaminoglycans (GAGs) in various organ tissues. It is a cutaneous condition, also characterized by mild mental retardation and corneal clouding. Respiratory problems, sleep apnea, and heart disease may develop in adolescence.Hurler–Scheie syndrome is classified as a lysosomal storage disease. Patients with Hurler–Scheie syndrome lack the ability to break down GAGs in their lysosomes due a deficiency of the enzyme iduronidase. All forms of mucopolysaccharidosis type I (MPS I) are a spectrum of the same disease. Hurler-Sheie is the subtype of MPS I with intermediate severity. Hurler syndrome is the most severe form, while Scheie syndrome is the least severe form. Some clinicians consider the differences between Hurler, Hurler-Scheie, and Scheie syndromes to be arbitrary. Instead, they classify these patients as having "severe", "intermediate", or "attenuated" MPS I. See also Mucopolysaccharidosis References == External links ==

Hey Aarogya, could you help me understand about Rabies

Rabies

Rabies is a viral disease that causes encephalitis in humans and other mammals. Early symptoms can include fever and tingling at the site of exposure. These symptoms are followed by one or more of the following symptoms: nausea, vomiting, violent movements, uncontrolled excitement, fear of water, an inability to move parts of the body, confusion, and loss of consciousness. Once symptoms appear, the result is virtually always death, regardless of treatment. The time period between contracting the disease and the start of symptoms is usually one to three months but can vary from less than one week to more than one year. The time depends on the distance the virus must travel along peripheral nerves to reach the central nervous system.Rabies is caused by lyssaviruses, including the rabies virus and Australian bat lyssavirus. It is spread when an infected animal bites or scratches a human or other animals. Saliva from an infected animal can also transmit rabies if the saliva comes into contact with the eyes, mouth, or nose. Globally, dogs are the most common animal involved. In countries where dogs commonly have the disease, more than 99% of rabies cases are the direct result of dog bites. In the Americas, bat bites are the most common source of rabies infections in humans, and less than 5% of cases are from dogs. Rodents are very rarely infected with rabies. The disease can be diagnosed only after the start of symptoms.Animal control and vaccination programs have decreased the risk of rabies from dogs in a number of regions of the world. Immunizing people before they are exposed is recommended for those at high risk, including those who work with bats or who spend prolonged periods in areas of the world where rabies is common. In people who have been exposed to rabies, the rabies vaccine and sometimes rabies immunoglobulin are effective in preventing the disease if the person receives the treatment before the start of rabies symptoms. Washing bites and scratches for 15 minutes with soap and water, povidone-iodine, or detergent may reduce the number of viral particles and may be somewhat effective at preventing transmission. As of 2016, only fourteen people were documented to have survived a rabies infection after showing symptoms. However, research conducted in 2010 among a population of people in Perú with a self-reported history of one or more bites from vampire bats (commonly infected with rabies), found that out of 73 individuals reporting previous bat bites, 7 people had rabies virus-neutralizing antibodies (rVNA). Since only one member of this group reported prior vaccination for rabies, the findings of the research suggest previously undocumented cases of infection and viral replication followed by an abortive infection. This could indicate that in rare cases people may have an exposure to the virus without treatment and develop natural antibodies as a result. Rabies causes about 59,000 deaths worldwide per year, about 40% of which are in children under the age of 15. More than 95% of human deaths from rabies occur in Africa and Asia.Rabies is present in more than 150 countries and on all continents but Antarctica. More than 3 billion people live in regions of the world where rabies occurs. A number of countries, including Australia and Japan, as well as much of Western Europe, do not have rabies among dogs. Many Pacific islands do not have rabies at all. It is classified as a neglected tropical disease. Etymology The name rabies is derived from the Latin rabies, "madness". This, in turn, may be related to the Sanskrit rabhas, "to rage". The Greeks derived the word lyssa, from lud or "violent"; this root is used in the genus name of the rabies virus, Lyssavirus. Signs and symptoms The period between infection and the first symptoms (incubation period) is typically 1–3 months in humans. This period may be as short as four days or longer than six years, depending on the location and severity of the wound and the amount of virus introduced. Initial symptoms of rabies are often nonspecific such as fever and headache. As rabies progresses and causes inflammation of the brain and meninges, symptoms can include slight or partial paralysis, anxiety, insomnia, confusion, agitation, abnormal behavior, paranoia, terror, and hallucinations. The person may also have fear of water.The symptoms eventually progress to delirium, and coma. Death usually occurs 2 to 10 days after first symptoms. Survival is almost unknown once symptoms have presented, even with intensive care.Rabies has also occasionally been referred to as hydrophobia ("fear of water") throughout its history. It refers to a set of symptoms in the later stages of an infection in which the person has difficulty swallowing, shows panic when presented with liquids to drink, and cannot quench their thirst. Any mammal infected with the virus may demonstrate hydrophobia. Saliva production is greatly increased, and attempts to drink, or even the intention or suggestion of drinking, may cause excruciatingly painful spasms of the muscles in the throat and larynx. Since the infected individual cannot swallow saliva and water, the virus has a much higher chance of being transmitted, because it multiplies and accumulates in the salivary glands and is transmitted through biting. Hydrophobia is commonly associated with furious rabies, which affects 80% of rabies-infected people. The remaining 20% may experience a paralytic form of rabies that is marked by muscle weakness, loss of sensation, and paralysis; this form of rabies does not usually cause fear of water. Cause Rabies is caused by a number of lyssaviruses including the rabies virus and Australian bat lyssavirus. Duvenhage lyssavirus may cause a rabies-like infection.The rabies virus is the type species of the Lyssavirus genus, in the family Rhabdoviridae, order Mononegavirales. Lyssavirions have helical symmetry, with a length of about 180 nm and a cross-section of about 75 nm. These virions are enveloped and have a single-stranded RNA genome with negative sense. The genetic information is packed as a ribonucleoprotein complex in which RNA is tightly bound by the viral nucleoprotein. The RNA genome of the virus encodes five genes whose order is highly conserved: nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G), and the viral RNA polymerase (L).To enter cells, trimeric spikes on the exterior of the membrane of the virus interact with a specific cell receptor, the most likely one being the acetylcholine receptor. The cellular membrane pinches in a procession known as pinocytosis and allows entry of the virus into the cell by way of an endosome. The virus then uses the acidic environment, which is necessary, of that endosome and binds to its membrane simultaneously, releasing its five proteins and single-strand RNA into the cytoplasm.Once within a muscle or nerve cell, the virus undergoes replication. The L protein then transcribes five mRNA strands and a positive strand of RNA all from the original negative strand RNA using free nucleotides in the cytoplasm. These five mRNA strands are then translated into their corresponding proteins (P, L, N, G and M proteins) at free ribosomes in the cytoplasm. Some proteins require post-translative modifications. For example, the G protein travels through the rough endoplasmic reticulum, where it undergoes further folding, and is then transported to the Golgi apparatus, where a sugar group is added to it (glycosylation).When there are enough viral proteins, the viral polymerase will begin to synthesize new negative strands of RNA from the template of the positive-strand RNA. These negative strands will then form complexes with the N, P, L and M proteins and then travel to the inner membrane of the cell, where a G protein has embedded itself in the membrane. The G protein then coils around the N-P-L-M complex of proteins taking some of the host cell membrane with it, which will form the new outer envelope of the virus particle. The virus then buds from the cell.From the point of entry, the virus is neurotropic, traveling along the neural pathways into the central nervous system. The virus usually first infects muscle cells close to the site of infection, where they are able to replicate without being noticed by the hosts immune system. Once enough virus has been replicated, they begin to bind to acetylcholine receptors at the neuromuscular junction. The virus then travels through the nerve cell axon via retrograde transport, as its P protein interacts with dynein, a protein present in the cytoplasm of nerve cells. Once the virus reaches the cell body it travels rapidly to the central nervous system (CNS), replicating in motor neurons and eventually reaching the brain. After the brain is infected, the virus travels centrifugally to the peripheral and autonomic nervous systems, eventually migrating to the salivary glands, where it is ready to be transmitted to the next host.: 317 Transmission All warm-blooded species, including humans, may become infected with the rabies virus and develop symptoms. Birds were first artificially infected with rabies in 1884; however, infected birds are largely, if not wholly, asymptomatic, and recover. Other bird species have been known to develop rabies antibodies, a sign of infection, after feeding on rabies-infected mammals.The virus has also adapted to grow in cells of cold-blooded vertebrates. Most animals can be infected by the virus and can transmit the disease to humans. Worldwide, about 99% of human rabies cases come from domestic dogs. Other sources of rabies in humans include bats, monkeys, raccoons, foxes, skunks, cattle, wolves, coyotes, cats, and mongooses (normally either the small Asian mongoose or the yellow mongoose).Rabies may also spread through exposure to infected bears, domestic farm animals, groundhogs, weasels, and other wild carnivorans. However, lagomorphs, such as hares and rabbits, and small rodents, such as chipmunks, gerbils, guinea pigs, hamsters, mice, rats, and squirrels, are almost never found to be infected with rabies and are not known to transmit rabies to humans. Bites from mice, rats, or squirrels rarely require rabies prevention because these rodents are typically killed by any encounter with a larger, rabid animal, and would, therefore, not be carriers. The Virginia opossum (a marsupial, unlike the other mammals named in this paragraph, which are all eutherians/placental), has a lower internal body temperature than the rabies virus prefers and therefore is resistant but not immune to rabies. Marsupials, along with monotremes (platypuses and echidnas), typically have lower body temperatures than similarly sized eutherians.The virus is usually present in the nerves and saliva of a symptomatic rabid animal. The route of infection is usually, but not always, by a bite. In many cases, the infected animal is exceptionally aggressive, may attack without provocation, and exhibits otherwise uncharacteristic behavior. This is an example of a viral pathogen modifying the behavior of its host to facilitate its transmission to other hosts. After a typical human infection by bite, the virus enters the peripheral nervous system. It then travels retrograde along the efferent nerves toward the central nervous system. During this phase, the virus cannot be easily detected within the host, and vaccination may still confer cell-mediated immunity to prevent symptomatic rabies. When the virus reaches the brain, it rapidly causes encephalitis, the prodromal phase, which is the beginning of the symptoms. Once the patient becomes symptomatic, treatment is almost never effective and mortality is over 99%. Rabies may also inflame the spinal cord, producing transverse myelitis.Although it is theoretically possible for rabies-infected humans to transmit it to others by biting or otherwise, no such cases have ever been documented, because infected humans are usually hospitalized and necessary precautions taken. Casual contact, such as touching a person with rabies or contact with non-infectious fluid or tissue (urine, blood, feces), does not constitute an exposure and does not require post-exposure prophylaxis. But as the virus is present in sperm and vaginal secretions, it might be possible for rabies to spread through sex. There are only a handful of recorded cases of human-to-human transmission of rabies, and all occurred through organ transplants from infected donors. Diagnosis Rabies can be difficult to diagnose because, in the early stages, it is easily confused with other diseases or even with a simple aggressive temperament. The reference method for diagnosing rabies is the fluorescent antibody test (FAT), an immunohistochemistry procedure, which is recommended by the World Health Organization (WHO). The FAT relies on the ability of a detector molecule (usually fluorescein isothiocyanate) coupled with a rabies-specific antibody, forming a conjugate, to bind to and allow the visualisation of rabies antigen using fluorescent microscopy techniques. Microscopic analysis of samples is the only direct method that allows for the identification of rabies virus-specific antigen in a short time and at a reduced cost, irrespective of geographical origin and status of the host. It has to be regarded as the first step in diagnostic procedures for all laboratories. Autolysed samples can, however, reduce the sensitivity and specificity of the FAT. The RT PCR assays proved to be a sensitive and specific tool for routine diagnostic purposes, particularly in decomposed samples or archival specimens. The diagnosis can be reliably made from brain samples taken after death. The diagnosis can also be made from saliva, urine, and cerebrospinal fluid samples, but this is not as sensitive or reliable as brain samples. Cerebral inclusion bodies called Negri bodies are 100% diagnostic for rabies infection but are found in only about 80% of cases. If possible, the animal from which the bite was received should also be examined for rabies.Some light microscopy techniques may also be used to diagnose rabies at a tenth of the cost of traditional fluorescence microscopy techniques, allowing identification of the disease in less-developed countries. A test for rabies, known as LN34, is easier to run on a dead animals brain and might help determine who does and does not need post-exposure prevention. The test was developed by the CDC in 2018.The differential diagnosis in a case of suspected human rabies may initially include any cause of encephalitis, in particular infection with viruses such as herpesviruses, enteroviruses, and arboviruses such as West Nile virus. The most important viruses to rule out are herpes simplex virus type one, varicella zoster virus, and (less commonly) enteroviruses, including coxsackieviruses, echoviruses, polioviruses, and human enteroviruses 68 to 71.New causes of viral encephalitis are also possible, as was evidenced by the 1999 outbreak in Malaysia of 300 cases of encephalitis with a mortality rate of 40% caused by Nipah virus, a newly recognized paramyxovirus. Likewise, well-known viruses may be introduced into new locales, as is illustrated by the outbreak of encephalitis due to West Nile virus in the eastern United States. Prevention Almost all human exposure to rabies was fatal until a vaccine was developed in 1885 by Louis Pasteur and Émile Roux. Their original vaccine was harvested from infected rabbits, from which the virus in the nerve tissue was weakened by allowing it to dry for five to ten days. Similar nerve tissue-derived vaccines are still used in some countries, as they are much cheaper than modern cell culture vaccines. The human diploid cell rabies vaccine was started in 1967. Less expensive purified chicken embryo cell vaccine and purified vero cell rabies vaccine are now available. A recombinant vaccine called V-RG has been used in Belgium, France, Germany, and the United States to prevent outbreaks of rabies in undomesticated animals. Immunization before exposure has been used in both human and nonhuman populations, where, as in many jurisdictions, domesticated animals are required to be vaccinated. The Missouri Department of Health and Senior Services Communicable Disease Surveillance 2007 Annual Report states the following can help reduce the risk of contracting rabies:Vaccinating dogs, cats, and ferrets against rabies Keeping pets under supervision Not handling wild animals or strays Contacting an animal control officer upon observing a wild animal or a stray, especially if the animal is acting strangely If bitten by an animal, washing the wound with soap and water for 10 to 15 minutes and contacting a healthcare provider to determine if post-exposure prophylaxis is required28 September is World Rabies Day, which promotes the information, prevention, and elimination of the disease.In Asia and in parts of the Americas and Africa, dogs remain the principal host. Mandatory vaccination of animals is less effective in rural areas. Especially in developing countries, pets may not be privately kept and their destruction may be unacceptable. Oral vaccines can be safely distributed in baits, a practice that has successfully reduced rabies in rural areas of Canada, France, and the United States. In Montreal, Quebec, Canada, baits are successfully used on raccoons in the Mount-Royal Park area. Vaccination campaigns may be expensive, but cost-benefit analysis suggests baits may be a cost-effective method of control. In Ontario, a dramatic drop in rabies was recorded when an aerial bait-vaccination campaign was launched.The number of recorded human deaths from rabies in the United States has dropped from 100 or more annually in the early 20th century to one or two per year due to widespread vaccination of domestic dogs and cats and the development of human vaccines and immunoglobulin treatments. Most deaths now result from bat bites, which may go unnoticed by the victim and hence untreated. Treatment After exposure Treatment after exposure can prevent the disease if given within 10 days. The rabies vaccine is 100% effective if given early, and still has a chance of success if delivery is delayed. Every year, more than 15 million people get vaccinated after potential exposure. While this works well, the cost is significant. In the US it is recommended people receive one dose of human rabies immunoglobulin (HRIG) and four doses of rabies vaccine over a 14-day period. HRIG is expensive and makes up most of the cost of post-exposure treatment, ranging as high as several thousand dollars. In the UK, one dose of HRIG costs the National Health Service £1,000, although this is not flagged as a "high-cost medication". A full course of vaccine costs £120–180. As much as possible of HRIG should be injected around the bites, with the remainder being given by deep intramuscular injection at a site distant from the vaccination site.People who have previously been vaccinated against rabies do not need to receive the immunoglobulin—only the postexposure vaccinations on days 0 and 3. The side effects of modern cell-based vaccines are similar to the side effects of flu shots. The old nerve-tissue-based vaccination required multiple injections into the abdomen with a large needle but is inexpensive. It is being phased out and replaced by affordable World Health Organization intradermal-vaccination regimens. In children less than a year old, the lateral thigh is recommended. Thoroughly washing the wound as soon as possible with soap and water for approximately five minutes is effective in reducing the number of viral particles. Povidone-iodine or alcohol is then recommended to reduce the virus further.Awakening to find a bat in the room, or finding a bat in the room of a previously unattended child or mentally disabled or intoxicated person, is an indication for post-exposure prophylaxis (PEP). The recommendation for the precautionary use of PEP in bat encounters where no contact is recognized has been questioned in the medical literature, based on a cost–benefit analysis. However, a 2002 study has supported the protocol of precautionary administration of PEP where a child or mentally compromised individual has been alone with a bat, especially in sleep areas, where a bite or exposure may occur with the victim being unaware. After onset At least two treatment schemes have been proposed for treating rabies after the onset of symptoms, the Milwaukee Protocol and the Recife Protocol. The Milwaukee Protocol was first used in 2004 on Jeanna Giese, who became the first person known to have survived rabies without preventive treatments before symptom onset. The protocol puts a person into a chemically induced coma and uses antiviral medications to prevent fatal dysautonomia. The overall protocol is complex; the sixth version of the protocol last updated in 2018 consists of 17 pages with 22 steps of treatment, detailed monitoring, and a timeline of expected complications. The Recife Protocol follows the same principle but differs in details like termination of sedation and supplementary medication. Prognosis Vaccination after exposure, PEP, is highly successful in preventing rabies. In unvaccinated humans, rabies is virtually always fatal after neurological symptoms have developed. Epidemiology In 2010, an estimated 26,000 people died from rabies, down from 54,000 in 1990. The majority of the deaths occurred in Asia and Africa. As of 2015, India, followed by China (approximately 6,000) and the Democratic Republic of the Congo (5,600), had the most cases. A 2015 collaboration between the World Health Organization, World Organization of Animal Health (OIE), Food and Agriculture Organization of the United Nation (FAO), and Global Alliance for Rabies Control has a goal of eliminating deaths from rabies by 2030. India India has the highest rate of human rabies in the world, primarily because of stray dogs, whose number has greatly increased since a 2001 law forbade the killing of dogs. Effective control and treatment of rabies in India is hindered by a form of mass hysteria known as puppy pregnancy syndrome (PPS). Dog bite victims with PPS, male as well as female, become convinced that puppies are growing inside them, and often seek help from faith healers rather than medical services. An estimated 20,000 people die every year from rabies in India, more than a third of the global total. Australia Australia has an official rabies-free status, although Australian bat lyssavirus (ABLV), discovered in 1996, is a strain of rabies prevalent in Australian native bat populations. United States Canine-specific rabies has been eradicated in the United States. But rabies is common among wild animals in the United States, and an average of 100 dogs become infected from other wildlife each year.Due to high public awareness of the virus, efforts at vaccination of domestic animals and curtailment of feral populations, and availability of postexposure prophylaxis, incidence of rabies in humans is very rare in the United States. From 1960 to 2018, a total of 125 human rabies cases were reported in the United States; 36 (28%) were attributed to dog bites during international travel. Among the 89 infections acquired in the United States, 62 (70%) were attributed to bats. The most recent rabies death in the United States was an Illinois man who refused treatment after waking up in the night with a bat on his neck; the man died a month later. Occurring in 2021, it was the first case of human rabies in the United States in nearly three years. Europe Either no or very few cases of rabies are reported each year in Europe; cases are contracted both during travel and in Europe.In Switzerland the disease was virtually eliminated after scientists placed chicken heads laced with live attenuated vaccine in the Swiss Alps. The foxes of Switzerland, proven to be the main source of rabies in the country, ate the chicken heads and immunized themselves.Italy, after being declared rabies-free from 1997 to 2008, has witnessed a reemergence of the disease in wild animals in the Triveneto regions (Trentino-Alto Adige/Südtirol, Veneto and Friuli-Venezia Giulia), due to the spreading of an epidemic in the Balkans that also affected Austria. An extensive wild animal vaccination campaign eliminated the virus from Italy again, and it regained the rabies-free country status in 2013, the last reported case of rabies being reported in a red fox in early 2011.The United Kingdom has been free of rabies since the early 20th century except for a rabies-like virus (EBLV-2) in a few Daubentons bats. There has been one fatal case of EBLV-2 transmission to a human. There have been four deaths from rabies, transmitted abroad by dog bites, since 2000. The last infection in the UK occurred in 1922, and the last death from indigenous rabies was in 1902.Sweden and mainland Norway have been free of rabies since 1886. Bat rabies antibodies (but not the virus) have been found in bats. On Svalbard, animals can cross the arctic ice from Greenland or Russia. Mexico Mexico was certified by the World Health Organization as being free of dog-transmitted rabies in 2019 because no case of dog-human transmission had been recorded in two years. History Rabies has been known since around 2000 BC. The first written record of rabies is in the Mesopotamian Codex of Eshnunna (c. 1930 BC), which dictates that the owner of a dog showing symptoms of rabies should take preventive measures against bites. If another person were bitten by a rabid dog and later died, the owner was heavily fined.In Ancient Greece, rabies was supposed to be caused by Lyssa, the spirit of mad rage.Ineffective folk remedies abounded in the medical literature of the ancient world. The physician Scribonius Largus prescribed a poultice of cloth and hyena skin; Antaeus recommended a preparation made from the skull of a hanged man.Rabies appears to have originated in the Old World, the first epizootic in the New World occurring in Boston in 1768.Rabies was considered a scourge for its prevalence in the 19th century. In France and Belgium, where Saint Hubert was venerated, the "St Huberts Key" was heated and applied to cauterize the wound. By an application of magical thinking, dogs were branded with the key in hopes of protecting them from rabies. It was not uncommon for a person bitten by a dog merely suspected of being rabid to commit suicide or to be killed by others.In ancient times the attachment of the tongue (the lingual frenulum, a mucous membrane) was cut and removed as this was where rabies was thought to originate. This practice ceased with the discovery of the actual cause of rabies. Louis Pasteurs 1885 nerve tissue vaccine was successful, and was progressively improved to reduce often severe side-effects.In modern times, the fear of rabies has not diminished, and the disease and its symptoms, particularly agitation, have served as an inspiration for several works of zombie or similarly themed fiction, often portraying rabies as having mutated into a stronger virus which fills humans with murderous rage or incurable illness, bringing about a devastating, widespread pandemic. Other animals Rabies is infectious to mammals; three stages of central nervous system infection are recognized. The first stage is a one- to three-day period characterized by behavioral changes and is known as the prodromal stage. The second is the excitative stage, which lasts three to four days. This stage is often known as "furious rabies" for the tendency of the affected animal to be hyper-reactive to external stimuli and bite at anything near. The third is the paralytic stage and is caused by damage to motor neurons. Incoordination is seen, owing to rear limb paralysis, and drooling and difficulty swallowing is caused by paralysis of facial and throat muscles. Death is usually caused by respiratory arrest. Research Biotechnological use The outer shell of the rabies virus, stripped of its RNA contents and thus unable to cause disease, may be used as a vector for the delivery of unrelated genetic material in a research setting. It has the advantage over other pseudotyping methods for gene delivery in that the cell targeting (tissue tropism) is more specific for the central nervous system, a difficult-to-reach site, obviating the need for invasive delivery methods. It is also capable of infecting neighboring "upstream" cells, moving from one cell to axons of the next at synapses, and is thus used for retrograde tracing in neuronal circuits. Potential treatment Evidence indicates artificially increasing the permeability of the blood–brain barrier, which normally does not allow most immune cells across, promotes viral clearance. See also Global Alliance for Rabies Control Rabies in Haiti Eradication of infectious diseases Madstone (folklore) References Further reading Pankhurst, Richard. "The history and traditional treatment of rabies in Ethiopia." Medical History 14, no. 4 (1970): 378-389. External links Rabies at Curlie "Rabies". Centers for Disease Control and Prevention. Retrieved 12 August 2012. Virus Pathogen Database and Analysis Resource (ViPR): Rhabdoviridae OIEs Rabies Portal Archived 13 August 2020 at the Wayback Machine Aerophobia and Hydrophobia in Rabies Videos "Rabies virus". NCBI Taxonomy Browser. 11292.

Aarogya, give me a short description about Anterograde amnesia

Anterograde amnesia

In neurology, anterograde amnesia is the inability to create new memories after the event that caused amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions of the brain involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions. Signs and symptoms People with anterograde amnesic syndromes may present with widely varying degrees of forgetfulness. Some with severe cases have a combined form of anterograde and retrograde amnesia, sometimes called global amnesia. In the case of drug-induced amnesia, it may be short-lived and patients can recover from it. In the other case, which has been studied extensively since the early 1970s, patients often have permanent damage, although some recovery is possible, depending on the nature of the pathophysiology. Usually, some capacity for learning remains, although it may be very elementary. In cases of pure anterograde amnesia, patients have recollections of events prior to the injury, but cannot recall day-to-day information or new facts presented to them after the injury occurred.In most cases of anterograde amnesia, patients lose declarative memory, or the recollection of facts, but they retain nondeclarative memory, often called procedural memory. For instance, they are able to remember and in some cases learn how to do things such as talking on the phone or riding a bicycle, but they may not remember what they had eaten earlier that day for lunch. One extensively studied anterograde amnesiac patient, codenamed H.M., demonstrated that despite his amnesia preventing him from learning new declarative information, procedural memory consolidation was still possible, albeit severely reduced in power. He, along with other patients with anterograde amnesia, were given the same maze to complete day after day. Despite having no memory of having completed the maze the day before, unconscious practice of completing the same maze over and over reduced the amount of time needed to complete it in subsequent trials. From these results, Corkin et al. concluded despite having no declarative memory (i.e. no conscious memory of completing the maze exists), the patients still had a working procedural memory (learning done unconsciously through practice). This supports the notion that declarative and procedural memory are consolidated in different areas of the brain. In addition, patients have a diminished ability to remember the temporal context in which objects were presented. Certain authors claim the deficit in temporal context memory is more significant than the deficit in semantic learning ability (described below). Causes This disorder is usually acquired in one of four ways: One cause is benzodiazepine drugs such as midazolam, flunitrazepam, lorazepam, temazepam, nitrazepam, triazolam, clonazepam, alprazolam, diazepam, and nimetazepam; all of these are known to have powerful amnesic effects. This has also been recorded in non-benzodiazepine sedatives or "z-drugs" which act on the same set of receptors; such as zolpidem (also known as Ambien), eszopiclone (also known as Lunesta), and zopiclone (also known by brand names Imovane and Zimovane). A second cause is a traumatic brain injury in which damage is usually done to the hippocampus or surrounding cortices. It may also be caused by a PTSD, a shocking event, or an emotional disorder.Illness, though much rarer, can also cause anterograde amnesia if it causes encephalitis, which is the inflammation of brain tissue. There are several types of encephalitis: one such is herpes simplex encephalitis (HSV), which, if left untreated, can lead to neurological deterioration. How HSV gains access to the brain is unknown; the virus shows a distinct predilection for certain parts of the brain. Initially, it is present in the limbic cortices; it may then spread to the adjacent frontal and temporal lobes. Damage to specific areas can result in reduced or eliminated ability to encode new explicit memories, giving rise to anterograde amnesia. Patients with anterograde amnesia may have episodic, semantic, or both types of explicit memory impaired for events after the trauma that caused the amnesia. This suggests that memory consolidation for different types of memory takes place in different regions of the brain. Despite this, current knowledge on human memory is still insufficient to "map out" the wiring of a human brain to discover which parts of which lobe are responsible for the various episodic and semantic knowledge within a persons memory. Amnesia is seen in patients who, for the reason of preventing another more serious disorder, have parts of their brains known to be involved in memory circuits removed, the most notable of which is known as the medial temporal lobe (MTL) memory system, described below. Patients with seizures originating in the MTL may have either side or both structures removed (there is one structure per hemisphere). In addition, patients with tumors who undergo surgery will often sustain damage to these structures, as is described in a case below. Damage to any part of this system, including the hippocampus and surrounding cortices, results in amnesic syndromes. This is why after a stroke people have a chance of developing cognitive deficits that result in anterograde amnesia, since strokes can involve the temporal lobe in the temporal cortex, and the temporal cortex houses the hippocampus. Finally, anterograde amnesia can be the first clinical sign that Alzheimers disease develops in within the brain. Although later the complications can be much more widespread and strongly impair cognitive processes, at the initial stage of Alzheimers the changes observed can be restricted to anterograde amnesia and a mild deficit in retaining newly learnt sequences. This is explained by the fact that the disease is initiated within the medial temporal lobe and first affacts the entorhinal cortex that directly sends and receives information from the hippocampal formation. Alcohol intoxication Anterograde amnesia can also be caused by alcohol intoxication, a phenomenon commonly known as a blackout. Studies show rapid rises in blood alcohol concentration over a short period of time severely impair or in some cases completely block the brains ability to transfer short-term memories created during the period of intoxication to long-term memory for storage and later retrieval. Such rapid rises are caused by drinking large amounts of alcohol in short periods of time, especially on an empty stomach, as the dilution of alcohol by food slows the absorption of alcohol. Alcohol-related anterograde amnesia is directly related to the rate of consumption of alcohol (and is often associated with binge drinking), and not just the total amount of alcohol consumed in a drinking episode. Test subjects have been found not to experience amnesia when drinking slowly, despite being heavily intoxicated by the end of the experiment. When alcohol is consumed at a rapid rate, the point at which most healthy peoples long-term memory creation starts to fail usually occurs at approximately 0.20% BAC, but can be reached as low as 0.14% BAC for infrequent drinkers. The exact duration of these blackout periods is hard to determine, because most people fall asleep before they end. Upon reaching sobriety, usually after waking, long-term memory creation is completely restored.Chronic alcoholism often leads to a thiamine (vitamin B1) deficiency in the brain, causing Korsakoffs syndrome, a neurological disorder which is generally preceded by an acute neurological condition known as Wernickes encephalopathy (WE). The memory impairment that is pathognomonic to Korsakoffs syndrome predominantly affects the declarative memory, leaving non-declarative memory that is often procedural in nature relatively intact. The disproportionate severity in anterograde episodic memory processes in contrast to other cognitive processes is what differentiates Korsakoff syndrome from other conditions such as alcohol-related dementia. Evidence for the preservation of certain memory processes in the presence of severe anterograde episodic memory serve as experimental paradigm to investigate the components of human memory. Pathophysiology The pathophysiology of anterograde amnesic syndromes varies with the extent of damage and the regions of the brain that were damaged. The most well-described regions indicated in this disorder are the medial temporal lobe (MTL), basal forebrain, and fornix. Beyond the details described below, the precise process of how we remember – on a micro scale – remains a mystery. Neuropsychologists and scientists are still not in total agreement over whether forgetting is due to faulty encoding, accelerated forgetting, or faulty retrieval, although a great deal of data seem to point to the encoding hypothesis. In addition, neuroscientists are also in disagreement about the length of time involved in memory consolidation. Though most researchers, including Hasselmo et al., have found the consolidation process is spread out over several hours before transitioning from a fragile to a more permanent state, others, including Brown et al., posit that memory consolidation can take months or even years in a drawn-out process of consolidation and reinforcement. Further research into the length of time of memory consolidation will shed more light on why anterograde amnesia sometimes affects some memories gained after the event(s) that caused the amnesia, but does not affect other such memories. Medial temporal lobe The MTL memory system includes the hippocampal formation (CA fields, dentate gyrus, subicular complex), perirhinal, entorhinal, and parahippocampal cortices. It is known to be important for the storage and processing of declarative memory, which allows for factual recall. It is also known to communicate with the neocortex in the establishment and maintenance of long-term memories, although its known functions are independent of long-term memory. Nondeclarative memory, on the other hand, which allows for the performance of different skills and habits, is not part of the MTL memory system. Most data point to a "division of labor" among the parts of this system, although this is still being debated and is described in detail below.In animal models, researchers have shown monkeys with damage to both the hippocampus and its adjacent cortical regions were more severely impaired in terms of anterograde amnesia than monkeys with damage localized to hippocampal structures. However, conflicting data in another primate study point to the observation that the amount of tissue damaged does not necessarily correlate with the severity of the memory loss. Furthermore, the data do not explain the dichotomy that exists in the MTL memory system between episodic memory and semantic memory (described below).An important finding in amnesic patients with MTL damage is the impairment of memory in all sensory modalities – sound, touch, smell, taste, and sight. This reflects the fact that the MTL is a processor for all of the sensory modalities, and helps store these kind of thoughts into memory. In addition, subjects can often remember how to perform relatively simple tasks immediately (on the order of 10 seconds), but when the task becomes more difficult, even on the same time scale, subjects tend to forget. This demonstrates the difficulty of separating procedural memory tasks from declarative memory; some elements of declarative memory may be used in learning procedural tasks.MTL amnesic patients with localized damage to the hippocampus retain other perceptual abilities, such as the ability to intelligently function in society, to make conversation, to make ones bed, etc. Additionally, anterograde amnesics without combined retrograde disorders (localized damage to the MTL system) have memories prior to the traumatic event. For this reason, the MTL is not the storage place of all memories; other regions in the brain also store memories. The key is the MTL is responsible for the learning of new materials. Other memory systems A limited number of cases have been described in which patients with damage to other parts of the brain acquired anterograde amnesia. Easton and Parker observed damage to either the hippocampus or the surrounding cortices does not seem to result in severe amnesia in primate models. They suggested damage to the hippocampus and surrounding structures alone does not explain the amnesia they saw in patients, or increasing damage does not correlate with the degree of impairment. Furthermore, the data do not explain the dichotomy that exists in the MTL memory system between episodic and semantic memory. To demonstrate their hypothesis, they used a primate model with damage to the basal forebrain. They proposed that the disruption of neurons that project from the basal forebrain to the MTL are responsible for some of the impairment in anterograde amnesia. Easton and Parker also reported MRI scans of patients with severe anterograde amnesia showed damage beyond to cortical areas around the hippocampus and amygdala (a region of brain involved in emotions) and to surrounding white matter (white matter in the brain consists of axons, long projections of neuronal cell bodies). Another case described the onset of anterograde amnesia as a result of cell death in the fornix, another structure that carries information from the hippocampus to the structures of the limbic system and the diencephalon. The patient in this case did not show any disconnection syndrome, which is unexpected since the structures involved divide the brain hemispheres (both sides of her brain were able to communicate). Instead, she showed signs of amnesia. The final diagnosis was made by MRI. This particular amnesic syndrome is difficult to diagnose and often is misdiagnosed by physicians as an acute psychiatric disorder. Reorganization of memory When there is damage to just one side of the MTL, there is opportunity for normal functioning or near-normal function for memories. Neuroplasticity describes the ability of the cortex to remap when necessary. Remapping can occur in cases like the one above and with time the patient can recover and become more skilled at memory retention. A case report describing a patient who had two lobectomies – in the first, doctors removed part of her right MTL first because of seizures originating from the region, and later her left because she developed a tumor – demonstrates this. This case is unique because it is the only one in which both sides of the MTL were removed at different times. The authors observed that the patient was able to recover some ability to learn when she had only one MTL, but observed the deterioration of function when both sides of the MTL were affected. The reorganization of brain function for epileptic patients has had limited investigation, but imaging results show that it may occur. Rehabilitation Approaches used to treat those with anterograde amnesia often use interventions which focus on compensatory techniques, such as beepers, written notes, diaries or through intensive training programs involving the active participation of the individual concerned, along with their supporting network of family and friends. In this perspective, environmental adaptation techniques are used, such as the compensatory technique education to training (exercise), organizational strategies, visual imagery and verbal labeling. In addition, other techniques are also used in rehabilitation, such as implicit tasks, speech and mnemotechnic methods. So far, it has been proven that education techniques of compensatory strategies for memory disorders are effective in individuals with minor traumatic brain injuries. In moderately or severely injured individuals, effective interventions are those appealing to external aids, such as reminders in order to facilitate particular knowledge or skill acquisition. Reality orientation techniques are also considered; their purpose is to enhance orientation using stimulation and repetition of the basic orientation information. These techniques are regularly applied in populations of patients primarily presenting with dementia and head injuries. Controversies Episodic versus semantic memory As described above, patients with anterograde amnesia have a wide range of forgetfulness. Declarative memory can be further subdivided into episodic and semantic memory. Episodic memory is the recollection of autobiographical information with a temporal and/or spatial context, whereas semantic memory involves recall of factual information with no such association (language, history, geography, etc.). In a case study of a girl who developed anterograde amnesia during childhood, it was determined that the patient ("C.L.") retained semantic memory while having an extreme impairment of episodic memory.One patient, known by the codename "Gene", was involved in a motorcycle accident that damaged significant portions of his frontal and temporal lobes, including his left hippocampus. As a result, he cannot remember any specific episode in his life, such as a train derailment near his house. However, his semantic memory is intact; he remembers that he owns a car and two motorcycles, and he can even remember the names of his classmates in a school photograph. In stark contrast, a woman whose temporal lobes were damaged in the front due to encephalitis lost her semantic memory; she lost her memory of many simple words, historical events, and other trivial information categorized under semantic memory. However, her episodic memory was left intact; she can recall episodes such as her wedding and her fathers death with great detail. Vicari et al. describe that it remains unclear whether neural circuits involved in semantic and episodic memory overlap partially or completely, and this case seems to suggest that the two systems are independent. Both of the patients hippocampal and diencephalic structures on the right and left sides were disconnected. When C.L. came to Vicari et al.s office, her chief complaint was forgetfulness involving both semantic and episodic memory. After administering a battery of neuropsychological tests, Vicari determined that C.L. performed well in tests of visual naming and sentence comprehension, visual-spatial ability, and "general semantic knowledge about the world". They also noted an improved vocabulary and general knowledge base after 18 months. C.L.s episodic memory, on the other hand, was far below expectations: She could not retain daily events, where she had gone on vacation, the names of places she had been, and other such information. However, this study and others like it are susceptible to subjectivity, since it is not always possible to clearly distinguish between episodic and semantic memory. For this reason, the topic remains controversial and debated. Familiarity and the fractionation of memory The right hippocampus is clearly necessary for familiarity in spatial tasks, whereas the left hippocampus is necessary for familiarity-based recollection in verbal tasks. Some researchers claim the hippocampus is important for the retrieval of memories, whereas adjacent cortical regions can support familiarity-based memories. These memory decisions are made based on matching already-existing memories (before the onset of pathology) to the current situation. According to Gilboa et al., patients with localized hippocampal damage can score well on a test if it is based on familiarity.Poreh et al. describe a case study of patient A.D., whose damage to the fornix rendered the hippocampus useless, but spared adjacent cortical areas – a fairly rare injury. When the patient was given a test with something with which he had some familiarity, the patient was able to score well. In general, however, A.D. had severely impaired episodic memory, but had some ability to learn semantic knowledge. Other studies show animals with similar injuries can recognize objects with which they are familiar, but, when the objects are presented in an unexpected context, they do not score well on recognition tests. Islands of memory Patients with anterograde amnesia have trouble recalling new information and new autobiographical events, but the data are less consistent in regard to the latter. Medveds and Hirst recorded the presence of islands of memory – detailed accounts – that were described by such patients. The island memories were a combination of semantic and episodic memories. The researchers recorded patients giving long narratives with a fair amount of detail that resembled memories that the patients had prior to the trauma. The appearance of islands of memory could have something to do with the functioning of adjacent cortical areas and the neocortex. In addition, the researchers suspect that the amygdala played a role in the narratives. Notable cases The most famous case reported is that of patient Henry Molaison, known as H.M., in March 1953. Molaisons chief complaint was the persistence of severe seizures and therefore had a bilateral lobectomy (both of his medial temporal lobes were removed). As a result, Molaison had bilateral damage to both the hippocampal formation and the perirhinal cortex. Molaison had average intelligence and perceptual ability and a decent vocabulary. However, he could not learn new words or remember things that had happened more than a few minutes earlier. He could remember anything from his childhood. If the memory was created from before his lobectomy, he still had the ability to retrieve it and remember. However, he was able to learn some new skills. He was the first well-documented case of severe anterograde amnesia, and was studied until his death in 2008.A similar case involved Clive Wearing, an accomplished musicologist who contracted a cold sore virus that attacked his brain, causing herpes simplex encephalitis. As a result, Wearing developed both anterograde and retrograde amnesia, so he has little memory of what happened before the virus struck him in 1985, and cannot learn new declarative knowledge after the virus struck him either. As a result of anterograde amnesia, Wearing repeatedly "wakes up" every day usually in 30-second intervals. He has a history of repeatedly recording these moments of waking up in his journal (e.g., On Sept 2, 2013, I woke up, etc. etc.) and crossing out prior entries, as if the other moments of waking up were not real. His episodic memory is nonfunctional (so he does not consciously recall having woken up 30 seconds prior). Clive is often elated to see his wife, as if he has not seen her for a while. Despite this, however, Wearing maintained his ability to play the piano and conduct choirs. This case is significant because it demonstrates declarative and procedural memory are separate. Therefore, despite anterograde amnesia preventing Wearing from learning new bits of information that can be explained in words (declarative memory), and also preventing him from storing new memories of events or episodes (also part of declarative memory), he has little trouble in retaining his musical abilities (procedural memory), though he has no conscious memory of having learned music.Another case in the literature is Eugene Pauly, known as E.P., a severely amnesic patient (owing to viral encephalitis) who was able to learn three-word sentences. He performed better on consecutive tests over a 12-week period (24 study sessions). However, when asked how confident he was about the answers, his confidence did not appear to increase. Bayley and Squire proposed his learning was similar to the process required by procedural memory tasks; E.P. could not get the answers right when one word in the three-word sentence was changed or the order of words was changed, and his ability to answer correctly, thus, became more of a "habit". Bayley and Squire claim the learning may have happened in the neocortex, and it happened without the conscious knowledge of E.P. They hypothesized the information may be acquired directly by the neocortex (to which the hippocampus projects) when there is repetition. This case illustrates the difficulty in separating procedural from declarative tasks; this adds another dimension to the complexity of anterograde amnesia. In fiction Notable examples include Lucy Whitmore in 50 First Dates, Jonathan Archer in the Star Trek: Enterprise episode "Twilight", Joseph Gordon-Levitt in The Lookout, Kaori Fujimiya in One Week Friends, Chihiro Shindou in Ef: A Fairy Tale of the Two, Christine Lucas in Before I Go to Sleep, Gus in Remember Sunday. Christopher Nolans psychological crime film Memento (2000) contains a distinguished depiction of anterograde amnesia, in that the memory-impaired protagonist Leonard Shelby is trying to identify and kill the man who raped and murdered his wife, and does so through a system of writing crucial details related to the search on his body and on the blank spaces of Polaroid photographs. Mental health experts have described Memento as one of the most accurate depictions of amnesia in film history, an accuracy that was enhanced by the films fragmented, non-linear structure that mimics the protagonists memory problems.Dory, the happy-go-lucky Regal Blue Tang from Finding Nemo (2003) and Finding Dory (2016), suffers from anterograde amnesia. While Dory forgets conversations within minutes of having them, she never quite forgets who she is, or the fact that she has short-term memory loss, and can therefore explain her bizarre behavior to those around her.Ghajini (2008), a Hindi language film of India based on Memento, in which the main protagonist Sanjay Singhania played by Amir Khan has short-term memory loss, this variant of amnesia. In the film he is behind Ghajini, the killer of his fiancée Kalpana. In the TV series Perception, an episode revolved around a crime victim with this condition. The main character Latro in Gene Wolfes novels Soldier of the Mist, and the anime characters Vash the Stampede from Trigun and Index and Tōma from A Certain Magical Index had both retrograde and anterograde amnesia. The disorder has also been portrayed in music by English the Caretaker in Theoretically Pure Anterograde Amnesia (2005).In the 1965 film 36 Hours, Rod Taylor plays Nazi Major Walter Gerber, a psychiatrist who has developed an effective method for treating German soldiers with what is now known as PTSD – and for painlessly extracting information from Allied prisoners. The technique involves convincing patients that years have passed, the war is over, and that they have anterograde amnesia, which supposedly can be cured with talk therapy. A few days before D-Day, U.S. Army Major Jeff Pike (James Garner) is drugged, kidnapped and taken to what appears to be a hospital run by American Occupation Forces, where his appearance is altered overnight. Pike knows that the invasion is aimed at Normandy, not Pas de Calais, as the Nazi high command expects. He buys Gerbers explanation of anterograde amnesia – using the double doors of a wardrobe as illustration – and speaks casually of Normandy. Salt in a papercut alerts him to the horrible truth, and the drama proceeds from there. In the 2011 light novel Danganronpa Zero, the protagonist and "Ultimate Analyst" Ryoko Otonashi has anterograde amnesia as a result of "The Tragedy", keeping note of her memories by writing into a journal at all times and using her speedreading to keep herself up to date. Seen to be her boyfriend and "Ultimate Neurologist" Yasuke Matsuda, Ryoko witnesses a murder committed by Junko Enoshima, before being mistaken for wanted murderer and Tragedy perpetrator Izuru Kamukura by the "Ultimate Bodyguard" Madarai octuplets. After teaming up with perverted "Ultimate Secret Agent" Yuto Kamishiro in an attempt to discover the perpetrator behind the Tragedy, Ryoko learns that she herself was personally involved in the event as the true Junko, the Junko she met having been her non-identical twin sister Mukuro Ikusaba (with whom she shared Matsuda as a boyfriend) attempting to trigger her memories, which Matsuda had been suppressing on Junkos own request both to clear her of suspicion in the events off the Tragedy, attempt to cure her depression, and test wiping the memories of others. Attempting to subdue Ryoko, Matsuda accidentally restores her memories of being Junko and his fatally stabbed, before wishing Junko success in her planned actions with Izuru and Mukuro: collapsing world society and launching a "killing game". In the 2016 video game Phoenix Wright: Ace Attorney – Spirit of Justice, the character Sorin Sprocket is eventually revealed to have anterograde amnesia, which he developed after unintentionally causing a car accident which killed his sister. This causes his memories to completely reset every time he wakes up from sleeping, to the day after this accident. This depiction is notable for demonstrating the relationship issues that arise between Sorin and his fiancée, Ellen Wyatt, as a result of this disorder, most noticeably with how Sorins feelings towards her to coming across as distant and cold. As the storyline continues, however, the player comes to uncover that Sorin in fact deeply loves his fiancée, and is able to maintain this love despite his disorder, but in fact feels a sense of guilt over the fact that he has to constantly remind himself of the fact that this love exists inside of him every day, due to his disorder. It is also noticeable in that it depicts how Sorin deals with his disorder, by keeping a journal where he writes down every detail of every day after his sisters death. He carries this journal around everywhere he goes as a substitution to his memories, and uses what is written in the notebook to become aware each time he wakes up of the fact that he has his condition, what the current date apparently is, and everything important that have apparently occurred on every day since he first developed the condition. The episode also deals with legal issues concerning the disorder, when it is debated during Ellen Wyatts trial as to whether Sorins journal can be considered a proper substitution to his memories for the sake of viable witness testimony. Dangers imposed by this also come into play when it is revealed that a page in Sorins journal had been altered by someone, which causes him to go into mental collapse that any of his other memories and thoughts could also have arisen from someone elses manipulation.In the episode "Pimemento" of Brooklyn Nine-Nine, Adrian Pimento develops an artificial form of anterograde amnesia after being drugged by his therapist, which is a main plot point of the episode. See also Transient global amnesia References Other sources == External links ==

Aarogya what is Typhus

Typhus

Typhus, also known as typhus fever, is a group of infectious diseases that include epidemic typhus, scrub typhus, and murine typhus. Common symptoms include fever, headache, and a rash. Typically these begin one to two weeks after exposure.The diseases are caused by specific types of bacterial infection. Epidemic typhus is due to Rickettsia prowazekii spread by body lice, scrub typhus is due to Orientia tsutsugamushi spread by chiggers, and murine typhus is due to Rickettsia typhi spread by fleas.Vaccines have been developed, but none are commercially available. Prevention is achieved by reducing exposure to the organisms that spread the disease. Treatment is with the antibiotic doxycycline. Epidemic typhus generally occurs in outbreaks when poor sanitary conditions and crowding are present. While once common, it is now rare. Scrub typhus occurs in Southeast Asia, Japan, and northern Australia. Murine typhus occurs in tropical and subtropical areas of the world.Typhus has been described since at least 1528. The name comes from the Greek tûphos (τῦφος) meaning fever or delusion, describing the state of mind of those infected. While "typhoid" means "typhus-like", typhus and typhoid fever are distinct diseases caused by different types of bacteria. Note, however, that in some languages such as German, typhus does mean "typhoid fever". Signs and symptoms These signs and symptoms refer to epidemic typhus, as it is the most important of the typhus group of diseases.Signs and symptoms begin with sudden onset of fever and other flu-like symptoms about one to two weeks after being infected. Five to nine days after the symptoms have started, a rash typically begins on the trunk and spreads to the extremities. This rash eventually spreads over most of the body, sparing the face, palms, and soles. Signs of meningoencephalitis begin with the rash and continue into the second or third weeks. Other signs of meningoencephalitis include sensitivity to light (photophobia), altered mental status (delirium), or coma. Untreated cases are often fatal. Causes Multiple diseases include the word "typhus" in their descriptions. Types include: Prevention As of 2020, no vaccine is commercially available. A vaccine has been in development for scrub typhus known as the scrub typhus vaccine. Treatment The American Public Health Association recommends treatment based upon clinical findings and before culturing confirms the diagnosis. Without treatment, death may occur in 10% to 60% of people with epidemic typhus, with people over age 60 having the highest risk of death. In the antibiotic era, death is uncommon if doxycycline is given. In one study of 60 people hospitalized with epidemic typhus, no one died when given doxycycline or chloramphenicol. Epidemiology According to the World Health Organization, the current death rate from typhus is about one of every 5,000,000 people per year.Only a few areas of epidemic typhus exist today. Since the late 20th century, cases have been reported in Burundi, Rwanda, Ethiopia, Algeria, and a few areas in South and Central America.Except for two cases, all instances of epidemic typhus in the United States have occurred east of the Mississippi River. An examination of a cluster of cases in Pennsylvania concluded the source of the infection was flying squirrels. Sylvatic cycle (diseases transmitted from wild animals) epidemic typhus remains uncommon in the US. The Centers for Disease Control and Prevention have documented only 47 cases from 1976 to 2010. An outbreak of flea-borne murine typhus was identified in downtown Los Angeles, California, in October 2018. History Middle Ages The first reliable description of typhus appears in 1489 AD during the Spanish siege of Baza against the Moors during the War of Granada (1482–1492). These accounts include descriptions of fever; red spots over arms, back, and chest; attention deficit, progressing to delirium; and gangrenous sores and the associated smell of rotting flesh. During the siege, the Spaniards lost 3,000 men to enemy action, but an additional 17,000 died of typhus.In historical times, "jail fever" or "gaol fever" was common in English prisons, and is believed by modern authorities to have been typhus. It often occurred when prisoners were crowded together into dark, filthy rooms where lice spread easily. Thus, "imprisonment until the next term of court" was often equivalent to a death sentence. Prisoners brought before the court sometimes infected members of the court. The Black Assize of Exeter 1586 was another notable outbreak. During the Lent assizes court held at Taunton in 1730, gaol fever caused the death of the Lord Chief Baron, as well as the High Sheriff, the sergeant, and hundreds of others. During a time when persons were executed for capital offenses, more prisoners died from gaol fever than were put to death by all the public executioners in the British realm. In 1759, an English authority estimated that each year, a quarter of the prisoners had died from gaol fever. In London, gaol fever frequently broke out among the ill-kept prisoners of Newgate Prison and then moved into the general city population. In May 1750, the Lord Mayor of London, Sir Samuel Pennant, and many court personnel were fatally infected in the courtroom of the Old Bailey, which adjoined Newgate Prison. Early modern epidemics Epidemics occurred routinely throughout Europe from the 16th to the 19th centuries, including during the English Civil War, the Thirty Years War, and the Napoleonic Wars. Pestilence of several kinds raged among combatants and civilians in Germany and surrounding lands from 1618 to 1648. According to Joseph Patrick Byrne, "By wars end, typhus may have killed more than 10 percent of the total German population, and disease in general accounted for 90 percent of Europes casualties." 19th century During Napoleons retreat from Moscow in 1812, more French soldiers died of typhus than were killed by the Russians.A major epidemic occurred in Ireland between 1816 and 1819, during the famine caused by a worldwide reduction in temperature known as the Year Without a Summer. An estimated 100,000 people perished. Typhus appeared again in the late 1830s, and yet another major typhus epidemic occurred during the Great Irish Famine between 1846 and 1849. The Irish typhus spread to England, where it was sometimes called "Irish fever" and was noted for its virulence. It killed people of all social classes, as lice were endemic and inescapable, but it hit particularly hard in the lower or "unwashed" social strata.In the United States, a typhus epidemic broke out in Philadelphia in 1837 and killed the son of Franklin Pierce (14th President of the United States) in Concord, New Hampshire, in 1843. Several epidemics occurred in Baltimore, Memphis, and Washington, DC, between 1865 and 1873. Typhus was also a significant killer during the US Civil War, although typhoid fever was the more prevalent cause of US Civil War "camp fever". Typhoid fever is caused by the bacterium Salmonella enterica Serovar Typhi.In Canada alone, the typhus epidemic of 1847 killed more than 20,000 people from 1847 to 1848, mainly Irish immigrants in fever sheds and other forms of quarantine, who had contracted the disease aboard the crowded coffin ships in fleeing the Great Irish Famine. Officials neither knew how to provide sufficient sanitation under conditions of the time nor understood how the disease spread. 20th century Typhus was endemic in Poland and several neighboring countries prior to World War I (1914–1918), but became epidemic during the war. Delousing stations were established for troops on the Western Front during World War I, but typhus ravaged the armies of the Eastern Front, where over 150,000 died in Serbia alone. Fatalities were generally between 10% and 40% of those infected and the disease was a major cause of death for those nursing the sick.In 1922, the typhus epidemic reached its peak in Soviet territory, with some 20 to 30 million cases in Russia. Although typhus had ravaged Poland with some 4 million cases reported, efforts to stem the spread of disease in that country had largely succeeded by 1921 through the efforts of public health pioneers such as Hélène Sparrow and Rudolf Weigl. In Russia during the civil war between the White and Red Armies, epidemic typhus killed 2–3 million people, many of whom were civilians. In 1937 and 1938 there was a typhus epidemic in Chile.During World War II, many German POWs after the loss at Stalingrad died of typhus. Typhus epidemics killed those confined to POW camps, ghettos, and Nazi concentration camps who were held in unhygienic conditions. Pictures of mass graves including people who died from typhus can be seen in footage shot at Bergen-Belsen concentration camp. Among thousands of prisoners in concentration camps such as Theresienstadt and Bergen-Belsen who died of typhus were Anne Frank, age 15, and her sister Margot, age 19 in the latter camp. The first typhus vaccine was developed by the Polish zoologist Rudolf Weigl in the interwar period; the vaccine did not prevent the disease but reduced its mortality. 21st century Beginning in 2018, a typhus outbreak spread through Los Angeles County primarily affecting homeless people. In 2019, city attorney Elizabeth Greenwood revealed that she, too, was infected with typhus as a result of a flea bite at her office in Los Angeles City Hall. Pasadena also experienced a sudden uptick in typhus with 22 cases in 2018 but, without being able to attribute this to one location, the Pasadena Public Health Department did not identify the cases as an "outbreak". == References ==

Hello Aarogya , Do you know what is Arteritis,

Arteritis

Arteritis is the inflammation of the walls of arteries, usually as a result of infection or autoimmune response. Arteritis, a complex disorder, is still not entirely understood. Arteritis may be distinguished by its different types, based on the organ systems affected by the disease. A complication of arteritis is thrombosis, which can be fatal. Arteritis and phlebitis are forms of vasculitis. Signs and Symptoms Symptoms of general arteritis may include: Inflammation Fever Increased production of red blood cells (erythrocytes) Limping Reduced pulse Diagnosis Diagnosis of arteritis is based on unusual medical symptoms. Similar symptoms may be caused by a number of other conditions, such as Ehlers-Danlos syndrome and Marfan syndrome (both heritable disorders of connective tissue), tuberculosis, syphilis, spondyloarthropathies, Cogans syndrome, Buergers, Behcets, and Kawasaki disease. Various imaging techniques may be used to diagnose and monitor disease progression. Imaging modalities may include direct angiography, magnetic resonance angiography, and ultrasonography.Angiography is commonly used in the diagnosis of Takayasu arteritis, especially in the advanced stages of the disease, when arterial stenosis, occlusion, and aneurysms may be observed. However, angiography is a relatively invasive investigation, exposing patients to large doses of radiation, so is not recommended for routine, long-term monitoring of disease progression in patients with Takayasu arteritis.Computed tomography angiography can determine the size of the aorta and its surrounding branches, and can identify vessel wall lesions in middle to late stages of arteritis. CTA can also show the blood flow within the blood vessels. Like angiography, CTA exposes patients to high dosages of radiation.Magnetic resonance angiography is used to diagnose Takayasu arteritis in the early stages, showing changes such as the thickening of the vessel wall. Even small changes may be measured, making MRA a useful tool for monitoring disease progression without exposing patients to the radiation of direct angiography or CTA. MRA is an expensive investigation, and shows calcification of the aorta and distal branches less clearly than other imaging methods.Ultrasonography is an ideal method of diagnosing patients in early stages of arteritis when inflammation in the vessel walls occurs. It can also show the blood flow within the blood vessels. Ultrasonography is a popular first-line investigation for diagnosis because it is relatively quick, cheap, noninvasive, and does not expose patients to radiation. It is also used for long-term monitoring of disease progression in Takayasu arteritis. Not all vascular lesions are visible on ultrasound, and the accuracy of the scan depends, to some extent, on the person reading the scan, as the results are observed in real time. Types Arteritis may be primary or secondary to some other disease process. The primary types are: An example of a secondary arteritis is arteritis caused by infection with the fungal pathogen Candida albicans. Giant cell arteritis Giant cell arteritis contains two different types of arteritides that are almost indistinguishable from one another. It includes two types, temporal arteritis and Takayasu arteritis. Both types contain an occupancy of medium- and larger-sized arteries which are categorized based on the infiltration of the giant cells. Takayasu arteritis This type of arteritis is most common in females, with a median age of 25 years. Takayasu arteritis is more common in women of Asian descent who are in their reproductive years. However, over the past decades, its incidence in Africa, Europe, and North America has been increasing. Takayasu arteritis is an inflammatory disease that mainly affects the larger vessels such as the aorta and its surrounding branches. Research focused on Takayasu arteritis in the western parts of the world remains limited. An estimation suggests that, each year, the number of cases per million people is 2.6. Temporal arteritis Temporal arteritis, the second type of giant cell arteritis, is also a chronic, inflammatory disease involving mid- to large-sized arteries. Temporal arteritis has a higher incidence in people of Scandinavian descent. However, the incidence rate differs based on population, region and races. Temporal arteritis is not uncommon in North America. The incidence rate is around 0.017% for individuals over 50 years of age.Symptoms of temporal arteritis are classified as specific and nonspecific.Nonspecific symptoms: Headache Low grade fever Sweating Anorexia (loss of appetite) Weight loss General malaiseSpecific symptoms: Claudication of the jaw Engorged, tender vesselsSpecific symptoms usually develop in the advanced stages of temporal arteritis.Polyarteritis nodosa of unknown mechanism can cause testicular pain. It is often associated with aneurysms and Hepatitis B. Treatment Medications The first-line treatment for arteritis is oral glucocorticoid (steroid) medication, such as prednisone, taken daily for a period of three months. After this initial phase, the medication may be reduced in dose or frequency, e.g. every other day, if possible. If the disease worsens with the new treatment schedule, a cytotoxic medication may be given, in addition to the glucocorticoid. Commonly used cytotoxic agents include azathioprine, methotrexate, or cyclophosphamide. The dose of glucocorticoid medication may be decreased if response to treatment is good. This medication may be reduced gradually once the disease becomes inactive, slowly tapering the dose (to allow the body time to adjust) until the medication may be stopped completely. Conversely, if the disease remains active, the medication will need to be increased. After six months, if the medication cannot be reduced in frequency to alternate days, or if in 12 months the medications cannot be stopped completely, then treatment is deemed to have failed.Pulsed therapy is an alternative method of administering the medications above, using much higher doses over a short period of time (a pulse), to reduce the inflammation within the arteries. Methylprednisolone, a glucocorticoid, is often used for pulse therapy; cyclophosphamide is an alternative. This method has been shown to be successful for some patients. Immunosuppressive pulse therapy, such as with cyclophosphamide, has also demonstrated relief of symptoms associated with arteritis. References == External links ==

Hello Aarogya , Do you know what is Ancylostomiasis,

Ancylostomiasis

Ancylostomiasis is a hookworm disease caused by infection with Ancylostoma hookworms. The name is derived from Greek ancylos αγκύλος "crooked, bent" and stoma στόμα "mouth". Ancylostomiasis is also known as miners anaemia, tunnel disease, brickmakers anaemia and Egyptian chlorosis. Helminthiasis may also refer to ancylostomiasis, but this term also refers to all other parasitic worm diseases as well. In the United Kingdom, if acquired in the context of working in a mine, the condition is eligible for Industrial Injuries Disability Benefit. It is a prescribed disease (B4) under the relevant legislation.§Ancylostomiasis is caused when hookworms, present in large numbers, produce an iron deficiency anemia by sucking blood from the hosts intestinal walls. Signs and symptoms Depending on the organism, the signs and symptoms vary. Ancylostoma duodenale and Necator americanus can enter the blood stream while Ancylostoma braziliensis cannot. Signs and symptoms of Ancylostoma duodenale and Necator americanus are given in corresponding page.In Ancylostoma braziliensis as the larvae are in an abnormal host, they do not mature to adults but instead migrate through the skin until killed by the hosts inflammatory response. This migration causes local intense itching and a red serpiginous lesion. Treatment with a single dose of oral ivermectin results in cure rates of 94–100%. Causes The infection is usually contracted by people walking barefoot over contaminated soil. In penetrating the skin, the larvae may cause an allergic reaction. It is due to the itchy patch at the site of entry that the early infection gets its nickname "ground itch". Once larvae have broken through the skin, they enter the bloodstream and are carried to the lungs (however, unlike ascarids, hookworms do not usually cause pneumonia). The larvae migrate from the lungs up the windpipe to be swallowed and carried back down to the intestine. If humans come into contact with larvae of the dog hookworm or the cat hookworm, or of certain other hookworms that do not infect humans, the larvae may penetrate the skin. Sometimes, the larvae are unable to complete their migratory cycle in humans. Instead, the larvae migrate just below the skin producing snake-like markings. This is referred to as a creeping eruption or cutaneous larva migrans. Diagnosis They commonly infect the skin, eyes, and viscera in humans. Ancylostoma brasiliensis causes cutaneous larva migrans. Toxocara causes visceral larva migrans. Prevention Control of this parasite should be directed against reducing the level of environmental contamination. Treatment of heavily infected individuals is one way to reduce the source of contamination (one study has estimated that 60% of the total worm burden resides in less than 10% of the population). Other obvious methods are to improve access to sanitation, e.g. toilets, but also convincing people to maintaining them in a clean, functional state, thereby making them conducive to use. Treatment The drug of choice for the treatment of hookworm disease is mebendazole which is effective against both species, and in addition, will remove the intestinal worm Ascaris also, if present. The drug is very efficient, requiring only a single dose and is inexpensive. However, treatment requires more than giving the anthelmintic, the patient should also receive dietary supplements to improve their general level of health, in particular iron supplementation is very important. Iron is an important constituent of a multitude of enzyme systems involved in energy metabolism, DNA synthesis and drug detoxification.An infection of N. americanus parasites can be treated by using benzimidazoles, albendazole, and mebendazole. A blood transfusion may be necessary in severe cases of anemia. Light infections are usually left untreated in areas where reinfection is common. Iron supplements and a diet high in protein will speed the recovery process. In a case study involving 56–60 men with Trichuris trichiura and/or N. americanus infections, both albendazole and mebendazole were 90% effective in curing T. trichiura. However, albendazole had a 95% cure rate for N. americanus, while mebendazole only had a 21% cure rate. This suggests albendazole is most effective for treating both T. trichiura and N. americanus.During the 1910s, common treatments for hookworm included thymol, 2-naphthol, chloroform, gasoline, and eucalyptus oil. By the 1940s, the treatment of choice was tetrachloroethylene, given as 3 to 4 cc in the fasting state, followed by 30 to 45 g of sodium sulfate. Tetrachloroethylene was reported to have a cure rate of 80 percent for Necator infections, but 25 percent in Ancylostoma infections, requiring re-treatment. Epidemiology Hookworm anaemia was first described by Wilhelm Griesenger in Egypt, Cairo in 1852. He found thousands of adult ancylostomes in the small bowel of a 20-year old soldier who was suffering from severe diarrhoea and anaemia (labelled at the time as Egyptian chlorosis). The subject was revisited in Europe when there was an outbreak of "miners anaemia" in Italy. During the construction of the Gotthard Tunnel in Switzerland (1871–81), a large number of miners suffered from severe anaemia of unknown cause. Medical investigations let to the understanding that it was caused by Ancylostoma duodenale (favoured by high temperatures and humidity) and to "major advances in parasitology, by way of research into the aetiology, epidemiology and treatment of ancylostomiasis".Hookworms still account for high proportion of debilitating disease in the tropics and 50–60,000 deaths per year can be attributed to this disease. References == External links ==

Aarogya, elaborate on Spasm

Spasm

A spasm is a sudden involuntary contraction of a muscle, a group of muscles, or a hollow organ such as the bladder. A spasmodic muscle contraction may be caused by many medical conditions, including dystonia. Most commonly, it is a muscle cramp which is accompanied by a sudden burst of pain. A muscle cramp is usually harmless and ceases after a few minutes. It is typically caused by ion imbalance or muscle overload. There are other causes of involuntary muscle contractions, and some of these may cause a health problem. Description and causes Various kinds of involuntary muscle activity may be referred to as a "spasm". A spasm may be a muscle contraction caused by abnormal nerve stimulation or by abnormal activity of the muscle itself. A spasm may lead to muscle strains or tears in tendons and ligaments if the force of the spasm exceeds the tensile strength of the underlying connective tissue. This can occur with a particularly strong spasm or with weakened connective tissue. A hypertonic muscle spasm is a condition of chronic, excessive muscle tone (i.e., tension in a resting muscle). This is the amount of contraction that remains when a muscle is not working. A true hypertonic spasm is caused by malfunctioning feedback nerves. This is much more serious and is permanent unless treated. In this case, the hypertonic muscle tone is excessive, and the muscles are unable to relax. A subtype of spasm is colic. This is an episodic pain caused by spasm of smooth muscle in a particular organ (e.g., the bile duct). A characteristic of colic is the sensation of having to move about, and the pain may induce nausea or vomiting. See also References External links NIH Medical Encyclopedia How Stuff Works "Spasm" . New International Encyclopedia. 1905.

Hello Aarogya, explain a situation where Gerstmann–Sträussler–Scheinker syndrome occurs

Gerstmann–Sträussler–Scheinker syndrome

Gerstmann–Sträussler–Scheinker syndrome (GSS) is an extremely rare, usually familial, fatal neurodegenerative disease that affects patients from 20 to 60 years in age. It is exclusively heritable, and is found in only a few families all over the world. It is, however, classified with the transmissible spongiform encephalopathies (TSE) due to the causative role played by PRNP, the human prion protein. GSS was first reported by the Austrian physicians Josef Gerstmann, Ernst Sträussler and Ilya Scheinker in 1936.Familial cases are associated with autosomal-dominant inheritance.Certain symptoms are common to GSS, such as progressive ataxia, pyramidal signs, and dementia; they worsen as the disease progresses. Symptoms and signs Symptoms start with slowly developing dysarthria (difficulty speaking) and cerebellar truncal ataxia (unsteadiness) and then the progressive dementia becomes more evident. Loss of memory can be the first symptom of GSS. Extrapyramidal and pyramidal symptoms and signs may occur and the disease may mimic spinocerebellar ataxias in the beginning stages. Myoclonus (spasmodic muscle contraction) is less frequently seen than in Creutzfeldt–Jakob disease. Many patients also exhibit nystagmus (involuntary movement of the eyes), visual disturbances, and even blindness or deafness. The neuropathological findings of GSS include widespread deposition of amyloid plaques composed of abnormally folded prion protein.Four clinical phenotypes are recognized: typical GSS, GSS with areflexia and paresthesia, pure dementia GSS and Creutzfeldt-Jakob disease-like GSS. Causes GSS is part of a group of diseases called transmissible spongiform encephalopathies. These diseases are caused by prions, which are a class of pathogenic proteins that are resistant to proteases. These prions then form clusters in the brain, which are responsible for the neurodegenerative effects seen in patients.The P102L mutation, which causes a substitution of proline to a leucine in codon 102, has been found in the prion protein gene (PRNP, on chromosome 20) of most affected individuals. Therefore, it appears this genetic change is usually required for the development of the disease. Diagnosis GSS can be identified through genetic testing. Testing for GSS involves a blood and DNA examination in order to attempt to detect the mutated gene at certain codons. If the genetic mutation is present, the patient will eventually develop GSS. Treatment There is no cure for GSS, nor is there any known treatment to slow the progression of the disease. Therapies and medication are aimed at treating or slowing down the effects of the symptoms. The goal of these treatments is to try to improve the patients quality of life as much as possible. There is some ongoing research to find a cure, with one of the most prominent examples being the PRN100 monoclonal antibody. Prognosis GSS is a disease that progresses slowly, lasting roughly 2–10 years, with an average of approximately five years. The disease ultimately results in death, most commonly from the patient either going into a coma, or from a secondary infection due to the patients loss of bodily functions. Research Prion diseases, also called transmissible spongiform encephalopathies (TSEs), are neurodegenerative diseases of the brain thought to be caused by a protein that converts to an abnormal form called a prion. GSS is a very rare TSE, making its genetic origin nearly impossible to determine. It is also challenging to find any patients with GSS, as the disease tends to be underreported, due to its clinical similarity to other diseases, and has been found in only a few countries. In 1989, the first mutation of the prion protein gene was identified in a GSS family. The largest of these families affected by GSS is the Indiana Kindred, spanning over 8 generations, and includes over 3,000 people, with 57 individuals known to be affected. GSS was later realized to have many different gene mutation types, varying in symptom severity, timing and progression. Doctors in different parts of the world are in the process of uncovering more generations and families who have the mutation. Notes External links Gerstmann–Sträussler–Scheinker syndrome, MedicineNet.com

Hi Aarogya, could you help me understand about Fear of flying

Fear of flying

Fear of flying is a fear of being on an airplane, or other flying vehicle, such as a helicopter, while in flight. It is also referred to as flying anxiety, flying phobia, flight phobia, aviophobia, aerophobia, or pteromechanophobia (although aerophobia also means a fear of drafts or of fresh air).Acute anxiety caused by flying can be treated with anti-anxiety medication. The condition can be treated with exposure therapy, which works better when combined with cognitive behavioral therapy. Signs and symptoms People with fear of flying experience intense, persistent fear or anxiety when they consider flying, as well as during flying. They will avoid flying if they can, and the fear, anxiety, and avoidance cause significant distress and impair their ability to function. Take-off, bad weather, and turbulence appear to be the most anxiety provoking aspects of flying.The most extreme manifestations can include panic attacks or vomiting at the mere sight or mention of an aircraft or air travel.Around 60% of people with fear of flying report having some other anxiety disorder. Cause The causes of flight phobia and the mechanisms by which it is maintained were not well understood as of 2016. It is not clear if it is really one condition; it appears to be heterogenous. It appears that some people get aerophobia from being or having claustrophobia to the small spaces inside the fuselage of the plane or helicopter. Diagnosis The diagnosis is clinical. It is often difficult to determine if the specific phobia of fear of flight should be the primary diagnosis, or if fear of flying is a symptom of a generalized anxiety disorder or another anxiety disorder such as agoraphobia or claustrophobia. Classification Fear of flying is a specific phobia classified as such in the DSM-5. Management Acute anxiety caused by flying can be treated with anti-anxiety medication. The condition can be treated with exposure therapy, including use of virtual reality equipment, which works better when combined with cognitive behavioral therapy. Relaxation techniques and education about aviation safety can also be helpful in combination with other approaches.A new and advanced treatment for aviophobia is virtual reality exposure therapy. This type of treatment uses computer technology where the patient enters a virtual reality of flying. Virtual reality exposure therapy Effective treatment for phobias such as fear of flying would be one that activates and modifies the fear structure. Activation of the fear structure can be achieved by exposing the patient to the feared stimuli, flying in this case, to elicit the fearful response. Modification of the fear structure can be achieved by the processes of habituation and extinction after eliciting the fearful response several times. A new and advanced treatment for aviophobia is virtual reality exposure therapy (VRET). This type of treatment uses computer technology where the patient virtually experiences flying. This experience includes visual, auditory, and motion stimuli to imitate flying in a plane as close as possible. Thus, VRET is considered an effective treatment for aviophobia. While it can be argued that vivo exposure treatment, patients being exposed to an aircraft, is the most effective way of treatment, but VRET is more cost-effective, accessible, less time-consuming, and requires less organization. Another advantage of VRET over vivo exposure treatment is that it focuses on the main reason that elicits fear of flying easily. For example, if the patients most anxiety-inducing-component is takeoff, in VRET the patient would be exposed to a plane takeoff repeatedly while in vivo exposure the patient would have to wait for the plane to land and then take off again. Outcomes Studies of interventions like CBT have reported rates of reduction in anxiety of around 80%; however, there is little evidence that any treatment can eliminate fear of flying. Epidemiology Estimates for prevalence have ranged between 2.5% and 40%; estimates on the lower end are probably generated through studies where the condition is diagnosed by a professional, and the higher end probably includes people who have diagnosed themselves. History Fear of flying was first discussed in the biomedical literature by a doctor in the UK at the end of World War I, who called it "aero-neurosis" and was describing pilots and crew who were or became anxious about flying. It was not much discussed until the 1950s and rise of commercial air travel and the vogue in psychoanalysis. Starting in the 1970s fear of flying was addressed through behavioral and cognitive approaches. Society and culture Immediately after the September 11 attacks, Americans chose to travel more by car instead of flying; because of the extra traffic, around 350 more people died in traffic accidents than would have normally occurred.A number of celebrities have suffered from a fear of flying, including former Arsenal FC and Netherlands footballer Dennis Bergkamp, famously dubbed the "non-flying Dutchman", Agnetha Fältskog, and rockstar David Bowie. Research directions As of 2016, the causes of fear of flying as well as the psychological mechanisms through which it were persists had not been well researched. A few studies had looked at whether mechanisms like illusory correlation and expectancy bias were present in all or most people with fear of flying as well as other specific phobias; these studies have not led to clear outcomes.Research into the most effective ways to treat or manage fear of flying is difficult (as it is with other counselling or behavioral interventions) due to the inability to include a placebo or other control arm in such studies. See also List of phobias Health hazards of air travel Flight shame == References ==

Aarogya, explain a scenario commonly referred as Less

Less

Less or LESS may refer to: fewer than,: not as much. Computing less (Unix), a Unix utility program Less (stylesheet language), a dynamic stylesheet language Large-Scale Scrum (LeSS), a product development framework that extends Scrum Other uses -less, a privative suffix in English Lunar Escape Systems, a series of proposed emergency spacecraft for the Apollo Program Christian Friedrich Lessing (1809–1862), (author abbreviation Less.) for German botanist Less (novel), a 2017 novel by Andrew Sean Greer See also Fewer versus less Less is more (disambiguation) All pages with titles beginning with Less All pages with titles containing Less

Hey Aarogya!, what is System

System

A system is a group of interacting or interrelated elements that act according to a set of rules to form a unified whole. A system, surrounded and influenced by its environment, is described by its boundaries, structure and purpose and expressed in its functioning. Systems are the subjects of study of systems theory and other systems sciences. Systems have several common properties and characteristics, including structure, function(s), behavior and interconnectivity. Etymology The term system comes from the Latin word systēma, in turn from Greek σύστημα systēma: "whole concept made of several parts or members, system", literary "composition". History According to Marshall McLuhan, "System" means "something to look at". You must have a very high visual gradient to have systematization. But in philosophy, prior to Descartes, there was no "system". Plato had no "system". Aristotle had no "system". In the 19th century the French physicist Nicolas Léonard Sadi Carnot, who studied thermodynamics, pioneered the development of the concept of a system in the natural sciences. In 1824 he studied the system which he called the working substance (typically a body of water vapor) in steam engines, in regards to the systems ability to do work when heat is applied to it. The working substance could be put in contact with either a boiler, a cold reservoir (a stream of cold water), or a piston (on which the working body could do work by pushing on it). In 1850, the German physicist Rudolf Clausius generalized this picture to include the concept of the surroundings and began to use the term working body when referring to the system. The biologist Ludwig von Bertalanffy became one of the pioneers of the general systems theory. In 1945 he introduced models, principles, and laws that apply to generalized systems or their subclasses, irrespective of their particular kind, the nature of their component elements, and the relation or forces between them.Norbert Wiener and Ross Ashby, who pioneered the use of mathematics to study systems, carried out significant development in the concept of a system.In the 1980s John Henry Holland, Murray Gell-Mann and others coined the term complex adaptive system at the interdisciplinary Santa Fe Institute. Concepts Environment and boundaries Systems theory views the world as a complex system of interconnected parts. One scopes a system by defining its boundary; this means choosing which entities are inside the system and which are outside—part of the environment. One can make simplified representations (models) of the system in order to understand it and to predict or impact its future behavior. These models may define the structure and behavior of the system.Natural and human-made systems There are natural and human-made (designed) systems. Natural systems may not have an apparent objective but their behavior can be interpreted as purposeful by an observer. Human-made systems are made with various purposes that are achieved by some action performed by or with the system. The parts of a system must be related; they must be "designed to work as a coherent entity" — otherwise they would be two or more distinct systems. Theoretical framework Most systems are open systems, exchanging matter and energy with their respective surroundings; like a car, a coffeemaker, or Earth. A closed system exchanges energy, but not matter, with its environment; like a computer or the project Biosphere 2. An isolated system exchanges neither matter nor energy with its environment. A theoretical example of such system is the Universe.Process and transformation process An open system can also be viewed as a bounded transformation process, that is, a black box that is a process or collection of processes that transform inputs into outputs. Inputs are consumed; outputs are produced. The concept of input and output here is very broad. For example, an output of a passenger ship is the movement of people from departure to destination.System model A system comprises multiple views. Man-made systems may have such views as concept, analysis, design, implementation, deployment, structure, behavior, input data, and output data views. A system model is required to describe and represent all these views.Systems architecture A systems architecture, using one single integrated model for the description of multiple views, is a kind of system model. Subsystem A subsystem is a set of elements, which is a system itself, and a component of a larger system. The IBM Mainframe Job Entry Subsystem family (JES1, JES2, JES3, and their HASP/ASP predecessors) are examples. The main elements they have in common are the components that handle input, scheduling, spooling and output; they also have the ability to interact with local and remote operators. A subsystem description is a system object that contains information defining the characteristics of an operating environment controlled by the system. The Data tests are performed to verify the correctness of the individual subsystem configuration data (e.g. MA Length, Static Speed Profile, …) and they are related to a single subsystem in order to test its Specific Application (SA). Analysis There are many kinds of systems that can be analyzed both quantitatively and qualitatively. For example, in an analysis of urban systems dynamics, A .W. Steiss defined five intersecting systems, including the physical subsystem and behavioral system. For sociological models influenced by systems theory, Kenneth D. Bailey defined systems in terms of conceptual, concrete, and abstract systems, either isolated, closed, or open. Walter F. Buckley defined systems in sociology in terms of mechanical, organic, and process models. Bela H. Banathy cautioned that for any inquiry into a system understanding its kind is crucial, and defined "natural" and "designed", i. e. artificial, systems. It is important not to confuse these abstract definitions. For example, natural systems include subatomic systems, living systems, the Solar System, galaxies, and the Universe, while artificial systems include man-made physical structures, hybrids of natural and artificial systems, and conceptual knowledge. The human elements of organization and functions are emphasized with their relevant abstract systems and representations. Artificial systems inherently have a major defect: they must be premised on one or more fundamental assumptions upon which additional knowledge is built. This is in strict alignment to the Gödels incompleteness theorems. The Artificial system can be defined as a "consistent formalized system which contains elementary arithmetic". These fundamental assumptions are not inherently deleterious, but they must by definition be assumed as true, and if they are actually false then the system is not as structurally integral as is assumed (i.e. it is evident that if the initial expession is false, then the Artificial system is not a "consistent formalized system"). For example, in geometry this is very evident in the postulation of theorems and extrapolation of proofs from them. George J. Klir maintained that no "classification is complete and perfect for all purposes", and defined systems as abstract, real, and conceptual physical systems, bounded and unbounded systems, discrete to continuous, pulse to hybrid systems, etc. The interactions between systems and their environments are categorized as relatively closed and open systems. It seems most unlikely that an absolutely closed system can exist or, if it did, that it could be known by man. Important distinctions have also been made between hard systems – technical in nature and amenable to methods such as systems engineering, operations research, and quantitative systems analysis – and soft systems that involve people and organisations, commonly associated with concepts developed by Peter Checkland and Brian Wilson through Soft Systems Methodology (SSM) involving methods such as action research and emphasis of participatory designs. Where hard systems might be identified as more "scientific", the distinction between them is often elusive. Cultural system A cultural system may be defined as the interaction of different elements of culture. While a cultural system is quite different from a social system, sometimes both together are referred to as a "sociocultural system". A major concern of the social sciences is the problem of order. Economic system An economic system is a mechanism (social institution) which deals with the production, distribution and consumption of goods and services in a particular society. The economic system is composed of people, institutions and their relationships to resources, such as the convention of property. It addresses the problems of economics, like the allocation and scarcity of resources. The international sphere of interacting states is described and analysed in systems terms by several international relations scholars, most notably in the neorealist school. This systems mode of international analysis has however been challenged by other schools of international relations thought, most notably the constructivist school, which argues that an over-large focus on systems and structures can obscure the role of individual agency in social interactions. Systems-based models of international relations also underlies the vision of the international sphere held by the liberal institutionalist school of thought, which places more emphasis on systems generated by rules and interaction governance, particularly economic governance. Applications Systems modeling is generally a basic principle in engineering and in social sciences. The system is the representation of the entities under concern. Hence inclusion to or exclusion from system context is dependent on the intention of the modeler. No model of a system will include all features of the real system of concern, and no model of a system must include all entities belonging to a real system of concern. Information and computer science In computer science and information science, system is a hardware system, software system, or combination, which has components as its structure and observable inter-process communications as its behavior. Again, an example will illustrate: There are systems of counting, as with Roman numerals, and various systems for filing papers, or catalogues, and various library systems, of which the Dewey Decimal Classification is an example. This still fits with the definition of components which are connected together (in this case to facilitate the flow of information). System can also refer to a framework, aka platform, be it software or hardware, designed to allow software programs to run. A flaw in a component or system can cause the component itself or an entire system to fail to perform its required function, e.g., an incorrect statement or data definition Engineering and physics In engineering and physics, a physical system is the portion of the universe that is being studied (of which a thermodynamic system is one major example). Engineering also has the concept of a system referring to all of the parts and interactions between parts of a complex project. Systems engineering is the branch of engineering that studies how this type of system should be planned, designed, implemented, built, and maintained. Expected result is the behavior predicted by the specification, or another source, of the component or system under specified conditions. Sociology, cognitive science and management research Social and cognitive sciences recognize systems in human person models and in human societies. They include human brain functions and mental processes as well as normative ethics systems and social/cultural behavioral patterns. In management science, operations research and organizational development (OD), human organizations are viewed as systems (conceptual systems) of interacting components such as subsystems or system aggregates, which are carriers of numerous complex business processes (organizational behaviors) and organizational structures. Organizational development theorist Peter Senge developed the notion of organizations as systems in his book The Fifth Discipline. Organizational theorists such as Margaret Wheatley have also described the workings of organizational systems in new metaphoric contexts, such as quantum physics, chaos theory, and the self-organization of systems. Pure logic There is also such a thing as a logical system. The most obvious example is the calculus developed simultaneously by Leibniz and Isaac Newton. Another example is George Booles Boolean operators. Other examples have related specifically to philosophy, biology, or cognitive science. Maslows hierarchy of needs applies psychology to biology by using pure logic. Numerous psychologists, including Carl Jung and Sigmund Freud have developed systems which logically organize psychological domains, such as personalities, motivations, or intellect and desire. Often these domains consist of general categories following a corollary such as a theorem. Logic has been applied to categories such as taxonomy, ontology, assessment, and hierarchies. Strategic thinking In 1988, military strategist, John A. Warden III introduced the Five Ring System model in his book, The Air Campaign, contending that any complex system could be broken down into five concentric rings. Each ring—Leadership, Processes, Infrastructure, Population and Action Units—could be used to isolate key elements of any system that needed change. The model was used effectively by Air Force planners in the First Gulf War. In the late 1990s, Warden applied his model to business strategy. See also References Bibliography External links Definitions of Systems and Models by Michael Pidwirny, 1999–2007. Publications with the title "System" (1600–2008) by Roland Müller. Definitionen von "System" (1572–2002) by Roland Müller, (most in German).

Hi Aarogya , Do you know what is Hyperandrogenism,

Hyperandrogenism

Hyperandrogenism is a medical condition characterized by high levels of androgens. It is more common in women than men. Symptoms of hyperandrogenism may include acne, seborrhea (inflamed skin), hair loss on the scalp, increased body or facial hair, and infrequent or absent menstruation. Complications may include high blood cholesterol and diabetes. It occurs in approximately 5% of women of reproductive age.Polycystic ovary syndrome accounts for about 70% of hyperandrogenism cases. Other causes include adrenal hyperplasia, hirsutism, insulin resistance, hyperprolactinemia, Cushings disease, certain types of cancers, and certain medications. Diagnosis often involves blood tests for testosterone, 17-hydroxyprogesterone, and prolactin, as well as a pelvic ultrasound.Treatment depends on the underlying cause. Symptoms of hyperandrogenism can be treated with birth control pills or antiandrogens, such as cyproterone acetate or spironolactone. Other palliative measures may include hair removal techniques.The earliest known description of the condition is attributed to Hippocrates.In 2011, the International Association of Athletics Federations (now World Athletics) and IOC (International Olympic Committee) released statements restricting the eligibility of female athletes with high testosterone, whether through hyperandrogenism or as a result of a difference in sex development (DSD). These regulations were referred to by both bodies as hyperandrogenism regulations and have led to athletes with DSDs being described as having hyperandrogenism. They were revised in 2019 to focus more specifically on DSDs. Signs and symptoms Hyperandrogenism affects 5–10% of women of reproductive age. Hyperandrogenism can affect both men and women but is more noticeable in women since elevated levels of androgens in women may facilitate virilization. Because hyperandrogenism is characterized by elevated male sex hormone levels, symptoms of hyperandrogenism in men are often negligible. Hyperandrogenism in women is typically diagnosed in late adolescence with a medical evaluation. The medical evaluation usually consists of a pelvic exam, observation of external symptoms, and a blood test measuring androgen levels. Symptoms may include the following: Women Hyperandrogenism, especially high levels of testosterone, can cause serious adverse effects if left untreated. High testosterone levels are associated with other health conditions such as obesity, hypertension, amenorrhea (cessation of menstrual cycles), and ovulatory dysfunction, which can lead to infertility. Prominent signs of hyperandrogenism are hirsutism (unwanted growth of hair, especially in the abdominal region and on the back), adult acne, deepening of the voice, and alopecia (balding).Hyperandrogenism has also been observed to increase insulin tolerance, which can lead to type two diabetes and dyslipidemia, such as high cholesterol. These effects may have psychological impacts, sometimes leading to social anxiety and depression, especially in adolescent girls and young women. Paired with obesity and hirsutism, it can cause the individual to have low self-esteem. Men Administration of high-dose testosterone in men over a course of weeks can cause an increase in aggression and hypomanic symptoms, though these were see in only a minority of subjects. Acute high-dose anabolic-androgenic steroid administration in males attenuates endogenous sex hormone production and affects the thyroid hormone axis. Effects on mood and aggression observed during high-dose anabolic-androgenic steroid administration may occur secondarily to hormonal changes. Many of the same signs and symptoms that are seen in women, such as alopecia and acne, may also be found in men. Enlargement of the prostate may also occur. Causes While hyperandrogenism in women can be caused by external factors, it can also appear spontaneously. Polycystic ovary syndrome Polycystic ovary syndrome (PCOS) is an endocrine disorder characterized by an excess of androgens produced by the ovaries. It is estimated that approximately 90% of women with PCOS demonstrate hypersecretion of these hormones. The cause of this condition is unknown. Speculations include genetic predisposition; however, the gene or genes responsible for this remain unidentified. The condition may have a hereditary basis. Other possible causes include elevated insulin production. Most cases of PCOS involve insulin resistance. It is thought that adipose tissue dysfunction plays a role in the insulin resistance seen in PCOS. Insulin can induce excess testosterone secretion from the ovaries. A complication associated with polycystic ovary syndrome is high cholesterol, which is treated with statins. In a meta-analysis, atorvastatin was shown to decrease androgen concentrations in people with hyperandrogenism.Elevated insulin leads to lower production of sex hormone binding globulin (SHBG), a regulatory glycoprotein that suppresses the function of androgens. High blood levels of insulin also work in conjunction with ovarian sensitivity to insulin to cause hyperandrogenemia, the primary symptom of PCOS. Obese individuals may be more biologically inclined to PCOS due to markedly higher insulin. This hormonal imbalance can lead to chronic anovulation, in which the ovaries fail to release mature eggs. These cases of ovulatory dysfunction are linked to infertility and menstrual disturbances. A post hoc analysis from a randomized, placebo-controlled, multi-centre study carried out at 11 secondary care centres, as well as a longitudinal single-centre study on pregnant women in Norway, also determined that metformin had no effect on maternal androgens in pregnancies occurring in the setting of PCOS.One systemic review suggested that polymorphisms in the vitamin D receptor gene are associated with the prognosis of polycystic ovary syndrome, though this is based on small sample sizes and is debated. Studies have shown benefits for vitamin D supplementation in women with vitamin D deficiency and PCOS.Hyperinsulinemia can increase the production of androgens in the ovaries. One context in which this occurs is HAIR-AN syndrome, a rare subtype of PCOS. Hyperthecosis and hyperinsulinemia Hyperthecosis occurs when the cells of the ovarian stroma transition from interstitial cells, located between other cells, into luteinized theca cells. Theca cells are located in the ovarian follicles and become luteinized when the ovarian follicle bursts and a new corpus luteum is formed. The dispersal of luteinized theca cells throughout the ovarian stroma — in contrast to their distribution in PCOS, in which luteinized theca cells occur around cystic follicles only — causes women with hyperthecosis to have higher testosterone levels and virilization) than women with PCOS. Elevated insulin is also characteristic of hyperthecosis. Hyperthecosis most commonly develops in postmenopausal women and is linked to acne, hirsutism, growth of the clitoris, baldness, and voice deepening.Obesity can play a role in insulin resistance. It makes thecal cells more responsive to luteinizing hormone. Therefore, obesity increases ovarian androgen production. Additionally, obesity elevates inflammatory adipokines which leads to not only adipogenesis, but also heightened insulin resistance. Cushing’s syndrome Cushings syndrome develops as a result of long-term exposure to the hormone cortisol. Cushings syndrome can either be exogenous or endogenous, depending on whether it is caused by an external or internal source, respectively. The intake of glucocorticoids, a type of corticosteroid, is a common cause for the development of exogenous Cushings syndrome. Endogenous Cushings syndrome can occur when the body produces excess cortisol. This occurs when the hypothalamus of the brain signals to the pituitary gland with excess corticotropin-releasing hormone, which in turn secretes adrenocorticotropin hormone (ACTH). ACTH then causes the adrenal glands to release cortisol into the blood. Signs of Cushings syndrome include muscle weakness, easy bruising, weight gain, male-pattern hair growth (hirsutism), coloured stretch marks, and an excessively reddish complexion in the face. Cushings syndrome can cause androgen excess and hence the signs and symptoms of hyperandrogenism. Congenital adrenal hyperplasia Congenital adrenal hyperplasia (CAH) describes a group of autosomal recessive disorders that cause a lack of an enzyme necessary for the production of cortisol and/or aldosterone, steroid hormones produced by the adrenal cortex. Most cases of CAH are due to 21-hydroxylase deficiencies. The heightened androgen levels seen in congenital adrenal hyperplasia affect the hypothalamic–pituitary–gonadal axis. Heightened androgen levels can also affect the ovaries, which can lead to infertility as well as chronic anovulation.Since CAH consists of multiple disorders, the signs, symptoms and severity of hyperandrogenism may stem from a variety of specific mutations. Genotyping is therefore critical to verify diagnoses and to establish prognostic factors for individuals. Genotyping is also crucial for people seeking to use genetic counselling as an aid to family planning.In women, CAH causes ambiguous genitals at birth and excessive pubic hair, enlargement of the clitoris, and hirsutism in adolescence. Although CAH causes rapid growth in childhood, adult women with CAH are shorter than average due to early puberty and closure of the growth plates in the long bones. Symptoms in males include early showings of pubic hair, enlargement of the penis, and rapid musculoskeletal growth. Tumors Adrenocortical carcinoma and tumors Adrenocortical carcinoma occurs rarely; the average incidence rate is estimated to be 1–2 cases per million annually. The disease involves the formation of cancerous cells within the cortex of one or both of the adrenal glands. Although these tumors are identified in fewer than two percent of patients diagnosed with hyperandrogenism, the possibility must be considered within this population. In one study, more than half of tumor-affected patients had elevated levels of the androgens androstenedione, dehydroepiandrosterone sulfate, and testosterone. The elevation of androgens caused by adrenocortical carcinomas often causes patients to develop Cushings syndrome, primary aldosteronism, and hyperandrogenism. The molecular basis of the disease has yet to be elucidated. Adenoma of the adrenal gland Adrenal adenomas are benign tumors of the adrenal gland. In most cases, the tumors display no symptoms and require no treatment. In rare cases, however, some adrenal adenomas may become activated. When activated, the adenoma begins to produce hormones in much larger quantities than what the adrenal glands would normally produce, leading to health complications including primary aldosteronism and hyperandrogenism. Arrhenoblastoma Arrhenoblastoma is an uncommon tumor of the ovary. It is composed of sterol cells, Leydig cells, or some combination of the two. The tumor can produce male or female hormones and may cause masculinization. In a prepubescent child, a tumor may cause precocious puberty. Malignant arrhenoblastoma accounts for 30% of cases of arrhenoblastoma, the other 70% being largely benign and curable with surgery. Hilar cell tumor A hilar cell tumor is an androgen-producing ovarian tumor that is most commonly found in older women and often leads to the development of male sex characteristics. The tumor tends to occur around the region of the ovary where the blood vessels enter the organ, known as the hilum. This type of tumor tends to be small in size and in most cases can be entirely removed and its symptoms reversed through surgery. Krukenberg tumor A Krukenberg tumor is a quickly developing malignant tumor found in one or both ovaries. In most cases, the tumor primarily originates from tissues in the stomach, pancreas, gallbladder, colon, or breast. It colonized the ovary by spreading through the peritoneal cavity. These tumors cause virilization. Increased androgen production due to elevations in human chorionic gonadotropin is hypothesized as the main cause of hyperandrogenism in people with Krukenberg tumors. Menopause The end of ovulation and the beginning of menopause can result in hyperandrogenism. During this transition, the body stops releasing estrogen at a faster rate than it stops releasing androgens. In some cases, the difference between the lower estrogen levels and higher androgen levels can produce hyperandrogenism. A decrease in sex hormone levels while the free androgen index increases can also contribute to this process. Drugs Many drugs can provoke symptoms of hyperandrogenism. These symptoms include, but are not limited to hirsutism, acne, dermatitis, androgenic alopecia, irregularities in menstruation, clitoral hypertrophy, and the deepening of the voice. Drugs most frequently implicated in hyperandrogenism include anabolic steroids, synthetic progestins, and antiepileptics; however, many other drugs may also cause hyperandrogenism. This can happen through one of five mechanisms: the direct introduction of androgens to the body, the binding of the drug to androgen receptors (as is the case with anabolic-androgenic steroids), a reduction of sex hormone-binding globulin plasma concentration that leads to an increase in free testosterone, interference with the hypothalamic–pituitary–ovarian (HPO) axis, or an increase in the release of adrenal androgens. Certain drugs cause hyperandrogenism through mechanisms that remain unclear. For example, the molecular basis by which valproate induces hyperandrogenism and polycystic ovary syndrome has yet to be determined. However, one study showed that women taking valproic acid had higher testosterone levels and incidences of hyperandrogenism compared to women who were not taking valproic acid. Heredity Hyperandrogenism can appear as a symptom of many different genetic and medical conditions. Some of the conditions with hyperandrogenic symptoms, including PCOS, may sometimes be hereditary. Additionally, it is thought that epigenetics may contribute to the pathogenesis of polycystic ovary syndrome.One potential cause of PCOS is maternal hyperandrogenism, whereby hormonal irregularities in the mother can affect the development of the child during gestation, resulting in the passing of polycystic ovary syndrome from mother to child. However, no androgen elevations in were found in the umbilical cord blood of children born to mothers with PCOS. Diagnosis Diagnosing hyperandrogenism can be complex due to the wide variety and severity of signs and symptoms that may present. It is most often diagnosed by checking for signs of hirsutism according to a standardized method that scores the range of excess hair growth.Girls may show symptoms of hyperandrogenism early in life, but physicians become more concerned when the patient is in her late teens or older.Checking medical history and a physical examination of symptoms are used for an initial diagnosis. Patient history assessed includes age at thelarche, adrenarche, and menarche; patterns of menstruation; obesity; reproductive history; and the start and advancement of hyperandrogenism symptoms. Patterns of menstruation are examined since irregular patterns may accompany hyperandrogenism. Other conditions that may present alongside hirsutism that can contribute to diagnosis include androgenic alopecia and acne. If hyperandrogenism is severe, virilization may occur.Family history is also assessed for occurrences of hyperandrogenism symptoms or obesity in other family members.Laboratory tests can measure FSH, luteininzing hormone, DHEAS, prolactin, 17α-hydroxyprogesterone, and total and free testosterone in the blood. Abnormally high levels of any of these hormones help in diagnosing hyperandrogenism. Prevention Since risk factors are not known and vary among individuals with hyperandrogenism, there is no sure method to prevent the condition. Accordingly, more long-term studies are needed to find a cause of the condition before a sufficient method of prevention can be established.Despite this, there are a few things that can help avoid long-term medical issues related to hyperandrogenism and PCOS. Getting checked by a medical professional for hyperandrogenism — especially if one has a family history of the condition, irregular periods, or diabetes — can be beneficial. A healthy weight and diet may reduce the chances, as continued exercise and a healthy diet lead to an improved menstrual cycle, decreased insulin levels, and lowered androgen concentrations. Treatment There is no definitive treatment for hyperandrogenism as it varies with the underlying condition that causes it. As a hormonal symptom of PCOS, menopause, and other endocrine conditions, it is primarily treated as a symptom of these conditions. Drugs may be considered only in women who do not plan on becoming pregnant in the near future. Some effective drugs for facial hirsutism includes eflornithine, which may cause birth defects in pregnant women. Retinoids and antibiotics can be used for acne and minoxidil for alopecia. Systemically, it is treated with antiandrogens such as cyproterone acetate, flutamide and spironolactone to reduce androgenic signaling. For hyperandrogenism caused by late-onset congenital adrenal hyperplasia (LOCAH), treatment is primarily focused on providing the patient with glucocorticoids to combat the low cortisol production and the corresponding increase in androgens caused by the increase in size of the adrenal glands. Estrogen-based oral contraceptives are used to treat both LOCAH- and PCOS-associated hyperandrogenism. These hormonal treatments reduce the androgen excess and suppress adrenal androgen production, bringing about a significant decrease in hirsutism.Hyperandrogenism is often managed symptomatically. Hirsutism and acne both respond well to the hormonal treatments described above, with 60–100% of patients reporting an improvement in hirsutism. Androgenic alopecia however, does not show an improvement with hormonal treatments and requires other treatments, such as hair transplantation.Supplementation can also contribute to the managing the symptomatic effects of hyperandrogenism. In a meta-analysis, high-dose vitamin D supplements given to women with vitamin D deficiency due to PCOS improved glucose levels, insulin sensitivity, and cholesterol levels, as well as lowering testosterone, sex hormone-binding globulin, and the free androgen index, all of which are associated with hyperandrogenism. Vitamin D supplementation in women with vitamin D deficiency but without PCOS did not show the same results. Targeting insulin resistance and obesity Lifestyle modifications are the first-line treatment for PCOS. They help improve body composition, insulin resistance, and hyperandrogenism. However, it is unclear whether they help improve mood, quality of life, and reproductive outcomes. A meta-analysis study in 2017 showed that bariatric surgery in women with severe obesity and PCOS decreased levels of total and free testosterone and helped correct hirsutism and menstrual dysfunction.Insulin resistance in women with PCOS is typically treated with insulin-sensitizer drugs such as metformin. Metformin can help to decrease weight and androgen levels. When combined with lifestyle modifications (changes in diet and exercise), it has been linked with lower body mass index and a reduction in menstrual problems. However, the use of metformin in women with PCOS should only be considered in patients with impaired glucose tolerance. Society and culture Because androgen excess is manifested in noticeable physical features (such as hirsutism), social stigma may be associated with it. Sports Current evidence-based studies show that unusually high levels of circulating testosterone are associated with increased athletic performance in women, unless they lack androgen sensitivity. However, controversy has emerged in the form of the claim that testosterone is not unlike any other physical parameter with reference to bestowing advantages or disadvantages on female athletes. Existing regulations throughout competitive sports are currently being refined to specifically address this particular claim. Following the case of South African athlete Caster Semenya, an athlete with a difference in sex development (DSD), the International Association of Athletics Federations introduced its hyperandrogenism regulations, which restricted women with high testosterone levels, whether the hormones were produced by ovaries, adrenals, or testes. These regulations replaced the earlier sex verification rules.Following a series of legal challenges, regulations called the Eligibility Regulations for the Female Classification (Athletes with Differences of Sexual Development) were released on 1 May 2019. These regulations apply only to athletes who have a DSD, high testosterone and virilization, and no longer include hyperandrogenism from non-DSD-related causes such as PCOS. Such DSDs, often seen in people who have a Y chromosome and testes, include 5α‐reductase deficiency, partial androgen insensitivity, and congenital adrenal hyperplasia. Social definition Cultural variation can define hyperandrogenism socially—apart from clinical and chemical definitions—to make some hair growth unacceptable even if it is considered clinically normal based on metrics like the Ferriman-Gallwey score. For example, only pubic and axillary hair may be tolerated in North American women, while other androgen-dependent hair such as growth on the upper lip, over the linea alba, on the thighs, and around the areola is not. Organizations Professional organizations such as the Androgen Excess and PCOS Society exist to promote the research, treatment, diagnosis, and prevention of such disorders and to educate the public and scientific community about them. See also Hypoandrogenism Hypergonadism Hypergonadotropic hypergonadism Hypogonadism Hyperestrogenism Hypoestrogenism Androgen-dependent condition References == External links ==

Hi Aarogya, could you help me understand about Mucositis

Mucositis

Mucositis is the painful inflammation and ulceration of the mucous membranes lining the digestive tract, usually as an adverse effect of chemotherapy and radiotherapy treatment for cancer. Mucositis can occur anywhere along the gastrointestinal (GI) tract, but oral mucositis refers to the particular inflammation and ulceration that occurs in the mouth. Oral mucositis is a common and often debilitating complication of cancer treatment.Oral and gastrointestinal (GI) mucositis affects almost all patients undergoing high-dose chemotherapy and hematopoietic stem cell transplantation (HSCT), 80% of patients with malignancies of the head and neck receiving radiotherapy, and a wide range of patients receiving chemotherapy. Alimentary tract mucositis increases mortality and morbidity and contributes to rising health care costs.For most cancer treatment, about 5–15% of patients get mucositis. However, with 5-fluorouracil (5-FU), up to 40% get mucositis, and 10–15% get grade 3–4 oral mucositis. Irinotecan is associated with severe GI mucositis in over 20% of patients. Seventy-five to eighty percent of bone marrow transplantation recipients experience mucositis, of which oral mucositis is the most common and most debilitating, especially when melphalan is used. In grade 3 oral mucositis, the patient is unable to eat solid food, and in grade 4, the patient is unable to consume liquids as well.Radiotherapy to the head and neck or to the pelvis or abdomen is associated with Grade 3 and Grade 4 oral or GI mucositis, respectively, often exceeding 50% of patients. Among patients undergoing head and neck radiotherapy, pain and decreased oral function may persist long after the conclusion of therapy. Fractionated radiation dosage increases the risk of mucositis to > 70% of patients in most trials. Oral mucositis is particularly profound and prolonged among HSCT recipients who receive total-body irradiation. Signs and symptoms Cancer patients undergoing chemotherapy usually become symptomatic four to five days after beginning treatment, reaching a peak at around day 10, and then slowly improving over the course of a few weeks. Mucositis associated with radiotherapy usually appears at the end of the second week of treatment and may last for six to eight weeks.As a result of cell death in reaction to chemo- or radio-therapy, the mucosal lining of the mouth becomes thin, may slough off and then become red, inflamed and ulcerated. The ulcers may become covered by a yellowish-white fibrin clot called a pseudomembrane. Peripheral erythema is usually present. Ulcers may range from 0.5 cm to greater than 4 cm. Oral mucositis can be severely painful. The degree of pain is usually related to the extent of the tissue damage. Pain is often described as a burning sensation accompanied by reddening. Due to pain, the patient may experience trouble speaking, eating, or even opening the mouth.Dysgeusia, or an alteration in taste perception, is common, especially for those who are receiving concomitant radiation therapy to the neck and mouth area. "Taste blindness", or an altered sense of taste, is a temporary condition that occurs because of effects on taste buds that are mostly located in the tongue. Sometimes, only partial recovery of taste occurs. Common complaints are of food tasting too sweet or too bitter or of a continuous metallic taste. Complications Sores or ulcerations can become infected by virus, bacteria or fungus. Pain and loss of taste perception makes it more difficult to eat, which leads to weight loss. Ulcers may act as a site for local infection and a portal of entry for oral flora that, in some instances, may cause septicaemia (especially in immunosuppressed patients). Therefore, oral mucositis can be a dose-limiting condition, disrupting a patient’s optimal cancer treatment plan and consequentially decreasing their chances of survival. Pathophysiology The pathophysiology of mucositis is complex and multifactorial. Currently, Sonis five phase model is the accepted explanation for the process. The 5 stages are: Initiation phase. Free radicals are produced due to DNA damage caused by chemo- or radiotherapy. Primary damage response. Chemotherapy, radiotherapy and free radicals all contribute to the activation of transcription factors, such as NF-κB. This results in the upregulation of pro-inflammatory cytokines, ceramide, nitric oxide and matrix metalloproteinases. The consequence of this is mucosal destruction, caused by thinning of the epithelium due to tissue injury and cell death. Signal amplification. Positive or negative feedback loops involving some of the molecules in the previous phase can exacerbate or prolong tissue injury. For example, the pro-inflammatory cytokine TNF-α can positively feedback on NF-κB thus inducing more pro-inflammatory cytokine production. Ulceration. Bacteria colonise ulcers and their cell wall products infiltrate the submucosa. This leads to activation of tissue macrophages, which causes further production of pro-inflammatory cytokines. In addition, bacteria-mediated immune signalling via Toll-like receptors (TLRs) ambiguously shapes chemotherapy-induced genotoxic damage in the gastrointestinal tract. Healing. Signalling from the extracellular matrix of the submucosa results in epithelial proliferation and differentiation, and thus a thickening of the epithelium. The local oral flora are reinstated. Diagnosis Diagnosis is based on the symptoms the patient is experiencing and the appearance of the tissues of the mouth following chemotherapy, bone marrow transplants or radiotherapy. Red burn-like sores or ulcers throughout the mouth is enough to diagnose mucositis.The severity of oral mucositis can be evaluated using several different assessment tools. Two of the most commonly used are the World Health Organization (WHO) Oral Toxicity score and the National Cancer Institute Common Toxicity Criteria (NCI-CTC) for Oral Mucositis. While the NCI system has separate scores for appearance (erythema and ulceration) and function (pain and ability to eat solids, liquids, or nothing by mouth), the WHO score combines both elements into a single score that grades the severity of the condition from 0 (no oral mucositis) to 4 (swallowing not possible such that patient needs supplementary nutrition). Another scale developed in 1999, the Oral Mucositis Assessment Scale (OMAS) has been shown to be highly reproducible between observers, responsive over time, and accurate in recording symptoms associated with mucositis. The OMAS provides an objective assessment of oral mucositis based on assessment of the appearance and extent of redness and ulceration in various areas of the mouth. Prevention A 2015 Cochrane systematic review assessing the prevention of chemotherapy-induced oral mucositis concluded that oral cryotherapy leads to large reductions in the incidence of oral mucositis of all severities in adults receiving 5-FU treatment for solid cancers. The evidence also indicates a reduction of oral mucositis in adults receiving high-dose melphalan-based cancer treatment prior to haematopoietic stem cell transplantation, although there is uncertainty regarding the size of the reduction in this instance. No evidence was found for use of this preventive measure in children. Oral cryotherapy involves the placement of rounded ice chips in the mouth, which cools the oral tissues and causes vasoconstriction. This decreases blood flow to the region and, hence, also restricts the amounts of the chemotherapy drugs delivered to the tissues. Treatment Treatment of mucositis is mainly supportive. Oral hygiene is the mainstay of treatment; patients are encouraged to clean their mouth every four hours and at bedtime, more often if the mucositis becomes worse.Water-soluble jellies can be used to lubricate the mouth. Salt mouthwash can soothe the pain and keep food particles clear so as to avoid infection. Patients are also encouraged to drink plenty of liquids, at least three liters a day, and avoid alcohol. Citrus fruits, alcohol, and foods that are hot are all known to aggravate mucositis lesions. Medicinal mouthwashes may be used such as Chlorhexidine gluconate and viscous Lidocaine for relief of pain. However, care should be taken as the high doses of viscous lidocaine my cause adverse effects. A study reported that lidocaine has a potential toxicity; when it was tested on patients with oral mucositis who underwent a bone marrow transplant, lidocaine anesthetic mouthwash was found to be systemically absorbed.Palifermin is a human KGF (keratinocyte growth factor) that has shown to enhance epithelial cell proliferation, differentiation, and migration. Experimental therapies have been reported, including the use of cytokines and other modifiers of inflammation (e.g., IL-1, IL-11, TGF-beta3), amino acid supplementation (e.g., glutamine), vitamins, colony-stimulating factors, cryotherapy, and laser therapy.Symptomatic relief of the pain of oral mucositis may be provided by barrier protection agents such as concentrated oral gel products (e.g. Gelclair). Caphosol is a mouth rinse which has been shown to prevent and treat oral mucositis caused by radiation and high-dose chemotherapy. MuGard is a FDA-cleared mucoadhesive oral protectant, developed by Access Pharmaceuticals, Inc., that is designed to form a protective hydrogel coating over the oral mucosa while a patient is undergoing chemotherapy and/or radiotherapy cancer treatments to the head and neck. Additionally, the efficacy of MuGard for the prevention or treatment of mucositis has been tested by a prospective, randomized clinical trial in which 43% of head and neck cancer patients using MuGard prophylactically never got oral mucositis. NeutraSal is an FDA-cleared calcium phosphate mouth rinse that has been shown in an open-label, observational registry trial to prevent and reduce the severity of oral mucositis caused by radiation and high-dose chemotherapy. In the trial, 56% of the radiotherapy patients reported 0 (WHO score) or no mucositis, which is significantly lower than historical rates. Another super saturated calcium phosphate rinse on the market and cleared by the FDA is the US based SalivaMAX. The Mayo Clinic has been testing the antidepressant doxepin in a mouthwash to help treat symptoms.In 2011, the FDA cleared episil oral liquid for the management and relief of pain of oral lesions with various etiologies, including oral mucositis/stomatitis which may be caused by chemotherapy or radiation therapy. The transformative mechanism of action of episil creates a lipid membrane that mechanically bonds to the oral cavity mucosa to coat and soothe inflammation and ulcerations, and blanket painful lesions. In a multicenter, randomized, double-blind, single-dose study involving 38 head and neck cancer patients with oral mucositis (WHO grades 2-3) undergoing radiation therapy, episil clinically demonstrated fast-acting relief that lasted up to 8 hours. Episil oral liquid is marketed in the US by Cangene. In a 2012 randomized controlled pilot study involving pediatric patients, topical application of honey was found to reduce recovery time compared to benzocaine gel in grade 2 and 3 chemotherapy-induced oral mucositis to a degree that was statistically significant. In grade 3 oral mucositis, honey was as effective as a mixture of honey, olive oil and propolis, while both treatments were found to reduce recovery time compared to the benzocaine control.Clinical research is ongoing in oral mucositis. A recent phase 2 exploratory trial in oral mucositis reported that dusquetide, a unique innate immune modulator with a mechanism that potentially addresses each of the phases of OM pathophysiology, is able to reduce the duration of severe oral mucositis, as well as reducing the incidence of infection See also Stomatitis References General sources Mucositis Resource Center of the MASCC/ISOO Mucositis Study Group. Medical journal articles, guidelines, recommendations, and slides and videos from conference presentations. == External links ==

What does Hermansky–Pudlak syndrome mean Aarogya

Hermansky–Pudlak syndrome

Heřmanský–Pudlák syndrome (often written Hermansky–Pudlak syndrome or abbreviated HPS) is an extremely rare autosomal recessive disorder which results in oculocutaneous albinism (decreased pigmentation), bleeding problems due to a platelet abnormality (platelet storage pool defect), and storage of an abnormal fat-protein compound (lysosomal accumulation of ceroid lipofuscin). It is considered to affect around 1 in 500,000 people worldwide, with a significantly higher occurrence in Puerto Ricans, with a prevalence of 1 in 1800. Many of the clinical research studies on the disease have been conducted in Puerto Rico. There are eight classic forms of the disorder, based on the genetic mutation from which the disorder stems. Signs and symptoms There are three main disorders caused by Hermansky–Pudlak syndrome, which result in these symptoms: Albinism and eye problems: Individuals will have varying amounts of skin pigment (melanin). Because of the albinism there are eye problems such as light sensitivity (photophobia), strabismus (crossed eyes), and nystagmus (involuntary eye movements). Hermansky–Pudlak syndrome also impairs vision. Bleeding disorders: Individuals with the syndrome have platelet dysfunction. Since platelets are necessary for blood clotting, individuals will bruise and bleed easily. Cellular storage disorders: The syndrome causes a wax-like substance (ceroid) to accumulate in the body tissues and cause damage, especially in the lungs and kidneys.It is also associated with granulomatous colitis,, an inflammation of the colon, and with pulmonary fibrosis, a potentially fatal lung disease. Causes HPS can be caused by mutations in several genes: HPS1, HPS3, HPS4, HPS5, HPS6 and HPS7.HPS type 2, which includes immunodeficiency in its phenotype, is caused by mutation in the AP3B1 gene.HPS type 7 may result from a mutation in the gene coding for dysbindin protein.Hermansky–Pudlak syndrome is thought to be inherited as an autosomal recessive genetic trait. The defective gene, called HSP, responsible for this disorder is located on the long arm of chromosome 10 (10q2). Some research suggests that an abnormality of lysosomal function may be responsible for the development of the disease. HPS1, AP3B1, HPS3, HPS4, HPS5, HPS6, DTNBP1 and Biogenesis of Lysosome-related Organelles Complex (BLOC1, BLOC1S2 and BLOC3) are associated with Hermansky–Pudlak syndrome.In autosomal recessive disorders, the condition does not appear unless a person inherits two copies of the defective gene responsible for the disorder, one copy coming from each parent. If an individual receives one normal gene and one gene for the disorder, the person will be a carrier for the disease, but usually will not show symptoms. The risk of transmitting the disease to the children of a couple, both of whom are carriers for a recessive disorder, is 25 percent. Fifty percent of their children risk being carriers of the disease, but generally will not show symptoms of the disorder. Twenty-five percent of their children may receive both normal genes, one from each parent, and will be genetically normal (for that particular trait). The risk is the same for each pregnancy. Pathophysiology The mechanism of Hermansky–Pudlak syndrome indicates that platelets in affected individuals accumulate abnormally with thrombin, epinephrine, and adenosine diphosphate, furthermore platelets in these individuals have a lower amount of dense bodies Diagnosis The diagnosis of HPS is established by clinical findings of hypopigmentation of the skin and hair, characteristic eye findings, and demonstration of absent dense bodies on whole mount electron microscopy of platelets. Molecular genetic testing of the HPS1 gene is available on a clinical basis for individuals from northwestern Puerto Rico. Molecular testing of the HPS3 gene is available on a clinical basis for individuals of central Puerto Rican or Ashkenazi Jewish heritage. Sequence analysis is available on a clinical basis for mutations in HPS1 and HPS4. Diagnosis of individuals with other types of HPS is available on a research basis only. Treatment While there is no cure for HPS, treatment for chronic hemorrhages associated with the disorder includes therapy with vitamin E and the antidiuretic dDAVP. Considerations for patients A preoperative pulmonology consultation is needed. The anesthesia team should be aware that patients may have postoperative pulmonary complications as part of the syndrome.Preoperative hematology consultation is advisable prior to elective ocular surgeries. Since patients with the syndrome have bleeding tendencies, intraoperative, perioperative, and postoperative hemorrhages should be prevented and treated. If platelet aggregation improves with desmopressin, it may be administered in the preoperative period. However, sometimes plasmapheresis is needed in the perioperative period.Ophthalmologists should try to avoid retrobulbar blocks in patients with the syndrome. Whenever possible, patients with HPS may benefit from general endotracheal anesthesia. Phacoemulsification may help prevent intraoperative and postoperative bleeding in patients with the syndrome. Prolonged bleeding has been reported following strabismus surgery in patients with the syndrome. Prognosis The course of HPS has been mild in rare instances of the disorder, however, the general prognosis is still considered to be poor.The disease can cause dysfunctions of the lungs, intestine, kidneys, and heart. The major complication of most forms of the disorder is pulmonary fibrosis, which typically exhibits in patients ages 40–50 years. This is a fatal complication seen in many forms of HPS, and is the usual cause of death from the disorder. HPS patients who develop pulmonary fibrosis typically have type 1 or type 4. Research HPS is one of the rare lung diseases currently being studied by The Rare Lung Diseases Consortium (RLDC). The RLDC is part of the Rare Diseases Clinical Research Network (RDCRN), an initiative of the Office of Rare Diseases Research (ORDR), of the National Center for Advancing Translational Sciences (NCATS). The RLDC is dedicated to developing new diagnostics and therapeutics for patients with rare lung diseases, through collaboration between the NIH, patient organizations and clinical investigators. Eponym It is named for František Heřmanský (1916–1980) and Pavel Pudlák (1927–1993). See also Biogenesis of lysosome-related organelles complex 1 List of cutaneous conditions References External links GeneReviews/NCBI/NIH/UW entry on Hermansky-Pudlak Syndrome

Aarogya, Please give me a short description about Vehicle

Vehicle

A vehicle (from Latin: vehiculum) is a machine that transports people or cargo. Vehicles include wagons, bicycles, motor vehicles (motorcycles, cars, trucks, buses, mobility scooters for disabled people), railed vehicles (trains, trams), watercraft (ships, boats, underwater vehicles), amphibious vehicles (screw-propelled vehicles, hovercraft), aircraft (airplanes, helicopters, aerostats) and spacecraft.Land vehicles are classified broadly by what is used to apply steering and drive forces against the ground: wheeled, tracked, railed or skied. ISO 3833-1977 is the standard, also internationally used in legislation, for road vehicles types, terms and definitions. History The oldest boats found by archaeological excavation are logboats, with the oldest logboat found, the Pesse canoe found in a bog in the Netherlands, being carbon dated to 8040 - 7510 BC, making it 9,500–10,000 years old, a 7,000-year-old seagoing boat made from reeds and tar has been found in Kuwait. Boats were used between 4000 -3000 BC in Sumer, ancient Egypt and in the Indian Ocean. There is evidence of camel pulled wheeled vehicles about 4000–3000 BC. The earliest evidence of a wagonway, a predecessor of the railway, found so far was the 6 to 8.5 km (4 to 5 mi) long Diolkos wagonway, which transported boats across the Isthmus of Corinth in Greece since around 600 BC. Wheeled vehicles pulled by men and animals ran in grooves in limestone, which provided the track element, preventing the wagons from leaving the intended route. In 200 CE, Ma Jun built a south-pointing chariot, a vehicle with an early form of guidance system. Railways began reappearing in Europe after the Dark Ages. The earliest known record of a railway in Europe from this period is a stained-glass window in the Minster of Freiburg im Breisgau dating from around 1350. In 1515, Cardinal Matthäus Lang wrote a description of the Reisszug, a funicular railway at the Hohensalzburg Fortress in Austria. The line originally used wooden rails and a hemp haulage rope and was operated by human or animal power, through a treadwheel. 1769 Nicolas-Joseph Cugnot is often credited with building the first self-propelled mechanical vehicle or automobile in 1769. In Russia, in the 1780s, Ivan Kulibin developed a human-pedalled, three-wheeled carriage with modern features such as a flywheel, brake, gear box and bearings; however, it was not developed further. 1783 Montgolfier brothers first balloon vehicle 1801 Richard Trevithick built and demonstrated his Puffing Devil road locomotive, which many believe was the first demonstration of a steam-powered road vehicle, though it could not maintain sufficient steam pressure for long periods and was of little practical use. 1817 Push bikes, draisines or hobby horses were the first human means of transport to make use of the two-wheeler principle, the draisienne (or Laufmaschine, "running machine"), invented by the German Baron Karl von Drais, is regarded as the forerunner of the modern bicycle (and motorcycle). It was introduced by Drais to the public in Mannheim in summer 1817. 1885 Karl Benz built (and subsequently patented) the first automobile, powered by his own four-stroke cycle gasoline engine in Mannheim, Germany 1885 Otto Lilienthal began experimental gliding and achieved the first sustained, controlled, reproducible flights. 1903 Wright brothers flew the first controlled, powered aircraft 1907 First helicopters Gyroplane no.1 (tethered) and Cornu helicopter (free flight) 1928 Opel RAK.1 rocket car 1929 Opel RAK.1 rocket glider 1961 Vostok vehicle carried the first human, Yuri Gagarin, into space 1969 Apollo Program first crewed vehicle landed on the moon 2010 The number of road motor vehicles in operation worldwide surpassed the 1 billion mark – roughly one for every seven people. Types of vehicles There are over 1 billion bicycles in use worldwide. In 2002 there were an estimated 590 million cars and 205 million motorcycles in service in the world. At least 500 million Chinese Flying Pigeon bicycles have been made, more than any other single model of vehicle. The most-produced model of motor vehicle is the Honda Super Cub motorcycle, having passed 60 million units in 2008. The most-produced car model is the Toyota Corolla, with at least 35 million made by 2010. The most common fixed-wing airplane is the Cessna 172, with about 44,000 having been made as of 2017. The Soviet Mil Mi-8, at 17,000, is the most-produced helicopter. The top commercial jet airliner is the Boeing 737, at about 10,000 in 2018. At around 14,000 for both, the most produced trams are the KTM-5 and Tatra T3. The most common trolleybus is ZiU-9. Locomotion Locomotion consists of a means that allows displacement with little opposition, a power source to provide the required kinetic energy and a means to control the motion, such as a brake and steering system. By far, most vehicles use wheels which employ the principle of rolling to enable displacement with very little rolling friction. Energy source It is essential that a vehicle have a source of energy to drive it. Energy can be extracted from external sources, as in the cases of a sailboat, a solar-powered car, or an electric streetcar that uses overhead lines. Energy can also be stored, provided it can be converted on demand and the storing mediums energy density and power density are sufficient to meet the vehicles needs. Human power is a simple source of energy that requires nothing more than humans. Despite the fact that humans cannot exceed 500 W (0.67 hp) for meaningful amounts of time, the land speed record for human-powered vehicles (unpaced) is 133 km/h (83 mph), as of 2009 on a recumbent bicycle.The most common type of energy source is fuel. External combustion engines can use almost anything that burns as fuel, whilst internal combustion engines and rocket engines are designed to burn a specific fuel, typically gasoline, diesel or ethanol. Another common medium for storing energy is batteries, which have the advantages of being responsive, useful in a wide range of power levels, environmentally friendly, efficient, simple to install, and easy to maintain. Batteries also facilitate the use of electric motors, which have their own advantages. On the other hand, batteries have low energy densities, short service life, poor performance at extreme temperatures, long charging times, and difficulties with disposal (although they can usually be recycled). Like fuel, batteries store chemical energy and can cause burns and poisoning in event of an accident. Batteries also lose effectiveness with time. The issue of charge time can be resolved by swapping discharged batteries with charged ones; however, this incurs additional hardware costs and may be impractical for larger batteries. Moreover, there must be standard batteries for battery swapping to work at a gas station. Fuel cells are similar to batteries in that they convert from chemical to electrical energy, but have their own advantages and disadvantages. Electrified rails and overhead cables are a common source of electrical energy on subways, railways, trams, and trolleybuses. Solar energy is a more modern development, and several solar vehicles have been successfully built and tested, including Helios, a solar-powered aircraft. Nuclear power is a more exclusive form of energy storage, currently limited to large ships and submarines, mostly military. Nuclear energy can be released by a nuclear reactor, nuclear battery, or repeatedly detonating nuclear bombs. There have been two experiments with nuclear-powered aircraft, the Tupolev Tu-119 and the Convair X-6. Mechanical strain is another method of storing energy, whereby an elastic band or metal spring is deformed and releases energy as it is allowed to return to its ground state. Systems employing elastic materials suffer from hysteresis, and metal springs are too dense to be useful in many cases.Flywheels store energy in a spinning mass. Because a light and fast rotor is energetically favorable, flywheels can pose a significant safety hazard. Moreover, flywheels leak energy fairly quickly and affect a vehicles steering through the gyroscopic effect. They have been used experimentally in gyrobuses. Wind energy is used by sailboats and land yachts as the primary source of energy. It is very cheap and fairly easy to use, the main issues being dependence on weather and upwind performance. Balloons also rely on the wind to move horizontally. Aircraft flying in the jet stream may get a boost from high altitude winds. Compressed gas is currently an experimental method of storing energy. In this case, compressed gas is simply stored in a tank and released when necessary. Like elastics, they have hysteresis losses when gas heats up during compression. Gravitational potential energy is a form of energy used in gliders, skis, bobsleds and numerous other vehicles that go down hill. Regenerative braking is an example of capturing kinetic energy where the brakes of a vehicle are augmented with a generator or other means of extracting energy. Motors and engines When needed, the energy is taken from the source and consumed by one or more motors or engines. Sometimes there is an intermediate medium, such as the batteries of a diesel submarine.Most motor vehicles have internal combustion engines. They are fairly cheap, easy to maintain, reliable, safe and small. Since these engines burn fuel, they have long ranges but pollute the environment. A related engine is the external combustion engine. An example of this is the steam engine. Aside from fuel, steam engines also need water, making them impractical for some purposes. Steam engines also need time to warm up, whereas IC engines can usually run right after being started, although this may not be recommended in cold conditions. Steam engines burning coal release sulfur into the air, causing harmful acid rain. While intermittent internal combustion engines were once the primary means of aircraft propulsion, they have been largely superseded by continuous internal combustion engines: gas turbines. Turbine engines are light and, particularly when used on aircraft, efficient. On the other hand, they cost more and require careful maintenance. They can also be damaged by ingesting foreign objects, and they produce a hot exhaust. Trains using turbines are called gas turbine-electric locomotives. Examples of surface vehicles using turbines are M1 Abrams, MTT Turbine SUPERBIKE and the Millennium. Pulse jet engines are similar in many ways to turbojets, but have almost no moving parts. For this reason, they were very appealing to vehicle designers in the past; however their noise, heat and inefficiency has led to their abandonment. A historical example of the use of a pulse jet was the V-1 flying bomb. Pulse jets are still occasionally used in amateur experiments. With the advent of modern technology, the pulse detonation engine has become practical and was successfully tested on a Rutan VariEze. While the pulse detonation engine is much more efficient than the pulse jet and even turbine engines, it still suffers from extreme noise and vibration levels. Ramjets also have few moving parts, but they only work at high speed, so that their use is restricted to tip jet helicopters and high speed aircraft such as the Lockheed SR-71 Blackbird.Rocket engines are primarily used on rockets, rocket sleds and experimental aircraft. Rocket engines are extremely powerful. The heaviest vehicle ever to leave the ground, the Saturn V rocket, was powered by five F-1 rocket engines generating a combined 180 million horsepower (134.2 gigawatt). Rocket engines also have no need to "push off" anything, a fact that the New York Times denied in error. Rocket engines can be particularly simple, sometimes consisting of nothing more than a catalyst, as in the case of a hydrogen peroxide rocket. This makes them an attractive option for vehicles such as jet packs. Despite their simplicity, rocket engines are often dangerous and susceptible to explosions. The fuel they run off may be flammable, poisonous, corrosive or cryogenic. They also suffer from poor efficiency. For these reasons, rocket engines are only used when absolutely necessary.Electric motors are used in electric vehicles such as electric bicycles, electric scooters, small boats, subways, trains, trolleybuses, trams and experimental aircraft. Electric motors can be very efficient: over 90% efficiency is common. Electric motors can also be built to be powerful, reliable, low-maintenance and of any size. Electric motors can deliver a range of speeds and torques without necessarily using a gearbox (although it may be more economical to use one). Electric motors are limited in their use chiefly by the difficulty of supplying electricity.Compressed gas motors have been used on some vehicles experimentally. They are simple, efficient, safe, cheap, reliable and operate in a variety of conditions. One of the difficulties met when using gas motors is the cooling effect of expanding gas. These engines are limited by how quickly they absorb heat from their surroundings. The cooling effect can, however, double as air conditioning. Compressed gas motors also lose effectiveness with falling gas pressure.Ion thrusters are used on some satellites and spacecraft. They are only effective in a vacuum, which limits their use to spaceborne vehicles. Ion thrusters run primarily off electricity, but they also need a propellant such as caesium, or more recently xenon. Ion thrusters can achieve extremely high speeds and use little propellant; however they are power-hungry. Converting energy to work The mechanical energy that motors and engines produce must be converted to work by wheels, propellers, nozzles, or similar means. Aside from converting mechanical energy into motion, wheels allow a vehicle to roll along a surface and, with the exception of railed vehicles, to be steered. Wheels are ancient technology, with specimens being discovered from over 5000 years ago. Wheels are used in a plethora of vehicles, including motor vehicles, armoured personnel carriers, amphibious vehicles, airplanes, trains, skateboards and wheelbarrows. Nozzles are used in conjunction with almost all reaction engines. Vehicles using nozzles include jet aircraft, rockets and personal watercraft. While most nozzles take the shape of a cone or bell, some unorthodox designs have been created such as the aerospike. Some nozzles are intangible, such as the electromagnetic field nozzle of a vectored ion thruster.Continuous track is sometimes used instead of wheels to power land vehicles. Continuous track has the advantages of a larger contact area, easy repairs on small damage, and high maneuverability. Examples of vehicles using continuous track are tanks, snowmobiles and excavators. Two continuous tracks used together allow for steering. The largest vehicle in the world, the Bagger 288, is propelled by continuous tracks. Propellers (as well as screws, fans and rotors) are used to move through a fluid. Propellers have been used as toys since ancient times, however it was Leonardo da Vinci who devised what was one of the earliest propeller driven vehicles, the "aerial-screw". In 1661, Toogood & Hays adopted the screw for use as a ship propeller. Since then, the propeller has been tested on many terrestrial vehicles, including the Schienenzeppelin train and numerous cars. In modern times, propellers are most prevalent on watercraft and aircraft, as well as some amphibious vehicles such as hovercraft and ground-effect vehicles. Intuitively, propellers cannot work in space as there is no working fluid, however some sources have suggested that since space is never empty, a propeller could be made to work in space.Similarly to propeller vehicles, some vehicles use wings for propulsion. Sailboats and sailplanes are propelled by the forward component of lift generated by their sails/wings. Ornithopters also produce thrust aerodynamically. Ornithopters with large rounded leading edges produce lift by leading-edge suction forces. Research at the University of Toronto Institute for Aerospace Studies lead to a flight with an actual ornithopter on July 31, 2010. Paddle wheels are used on some older watercraft and their reconstructions. These ships were known as paddle steamers. Because paddle wheels simply push against the water, their design and construction is very simple. The oldest such ship in scheduled service is the Skibladner. Many pedalo boats also use paddle wheels for propulsion. Screw-propelled vehicles are propelled by auger-like cylinders fitted with helical flanges. Because they can produce thrust on both land and water, they are commonly used on all-terrain vehicles. The ZiL-2906 was a Soviet-designed screw-propelled vehicle designed to retrieve cosmonauts from the Siberian wilderness. Friction All or almost all of the useful energy produced by the engine is usually dissipated as friction; so minimising frictional losses is very important in many vehicles. The main sources of friction are rolling friction and fluid drag (air drag or water drag). Wheels have low bearing friction and pneumatic tyres give low rolling friction. Steel wheels on steel tracks are lower still.Aerodynamic drag can be reduced by streamlined design features. Friction is desirable and important in supplying traction to facilitate motion on land. Most land vehicles rely on friction for accelerating, decelerating and changing direction. Sudden reductions in traction can cause loss of control and accidents. Control Steering Most vehicles, with the notable exception of railed vehicles, have at least one steering mechanism. Wheeled vehicles steer by angling their front or rear wheels. The B-52 Stratofortress has a special arrangement in which all four main wheels can be angled. Skids can also be used to steer by angling them, as in the case of a snowmobile. Ships, boats, submarines, dirigibles and aeroplanes usually have a rudder for steering. On an airplane, ailerons are used to bank the airplane for directional control, sometimes assisted by the rudder. Stopping With no power applied, most vehicles come to a stop due to friction. But it is often required to stop a vehicle faster than by friction alone: so almost all vehicles are equipped with a braking system. Wheeled vehicles are typically equipped with friction brakes, which use the friction between brake pads (stators) and brake rotors to slow the vehicle. Many airplanes have high performance versions of the same system in their landing gear for use on the ground. A Boeing 757 brake, for example, has 3 stators and 4 rotors. The Space Shuttle also uses frictional brakes on its wheels. As well as frictional brakes, hybrid/electric cars, trolleybuses and electric bicycles can also use regenerative brakes to recycle some of the vehicles potential energy. High-speed trains sometimes use frictionless Eddy-current brakes; however widespread application of the technology has been limited by overheating and interference issues.Aside from landing gear brakes, most large aircraft have other ways of decelerating. In aircraft, air brakes are aerodynamic surfaces that provide braking force by increasing the frontal cross section thus aerodynamic drag of the aircraft. These are usually implemented as flaps that oppose air flow when extended and are flush with aircraft when retracted. Reverse thrust is also used in many aeroplane engines. Propeller aircraft achieve reverse thrust by reversing the pitch of the propellers, while jet aircraft do so by redirecting their engine exhaust forwards. On aircraft carriers, arresting gears are used to stop an aircraft. Pilots may even apply full forward throttle on touchdown, in case the arresting gear does not catch and a go around is needed.Parachutes are used to slow down vehicles travelling very fast. Parachutes have been used in land, air and space vehicles such as the ThrustSSC, Eurofighter Typhoon and Apollo Command Module. Some older Soviet passenger jets had braking parachutes for emergency landings. Boats use similar devices called sea anchors to maintain stability in rough seas. To further increase the rate of deceleration or where the brakes have failed, several mechanisms can be used to stop a vehicle. Cars and rolling stock usually have hand brakes that, while designed to secure an already parked vehicle, can provide limited braking should the primary brakes fail. A secondary procedure called forward-slip is sometimes used to slow airplanes by flying at an angle, causing more drag. Legislation Motor vehicle and trailer categories are defined according to the following international classification: Category M: passenger vehicles. Category N: motor vehicles for the carriage of goods. Category O: trailers and semi-trailers. European Union In the European Union the classifications for vehicle types are defined by: Commission Directive 2001/116/EC of 20 December 2001, adapting to technical progress Council Directive 70/156/EEC on the approximation of the laws of the Member States relating to the type-approval of motor vehicles and their trailers Directive 2002/24/EC of the European Parliament and of the Council of 18 March 2002 relating to the type-approval of two or three wheeled motor vehicles and repealing Council Directive 92/61/EECEuropean Community, is based on the Communitys WVTA (whole vehicle type-approval) system. Under this system, manufacturers can obtain certification for a vehicle type in one Member State if it meets the EC technical requirements and then market it EU-wide with no need for further tests. Total technical harmonization already has been achieved in three vehicle categories (passenger cars, motorcycles, and tractors) and soon will extend to other vehicle categories (coaches and utility vehicles). It is essential that European car manufacturers be ensured access to as large a market as possible. While the Community type-approval system allows manufacturers to benefit fully from internal market opportunities, worldwide technical harmonization in the context of the United Nations Economic Commission for Europe (UNECE) offers a market beyond European borders. Licensing In many cases, it is unlawful to operate a vehicle without a license or certification. The least strict form of regulation usually limits what passengers the driver may carry or prohibits them completely (e.g., a Canadian ultra-light license without endorsements). The next level of licensing may allow passengers, but without any form of compensation or payment. A private drivers license usually has these conditions. Commercial licenses that allow the transport of passengers and cargo are more tightly regulated. The most strict form of licensing is generally reserved for school buses, hazardous materials transports and emergency vehicles. The driver of a motor vehicle is typically required to hold a valid drivers license while driving on public lands, whereas the pilot of an aircraft must have a license at all times, regardless of where in the jurisdiction the aircraft is flying. Registration Vehicles are often required to be registered. Registration may be for purely legal reasons, for insurance reasons or to help law enforcement recover stolen vehicles. Toronto Police Service, for example, offers free and optional bicycle registration online. On motor vehicles, registration often takes the form of a vehicle registration plate, which makes it easy to identify a vehicle. In Russia, trucks and buses have their licence plate numbers repeated in large black letters on the back. On aircraft, a similar system is used where a tail number is painted on various surfaces. Like motor vehicles and aircraft, watercraft also have registration numbers in most jurisdictions, however the vessel name is still the primary means of identification as has been the case since ancient times. For this reason, duplicate registration names are generally rejected. In Canada, boats with an engine power of 10 hp (7.5 kW) or greater require registration, leading to the ubiquitous "9.9 hp (7.4 kW)" engine. Registration may be conditional on the vehicle being approved for use on public highways, as in the case of the UK and Ontario. Many US states also have requirements for vehicles operating on public highways. Aircraft have more stringent requirements, as they pose a high risk of damage to people and property in event of an accident. In the US, the FAA requires aircraft to have an airworthiness certificate. Because US aircraft must be flown for some time before they are certified, there is a provision for an experimental airworthiness certificate. FAA experimental aircraft are restricted in operation, including no overflights of populated areas, in busy airspace or with unessential passengers. Materials and parts used in FAA certified aircraft must meet the criteria set forth by the technical standard orders. Mandatory safety equipment In many jurisdictions, the operator of a vehicle is legally obligated to carry safety equipment with or on them. Common examples include seat belts in cars, helmets on motorcycles and bicycles, fire extinguishers on boats, buses and airplanes and life jackets on boats and commercial aircraft. Passenger aircraft carry a great deal of safety equipment including inflatable slides are rafts, oxygen masks, oxygen tanks, life jackets, satellite beacons and first aid kits. Some equipment such as life jackets has led to debate regarding their usefulness. In the case of Ethiopian Airlines Flight 961, the life jackets saved many people but also led to many deaths when passengers inflated their vests prematurely. Right-of-way There are specific real-estate arrangements made to allow vehicles to travel from one place to another. The most common arrangements are public highways, where appropriately licensed vehicles can navigate without hindrance. These highways are on public land and are maintained by the government. Similarly, toll routes are open to the public after paying a toll. These routes and the land they rest on may be government or privately owned or a combination of both. Some routes are privately owned but grant access to the public. These routes often have a warning sign stating that the government does not maintain the way. An example of this are byways in England and Wales. In Scotland, land is open to un-motorised vehicles if the land meets certain criteria. Public land is sometimes open to use by off-road vehicles. On US public land, the Bureau of Land Management (BLM) decides where vehicles may be used. Railways often pass over land not owned by the railway company. The right to this land is granted to the railway company through mechanisms such as easement. Watercraft are generally allowed to navigate public waters without restriction as long as they do not cause a disturbance. Passing through a lock, however, may require paying a toll. Despite the common law tradition Cuius est solum, eius est usque ad coelum et ad inferos of owning all the air above ones property, the US Supreme Court ruled that aircraft in the US have the right to use air above someone elses property without their consent. While the same rule generally applies in all jurisdictions, some countries such as Cuba and Russia have taken advantage of air rights on a national level to earn money. There are some areas that aircraft are barred from overflying. This is called prohibited airspace. Prohibited airspace is usually strictly enforced due to potential damage from espionage or attack. In the case of Korean Air Lines Flight 007, the airliner entered prohibited airspace over Soviet territory and was shot down as it was leaving. Safety For a comparison of transportation fatality rates, see: Air safety statistics. Several different metrics used to compare and evaluate the safety of different vehicles. The main three are deaths per billion passenger-journeys, deaths per billion passenger-hours and deaths per billion passenger-kilometers. See also Automotive acronyms and abbreviations ISIRI 6924 Narrow-track vehicle Outline of vehicles Personal transporter Propulsion Single-track vehicle Vehicular dynamics Vehicular metrics == References ==

Aarogya, give me a short description about Hodgkin lymphoma

Hodgkin lymphoma

Hodgkin lymphoma (HL) is a type of lymphoma, in which cancer originates from a specific type of white blood cell called lymphocytes, where multinucleated Reed–Sternberg cells (RS cells) are present in the patients lymph nodes. The condition was named after the English physician Thomas Hodgkin, who first described it in 1832. Symptoms may include fever, night sweats, and weight loss. Often, nonpainful enlarged lymph nodes occur in the neck, under the arm, or in the groin. Those affected may feel tired or be itchy.The two major types of Hodgkin lymphoma are classic Hodgkin lymphoma and nodular lymphocyte-predominant Hodgkin lymphoma. About half of cases of Hodgkin lymphoma are due to Epstein–Barr virus (EBV) and these are generally the classic form. Other risk factors include a family history of the condition and having HIV/AIDS. Diagnosis is conducted by confirming the presence of cancer and identifying RS cells in lymph node biopsies. The virus-positive cases are classified as a form of the Epstein–Barr virus-associated lymphoproliferative diseases.Hodgkin lymphoma may be treated with chemotherapy, radiation therapy, and stem cell transplantation. The choice of treatment often depends on how advanced the cancer has become and whether or not it has favorable features. If the disease is detected early, a cure is often possible. In the United States, 88% of people diagnosed with Hodgkin Lymphoma survive for five years or longer. For those under the age of 20, rates of survival are 97%. Radiation and some chemotherapy drugs, however, increase the risk of other cancers, heart disease, or lung disease over the subsequent decades.In 2015, about 574,000 people globally had Hodgkin lymphoma, and 23,900 (4.2%) died. In the United States, 0.2% of people are affected at some point in their life. Most people are diagnosed with the disease between the ages of 20 and 40. Signs and symptoms People with Hodgkin lymphoma may present with the following symptoms: Lymphadenopathy: the most common symptom of Hodgkin is the painless enlargement of one or more lymph nodes. The nodes may also feel rubbery and swollen when examined. The nodes of the neck, armpits and groin (cervical and supraclavicular) are most frequently involved (80–90% of the time, on average). The lymph nodes of the chest are often affected, and these may be noticed on a chest radiograph. Systemic symptoms: about one-third of people with Hodgkin disease may also present with systemic symptoms, including:Itchy skin Night sweats. Unexplained weight loss of at least 10% of the persons total body mass in six months or less. Low-grade fever. Fatigue (lassitude). Systemic symptoms such as fever, night sweats, and weight loss are known as B symptoms; thus, presence of these indicate that the persons stage is, for example, 2B instead of 2A. Splenomegaly: enlargement of the spleen is often present in people with Hodgkin lymphoma. The enlargement is seldom massive, and the size of the spleen may fluctuate during the course of treatment. Hepatomegaly: enlargement of the liver, due to liver involvement, is infrequent in people with Hodgkin Lymphoma. Hepatosplenomegaly: the enlargement of both the liver and spleen caused by the same disease. Pain following alcohol consumption: classically, involved nodes are painful after alcohol consumption, though this phenomenon is very uncommon, occurring in only two to three percent of people with Hodgkin lymphoma, thus having a low sensitivity. On the other hand, its positive predictive value is high enough for it to be regarded as a pathognomonic sign of Hodgkin lymphoma. The pain typically has an onset within minutes after ingesting alcohol, and is usually felt as coming from the vicinity where there is an involved lymph node. The pain has been described as either sharp and stabbing or dull and aching. Back pain: nonspecific back pain (pain that cannot be localised or its cause determined by examination or scanning techniques) has been reported in some cases of Hodgkin lymphoma. The lower back is most often affected. Cyclical fever: people may also present with a cyclical high-grade fever known as the Pel–Ebstein fever, or more simply "P-E fever". However, there is debate as to whether the P-E fever truly exists. Nephrotic syndrome can occur in individuals with Hodgkin lymphoma and is most commonly caused by minimal change disease. May present with airway obstruction, pleural/pericardial effusion, hepatocellular dysfunction, bone marrow infiltration. Diagnosis Hodgkin lymphoma must be distinguished from non-cancerous causes of lymph node swelling (such as various infections) and from other types of cancer. Definitive diagnosis is by lymph node biopsy (usually excisional biopsy with microscopic examination). Blood tests are also performed to assess function of major organs and to assess safety for chemotherapy. Positron emission tomography (PET) is used to detect small deposits that do not show on CT scanning. PET scans are also useful in functional imaging (by using a radiolabeled glucose to image tissues of high metabolism). In some cases, a gallium scan may be used instead of a PET scan. Types There are two main types of Hodgkin lymphoma: classic Hodgkin lymphoma and nodular lymphocyte predominant Hodgkin lymphoma. The prevalence of classic Hodgkin lymphoma and nodular lymphocyte Hodgkin lymphoma are approximately 90% and 10%, respectively. The morphology, phenotype, molecular features, and, therefore, the clinical behaviour and presentation of the two types differ. Classic Classic Hodgkin lymphoma (excluding nodular lymphocyte predominant Hodgkin lymphoma) can be subclassified into four pathologic subtypes based upon Reed–Sternberg cell morphology and the composition of the reactive cell infiltrate seen in the lymph node biopsy specimen (the cell composition around the Reed–Sternberg cell(s)). Presence of EBV in Reed-Sternberg cells is most commonly found in the subtypes lymphocyte depleted HL (>70%) and mixed cellularity HL (70%), whilst being less prevalent in lymphocyte-rich HL (40%) and relatively uncommon by comparison in nodular sclerosing HL. For the other forms, although the traditional B-cell markers (such as CD20) are not expressed on all cells, Reed–Sternberg cells are usually of B cell origin. Although Hodgkins is now frequently grouped with other B-cell malignancies, some T-cell markers (such as CD2 and CD4) are occasionally expressed. However, this may be an artifact of the ambiguity inherent in the diagnosis. Hodgkin cells produce interleukin-21 (IL-21), which was once thought to be exclusive to T-cells. This feature may explain the behavior of classic Hodgkin lymphoma, including clusters of other immune cells gathered around HL cells (infiltrate) in cultures. Nodular lymphocyte predominant Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is another subtype of Hodgkin lymphoma distinct from classic Hodgkin lymphoma and is characterized by the presence of popcorn cells which express CD20. Due to these differences, among others, NLPHL is often treated differently from classic Hodgkin lymphoma, including using rituximab in combination with AVBD chemotherapy, though individual cases vary and clinical trials are ongoing. Staging The staging is the same for both Hodgkin and non-Hodgkin lymphomas. After Hodgkin lymphoma is diagnosed, a person will be staged: that is, they will undergo a series of tests and procedures that will determine what areas of the body are affected. These procedures may include documentation of their histology, a physical examination, blood tests, chest X-ray radiographs, computed tomography (CT)/positron emission tomography (PET)/magnetic resonance imaging (MRI) scans of the chest, abdomen and pelvis, and usually a bone marrow biopsy. PET scan is now used instead of the gallium scan for staging. On the PET scan, sites involved with lymphoma light up very brightly enabling accurate and reproducible imaging. In the past, a lymphangiogram or surgical laparotomy (which involves opening the abdominal cavity and visually inspecting for tumors) were performed. Lymphangiograms or laparotomies are very rarely performed, having been supplanted by improvements in imaging with the CT scan and PET scan.On the basis of this staging, the person will be classified according to a staging classification (the Ann Arbor staging classification scheme is a common one): Stage I is involvement of a single lymph node region (I) (mostly the cervical region) or single extralymphatic site (Ie); Stage II is involvement of two or more lymph node regions on the same side of the diaphragm (II) or of one lymph node region and a contiguous extralymphatic site (IIe); Stage III is involvement of lymph node regions on both sides of the diaphragm, which may include the spleen (IIIs) or limited contiguous extralymphatic organ or site (IIIe, IIIes); Stage IV is disseminated involvement of one or more extralymphatic organs.The absence of systemic symptoms is signified by adding "A" to the stage; the presence of systemic symptoms is signified by adding "B" to the stage. For localised extranodal extension from mass of nodes that does not advance the stage, subscript "E" is added. Splenic involvement is signified by adding "S" to the stage. The inclusion of "bulky disease" is signified by "X". Pathology MacroscopyAffected lymph nodes (most often, laterocervical lymph nodes) are enlarged, but their shape is preserved because the capsule is not invaded. Usually, the cut surface is white-grey and uniform; in some histological subtypes (e.g. nodular sclerosis) a nodular aspect may appear.A fibrin ring granuloma may be seen. Microscopy Microscopic examination of the lymph node biopsy reveals complete or partial effacement of the lymph node architecture by scattered large malignant cells known as Reed-Sternberg cells (RSC) (typical and variants) admixed within a reactive cell infiltrate composed of variable proportions of lymphocytes, histiocytes, eosinophils, and plasma cells. The Reed–Sternberg cells are identified as large often bi-nucleated cells with prominent nucleoli and an unusual CD45-, CD30+, CD15+/- immunophenotype. In approximately 50% of cases, the Reed–Sternberg cells are infected by the Epstein–Barr virus.Characteristics of classic Reed–Sternberg cells include large size (20–50 micrometres), abundant, amphophilic, finely granular/homogeneous cytoplasm; two mirror-image nuclei (owl eyes) each with an eosinophilic nucleolus and a thick nuclear membrane (chromatin is distributed close to the nuclear membrane). Almost all of these cells have an increased copy number of chromosome 9p/9p24.1.Variants: Hodgkin cell (atypical mononuclear RSC) is a variant of RS cell, which has the same characteristics but is mononucleated. Lacunar RSC is large, with a single hyperlobulated nucleus, multiple, small nucleoli and eosinophilic cytoplasm which is retracted around the nucleus, creating an empty space ("lacunae"). Pleomorphic RSC has multiple irregular nuclei. "Popcorn" RSC (lympho-histiocytic variant) is a small cell, with a very lobulated nucleus, small nucleoli. "Mummy" RSC has a compact nucleus with no nucleolus and basophilic cytoplasm.Hodgkin lymphoma can be sub-classified by histological type. The cell histology in Hodgkin lymphoma is not as important as it is in non-Hodgkin lymphoma: the treatment and prognosis in classic Hodgkin lymphoma usually depends on the stage of disease rather than the histotype. Management The current approach for treatment aims to reduce the acute and long-term toxicities associated with Hodgkin lymphoma (e.g. cardiac damage and secondary cancers) and increase overall survival.People with early stage disease (IA or IIA) are effectively treated with radiation therapy or chemotherapy. The choice of treatment depends on the age, sex, bulk and the histological subtype of the disease. Adding localised radiation therapy after the chemotherapy regimen may provide a longer progression-free survival compared with chemotherapy treatment alone. People with later disease (III, IVA, or IVB) are treated with combination chemotherapy alone. People of any stage with a large mass in the chest are usually treated with combined chemotherapy and radiation therapy. The common non-Hodgkin treatment, rituximab (which is a monoclonal antibody against CD20) is not routinely used to treat Hodgkin lymphoma due to the lack of CD20 surface antigens in most cases. The use of rituximab in Hodgkin lymphoma, including the lymphocyte predominant subtype has been recently reviewed. The evidence is very uncertain about the effect of Nivolumab for patients with a Hodgkins lymphoma e.g. on the overall survival.Increased age is an adverse risk factor for Hodgkin lymphoma, but in general elderly people (≥ 60 years of age) without major comorbidities are sufficiently fit to tolerate therapy with curative intent. Despite this, treatment outcome in the elderly patient is not comparable to that of younger people and the disease is a different entity in older people where different considerations enter into treatment decisions.Recently, two novel targeted drugs have been developed for relapsing and refractory HL patients; Brentuximab vedotin, a CD30 antibody conjugated with a cytotoxic component MMAE, and the checkpoint inhibitors, Nivolumab and Pembrolizumab. This has been an important step in the treatment for the few, but still existing refractory patients. For Hodgkin lymphomas, radiation oncologists typically use external beam radiation therapy (sometimes shortened to EBRT or XRT). Radiation oncologists deliver external beam radiation therapy to the lymphoma from a machine called a linear accelerator which produces high energy X-rays and electrons. People usually describe treatments as painless and similar to getting an X-ray. Treatments last less than 30 minutes each. For lymphomas, there are a few different ways radiation oncologists target the cancer cells. Involved site radiation is when the radiation oncologists give radiation only to those parts of the persons body known to have the cancer. Very often, this is combined with chemotherapy. Radiation therapy directed above the diaphragm to the neck, chest or underarms is called mantle field radiation. Radiation to below the diaphragm to the abdomen, spleen or pelvis is called inverted-Y field radiation. Total nodal irradiation is when the therapist gives radiation to all the lymph nodes in the body to destroy cells that may have spread. Adverse effects The high cure rates and long survival of many people with Hodgkin lymphoma has led to a high concern with late adverse effects of treatment, including cardiovascular disease and second malignancies such as acute leukemias, lymphomas, and solid tumors within the radiation therapy field. Most people with early-stage disease are now treated with abbreviated chemotherapy and involved site radiation therapy rather than with radiation therapy alone. Clinical research strategies are exploring reduction of the duration of chemotherapy and dose and volume of radiation therapy in an attempt to reduce late morbidity and mortality of treatment while maintaining high cure rates. Hospitals are also treating those who respond quickly to chemotherapy with no radiation.In childhood cases of Hodgkin lymphoma, long-term endocrine adverse effects are a major concern, mainly gonadal dysfunction and growth retardation. Gonadal dysfunction seems to be the most severe endocrine long-term effect, especially after treatment with alkylating agents or pelvic radiotherapy.It is possible that patients undergoing a chemotherapy need a platelet transfusion. If a stem cell transplantation is necessary for the treatment of a relapse, graft-versus-host diseases might occur. Supportive treatment Adding physical exercises to the standard treatment for adult patients with haematological malignancies like Hodgkin lymphoma may result in little to no difference in the mortality, the quality of life and the physical functioning. These exercises may result in a slight reduction in depression. Furthermore, aerobic physical exercises probably reduce fatigue. The evidence is very uncertain about the effect on anxiety and serious adverse events. Prognosis Treatment of Hodgkins disease has been improving over the past few decades. Recent trials that have made use of new types of chemotherapy have indicated higher survival rates than have previously been seen. In one recent European trial, the five-year survival rate for those people with a favorable prognosis (FFP) was 98%, while that for people with worse outlooks was at least 85%.In 1998, an international effort identified seven prognostic factors that accurately predict the success rate of conventional treatment in people with locally extensive or advanced-stage Hodgkin lymphoma. Freedom from progression (FFP) at five years was directly related to the number of factors present in a person. The five-year FFP for people with zero factors is 84%. Each additional factor lowers the five-year FFP rate by 7%, such that the five-year FFP for a person with five or more factors is 42%.The adverse prognostic factors identified in the international study are: Age ≥ 45 years Stage IV disease Hemoglobin < 10.5 g/dl Lymphocyte count < 600/µl or < 8% Male Albumin < 4.0 g/dl White blood count ≥ 15,000/µlOther studies have reported the following to be the most important adverse prognostic factors: mixed-cellularity or lymphocyte-depleted histologies, male sex, large number of involved nodal sites, advanced stage, age of 40 years or more, the presence of B symptoms, high erythrocyte sedimentation rate, and bulky disease (widening of the mediastinum by more than one third, or the presence of a nodal mass measuring more than 10 cm in any dimension.)More recently, the use of positron emission tomography (PET) early after commencing chemotherapy has demonstrated to have powerful prognostic ability. This enables assessment of an individuals response to chemotherapy as the PET activity switches off rapidly in people who are responding. In this study, after two cycles of ABVD chemotherapy, 83% of people were free of disease at 3 years if they had a negative PET versus only 28% in those with positive PET scans. This prognostic method improves on FFP estimates based on the seven conventional factors. Several trials are underway to see if PET-based risk adapted response can be used to improve a persons outcomes by changing chemotherapy early in people who are not responding. The evidence is very uncertain about the effect of negative (= good prognosis) or positive (= bad prognosis) interim PET scan results for patients with a Hodgkins lymphoma on the progression-free survival. Negative interim PET scan results may result in an increase in progression-free survival compared if the adjusted result was measured. Negative interim PET scan results probably result in a large increase in the overall survival compared to those with a positive interim PET scan result, Epidemiology Unlike some other lymphomas, whose number of new cases per year increases with age, Hodgkin lymphoma has a bimodal curve for the number of cases; that is, it occurs most frequently in two separate age groups, the first being young adulthood (age 15–35) and the second being in those over 55 years old although these peaks may vary slightly with nationality. Overall, it is more common in males, except for the nodular sclerosis variant, which is slightly more common in females. The annual number of cases of Hodgkin lymphoma is 2.7 per 100,000 per persons per year, and the disease accounts for slightly less than 1% of all cancers worldwide.In 2010, globally it resulted in about 18,000 deaths down from 19,000 in 1990. In 2012, there were an estimated 65,950 cases and 25,469 deaths from Hodgkin lymphoma worldwide, with 28,852 and 37,098 cases occurring in developed and developing countries, respectively. However, the age-standardized rates were higher in developed regions, with the greatest rates in the Americas (1.5 per 100,000), East Mediterranean Region (1.5 per 100,000), and Europe (2.0 per 100,000). The East Mediterranean Region also has the highest age-standardized mortality rate of 1.0 per 100,000, which is mainly attributed to lifestyle and environmental risk factors associated with transitional economies such as smoking, obesity, physical inactivity, and reproductive behaviors, as well as availability of diagnostic practices and awareness of the disease.The number of cases of Hodgkin lymphoma is increased in people with HIV infection. In contrast to many other lymphomas associated with HIV infection it occurs most commonly in people with higher CD4 T cell counts. Canada Hodgkin lymphoma accounts for 0.6% of all male cancer cases, and 0.4% of all female cancer cases in Canada. In 2017, approximately 990 Canadians will be diagnosed with Hodgkin lymphoma, and 140 will die of the disease. UK Hodgkin lymphoma accounts for less than 1% of all cancer cases and deaths in the UK. Around 1,800 people were diagnosed with the disease in 2011, and around 330 people died in 2012. United States In 2016, there were 8,389 new cases and 1,000 mortalities attributed to Hodgkin Lymphoma, a decrease from the 8,625 new cases and 1,120 mortalities in 2015. As of January 1, 2016, the 5-year limited duration prevalence of Hodgkin Lymphoma was 37,513 representing 0.71% of all diagnosed cancers in the U.S. History Hodgkin lymphoma was first described in an 1832 report by Thomas Hodgkin, although Hodgkin noted that perhaps an earlier reference to the condition was provided by Marcello Malpighi in 1666. While occupied as museum curator at Guys Hospital, London, Hodgkin studied seven people with painless lymph node enlargement. Of the seven cases, two were under the care of Richard Bright, one was of Thomas Addison, and one was of Robert Carswell. Carswells report of the seventh case was accompanied by numerous illustrations that aided early descriptions of the disease.Hodgkins report on the seven cases, entitled "On some morbid appearances of the absorbent glands and spleen", was presented to the Medical and Chirurgical Society of London in January 1832 and was subsequently published in the societys journal, Medical-Chirurgical Society Transactions. Hodgkins paper went largely unnoticed, however, even though Bright highlighted it in an 1838 publication. Indeed, Hodgkin himself did not view his contribution as particularly significant.In 1856, Samuel Wilks independently reported on a series of patients with the same disease that Hodgkin had previously described. Wilks, a successor to Hodgkin at Guys Hospital, was unaware of Hodgkins prior work on the subject. Bright informed Wilks of Hodgkins contribution and in 1865, Wilks published a second paper, entitled "Cases of enlargement of the lymphatic glands and spleen", in which he named the illness "Hodgkins disease" in honor of his predecessor.Theodor Langhans and WS Greenfield first described the microscopic characteristics of Hodgkin lymphoma in 1872 and 1878, respectively. In 1898 and 1902, respectively, Carl Sternberg and Dorothy Reed independently described the cytogenetic features of the malignant cells of Hodgkin lymphoma, now called Reed–Sternberg cells.Tissue specimens from Hodgkins seven cases were preserved at Guys Hospital. Nearly 100 years after Hodgkins initial publication, histopathologic reexamination confirmed Hodgkin lymphoma in only three of seven of these people. The remaining cases included non-Hodgkin lymphoma, tuberculosis, and syphilis.Hodgkin lymphoma was one of the first cancers to be treated successfully with radiation therapy and, later, it was one of the first to be treated by combination chemotherapy. Notable cases Paul Allen, co-founder of Microsoft was diagnosed with Hodgkin lymphoma in 1982. He later died from non-Hodgkin lymphoma, on October 15, 2018. Eric Berry, All-Pro strong safety for the Kansas City Chiefs of the National Football League, diagnosed in 2014. Howard Carter, Egyptologist and discoverer of the Tomb of Tutankhamun, died in 1939 from Hodgkins disease. Starchild Abraham Cherrix, a teenager whose refusal to undergo further conventional treatment after relapsing in 2006 resulted in a court battle and a change to Virginia laws about medical neglect. James Conner, running back and 2014 ACC Player of the Year for the Pittsburgh Steelers. Michael Cuccione, Canadian child actor, was diagnosed in 1994 at age 9. Treatments that rendered him cancer-free, including chemotherapy, a bone marrow transplant, and radiation, left him with permanent lung and respiratory problems and he died in 2001 just after turning 16. Victoria Duval, American tennis player, was diagnosed in 2014. Gerald Finzi, British composer, was diagnosed in 1951 and died in 1956. Mist Edvardsdóttir, Icelandic football player and member of the Icelandic womens national team. Diagnosed in June 2014 at the age of 23. Continued to play until becoming too ill due to chemotherapy. Made recovery in early 2015. Delta Goodrem, Australian singer, songwriter, and actress. She was diagnosed in July 2003 at the age of 18. Jiří Grossmann, Czechoslovak theatre actor, poet, and composer Michael C. Hall (born February 1, 1971), American actor, best known for his lead role as Dexter Morgan, in Showtimes crime series Dexter. In 2010, aged 38, Hall announced he was undergoing treatment for Hodgkin lymphoma; within two years, the disease was in full remission. Richard Harris, Irish actor who portrayed Albus Dumbledore in the first two Harry Potter movies, died on October 25, 2002, after being diagnosed earlier that year. Daniel Hauser, whose mother fled with him in 2009 in order to prevent him from undergoing chemotherapy. Tessa James, Australian actress, was diagnosed in 2014. Sean Kent, American stand up comedian and actor. Was diagnosed in 2002 while writing on a TV show. After three months in remission the cancer returned and he was given an autologous stem cell transplant at City of Hope Cancer Hospital in Los Angeles. Currently lives in Texas with his wife and family and still performs many weeks a year. Mario Lemieux, Hall of Fame NHL player, co-owner of the Pittsburgh Penguins and founder of the Mario Lemieux Foundation, diagnosed in 1993. Dinu Lipatti (1917–1950), Romanian classical pianist and composer. Diagnosed in 1947, received cortisone treatment in 1949; died from a burst abscess on his one lung. Jack Lisowski, English snooker player, diagnosed in 2008 at the age of 16. Mamta Mohandas, Indian film actress and producer, diagnosed in 2010. Nanni Moretti, Italian actor and director. Laura Packard, health care activist diagnosed in 2017, spoke at the 2020 Democratic National Convention. Nikola Pokrivač, Croatian soccer midfielder, diagnosed in 2015. Anthony Rizzo, MLB All-Star first baseman for the New York Yankees, diagnosed in May 2008 while signed as a minor league player for the Boston Red Sox. Dave Roberts, MLB outfielder and manager of the Los Angeles Dodgers. Diagnosed in March 2010 while he was a coach for the San Diego Padres. Chip Roy, Texas congressman. Flip Saunders, head coach of the NBA team Minnesota Timberwolves, announced in August 2015 that he was diagnosed with Hodgkins disease. He died of the disease in October 2015. Brandon Tartikoff, American television executive, diagnosed around 1974, died in 1997. Ethan Zohn, American professional soccer player and a winner of the Survivor reality television series. Zohn was diagnosed twice (in 2009 and 2011). Arlen Specter, United States Senator from Pennsylvania (1981 - 2011), diagnosed in 2005. He later died from non-Hodgkin lymphoma in 2012. David Brooks, Welsh professional footballer, diagnosed in 2021 while playing for AFC Bournemouth. Bernardo Tengarrinha, Portuguese professional footballer, diagnosed in 2017 Tengarrinha died on October 30, 2021, at the age of 32. [21] Hours later, his former teams FC Porto and Boavista FC paid tribute to him before the local derby. playing for FC Porto. References Further reading Charlotte DeCroes Jacobs. Henry Kaplan and the Story of Hodgkins Disease (Stanford University Press; 2010) 456 pages; combines a biography of the American radiation oncologist (1918–84) with a history of the lymphatic cancer whose treatment he helped to transform. External links Hodgkin lymphoma at Curlie Hodgkin Lymphoma at American Cancer Society Hodgkin Lymphoma at the American National Cancer Institute

Aarogya, share information about a health condition involving Outline of counseling

Outline of counseling

Counseling is the professional guidance of the individual by utilizing psychological methods especially in collecting case history data, using various techniques of the personal interview, and testing interests and aptitudes.This is a list of counseling topics. Therapeutic modalities Common areas See also List of psychotherapies Outline of communication Outline of psychology Outline of sociology Subfields of sociology Outline of self Psychopharmacology == References ==

Aarogya what is Dipylidium caninum

Dipylidium caninum

Dipylidium caninum, also called the flea tapeworm, double-pored tapeworm, or cucumber tapeworm (in reference to the shape of its cucumber-seed-like proglottids, though these also resemble grains of rice or sesame seeds), is a cyclophyllid cestode that infects organisms afflicted with fleas and canine chewing lice, including dogs, cats, and sometimes human pet-owners, especially children. Adult morphology The adult worm is about 18 inches (46 cm) long. Gravid proglottids containing the worms microscopic eggs are either passed in the definitive hosts feces or may leave their host spontaneously and are then ingested by microscopic flea larvae (the intermediate hosts) in the surrounding environment. As in all members of family Dipylidiidae, proglottids of the adult worm have genital pores on both sides (hence the name double-pore tapeworm). Each side has a set of male and female reproductive organs. The uterus is paired with 16 to 20 radial branches each. The scolex has a retractable rostellum with four rows of hooks, along with the four suckers that all cyclophyllid cestodes have. Life cycle The definitive host within this life cycle is primarily canines, and occasionally felines, and in rare cases young children. The intermediate hosts include fleas (Ctenocephalides spp.) and chewing lice. The first stage in the life cycle is when the gravid proglottids are either passed out through faecal matter, or actively crawl out of the anus of the host. The gravid proglottids once out of the definitive host release eggs. Then, an intermediate host (the larval stage of a flea or chewing louse) will ingest an egg, which develops into a cysticercoid larva. The cysticercoid larva remains viable, but is not infective to carnivores until the flea hatches to an adult and begins feeding on a host (e.g. a dog). Approximately 36 hours after the flea has consumed a blood meal, the infective metacestode develops inside the flea. The metacestode larva must be ingested in a flea by the dog or cat during grooming in order to develop. Humans can also become infected by D. caninum by accidentally ingesting an infected flea. In the small intestine of the definitive host, the metacestode develops into an adult tapeworm, which reaches maturity 4-6 weeks after ingestion. This adult tapeworm produces proglottids, and over time, the proglottids mature and become gravid and eventually detach from the tapeworm and the life cycle starts all over again. Geographic Distribution This parasite occurs worldwide in animals, such as dogs and cats, as well as in humans, though to a significantly lesser degree. It is the most common tapeworm of dogs and is relatively common in cats. Despite human diplydiasis being rare, instances have been reported from every inhabited continent.Human instances of diplydiasis are reported globally, and unsurprisingly roughly one third of the cases occur in children less than 6 months of age. The most at-risk age group is those that range from 2 months to 4 years old. Pet infections Tapeworm infection usually does not cause pathology in the dog or cat, and most pets show no adverse reaction to infection other than increased appetite. The bulk of infections are asymptomatic and the infections that do result in symptoms are generally mildly so. Pets behavior may reflect the presence of anal discomfort and itching, or pruritus. This could result in the ‘butt-scooching” across the floor, grass or carpeting. It may be accompanied by slight gastrointestinal disturbances, as this is the region where the worms inhabit. Though not a pathology of the diplydiasis, the most unnerving sign of the infection is the presence of proglottids in the animals, or child’s, feces. These proglottids can also be found near the perianal region, in the feces, and in diapers (children). The motile proglottids can actively crawl out of the anus of the infected animal/person and migrate small distances, thus potentially covering this array of neighboring surfaces. It is from these locations that the larval stage of the flea will come along and ingest them. Then the metacestode stage, a cysticercoid, develops in the coelomic cavity (abdominal cavity; main body cavity) of the flea larvae and remains there as the flea matures into an adult. These freshly passed proglottids are motile, allowing them to also be found on the floor and furniture, from a migration out of a pets anus and could be compared to resembling fly larvae, or maggots.The other tapeworm infecting cats is Taenia taeniaeformis, though this form is much less commonly encountered than D. caninum. A recent (2018) study using genetical analysis and experimental infections and life-cycles showed that two different distinct genotypes of D. caninum occur respectively in dogs and in cats, and suggested that two different species might be involved. Human infections A human infection with D. caninum is rare, but if an infection does occur, it is more likely to occur in young children. As of the early 1960s, the number of cases of D. caninum in the U.S. was a mere 21. Therefore, human infection of Dipylidium caninum, or diplydiasis, is a rare occasion. It is largely agreed across the parasitology community that despite the reports of this disease occurring, there are very likely numerous cases that have gone unnoticed and unreported because of its subtle and minor pathology in humans, in addition to its scarceness in clinical records. The adult tapeworm grows within the host for 3–4 weeks after initial infection. The number of parasites the host is initially infected with is directly related to the number of cysticercoid juveniles present in the fleas coelom. The load of parasites present in the humans is lower, luckily, as the life cycle is not occurring in the ideal conditions or species as humans are not the definitive host.Many cases have an unexciting course of infection, as can be depicted in two cases occurring in the 1960s. The first case occurred in a 9-month-old female. Mother found motile proglottids the child’s diaper, later identified as D. caninum. The child had no apparent signs or symptoms. The presumed source of infections was one of the family’s four Labrador retrievers, two of which were found to already have been infected with D. caninum. The second additional case occurred in an 18-month-old male. Mother found motile proglottids in the child’s diaper and again, the child was symptom-free. A puppy in the household was found to be infected and thus was the source of the child infection. Young children and toddlers are at a greater risk of infection because of how they interact with their pets. A human may attain an infection by accidentally ingesting an infected flea through food contamination or through the saliva of pets. Most infections are asymptomatic, but sometimes these symptoms may be identified in an infected individual: mild diarrhea, abdominal colic, anorexia, restlessness, constipation, rectal itching, and pain due to emerging proglottids through the anal cavity. Treatment and prevention As with most tapeworm infections, the drugs of choice to kill adult tapeworms are praziquantel or niclosamide. Pets can be prevented from becoming infested with tapeworm if they are treated prophylactically with a product which kills the intermediate host (the flea) before the infective metacestode can develop. Some isoxazoline products are registered to prevent flea tapeworm infestations using this method. Gallery References External links tapeworms from The Pet Health Library

Hello Aarogya , Do you know what is Periodontosis,

Periodontosis

Periodontosis is an obsolete term that was used to describe what was once thought to be certain type of unique and distinguishable chronic periodontal disease that manifested as degenerative bony changes without concomitant inflammation. Although utilized for more than 50 years, the term has since been dropped in favor of a more contemporary disease classification for periodontal disease. Described by Gottlieb as a "diffuse atrophy of the alveolar bone," the term periodontosis was later applied and it gained acceptance as a disease entity, being defined as: "a degenerative, noninflammatory destruction of the periodontium, originating in one or more of the periodontal structures and characterized by migrating and loosening of the teeth in the presence or absence of secondary epithelial proliferation and pocket formation or secondary gingival disease."Noted as a rare disease, periodontosis was said to have been seen primarily in young patients. And despite being defined as being a "noninflammatory destruction of the periodontium," almost all cases did exhibit varying degrees of gingival inflammation. References == External links ==

Please give me a short description about Human leg , Aarogya

Human leg

The human leg, in the general word sense, is the entire lower limb of the human body, including the foot, thigh or sometimes even the hip or gluteal region. However, the definition in human anatomy refers only to the section of the lower limb extending from the knee to the ankle, also known as the crus or, especially in non-technical use, the shank. Legs are used for standing, and all forms of locomotion including recreational such as dancing, and constitute a significant portion of a persons mass. Female legs generally have greater hip anteversion and tibiofemoral angles, but shorter femur and tibial lengths than those in males. Structure In human anatomy, the lower leg is the part of the lower limb that lies between the knee and the ankle. Anatomists restrict the term leg to this use, rather than to the entire lower limb. The thigh is between the hip and knee and makes up the rest of the lower limb. The term lower limb or lower extremity is commonly used to describe all of the leg. The leg from the knee to the ankle is called the crus. The calf is the back portion, and the tibia or shinbone together with the smaller fibula make up the front of the lower leg. Evolution has provided the human body with two distinct features: the specialization of the upper limb for visually guided manipulation and the lower limbs development into a mechanism specifically adapted for efficient bipedal gait. While the capacity to walk upright is not unique to humans, other primates can only achieve this for short periods and at a great expenditure of energy.The human adaption to bipedalism has also affected the location of the bodys center of gravity, the reorganization of internal organs, and the form and biomechanism of the trunk. In humans, the double S-shaped vertebral column acts as a great shock-absorber which shifts the weight from the trunk over the load-bearing surface of the feet. The human legs are exceptionally long and powerful as a result of their exclusive specialization for support and locomotion—in orangutans the leg length is 111% of the trunk; in chimpanzees 128%, and in humans 171%. Many of the legs muscles are also adapted to bipedalism, most substantially the gluteal muscles, the extensors of the knee joint, and the calf muscles. Skeleton The major bones of the leg are the femur (thigh bone), tibia (shin bone), and adjacent fibula, and these are all long bones. The patella (kneecap) is the sesamoid bone in front of the knee. Most of the leg skeleton has bony prominences and margins that can be palpated and some serve as anatomical landmarks that define the extent of the leg. These landmarks are the anterior superior iliac spine, the greater trochanter, the superior margin of the medial condyle of tibia, and the medial malleolus. Notable exceptions to palpation are the hip joint, and the neck and body, or shaft of the femur. Usually, the large joints of the lower limb are aligned in a straight line, which represents the mechanical longitudinal axis of the leg, the Mikulicz line. This line stretches from the hip joint (or more precisely the head of the femur), through the knee joint (the intercondylar eminence of the tibia), and down to the center of the ankle (the ankle mortise, the fork-like grip between the medial and lateral malleoli). In the tibial shaft, the mechanical and anatomical axes coincide, but in the femoral shaft they diverge 6°, resulting in the femorotibial angle of 174° in a leg with normal axial alignment. A leg is considered straight when, with the feet brought together, both the medial malleoli of the ankle and the medial condyles of the knee are touching. Divergence from the normal femorotibial angle is called genu varum if the center of the knee joint is lateral to the mechanical axis (intermalleolar distance exceeds 3 cm), and genu valgum if it is medial to the mechanical axis (intercondylar distance exceeds 5 cm). These conditions impose unbalanced loads on the joints and stretching of either the thighs adductors and abductors.The angle of inclination formed between the neck and shaft of the femur (collodiaphysial angle) varies with age—about 150° in the newborn, it gradually decreases to 126–128° in adults, to reach 120° in old age. Pathological changes in this angle result in abnormal posture of the leg: a small angle produces coxa vara and a large angle coxa valga; the latter is usually combined with genu varum, and coxa vara leads genu valgum. Additionally, a line drawn through the femoral neck superimposed on a line drawn through the femoral condyles forms an angle, the torsion angle, which makes it possible for flexion movements of the hip joint to be transposed into rotary movements of the femoral head. Abnormally increased torsion angles result in a limb turned inward and a decreased angle in a limb turned outward; both cases resulting in a reduced range of a persons mobility. Muscles Hip There are several ways of classifying the muscles of the hip: By location or innervation (ventral and dorsal divisions of the plexus layer); By development on the basis of their points of insertion (a posterior group in two layers and an anterior group); and By function (i.e. extensors, flexors, adductors, and abductors).Some hip muscles also act either on the knee joint or on vertebral joints. Additionally, because the areas of origin and insertion of many of these muscles are very extensive, these muscles are often involved in several very different movements. In the hip joint, lateral and medial rotation occur along the axis of the limb; extension (also called dorsiflexion or retroversion) and flexion (anteflexion or anteversion) occur along a transverse axis; and abduction and adduction occur about a sagittal axis.The anterior dorsal hip muscles are the iliopsoas, a group of two or three muscles with a shared insertion on the lesser trochanter of the femur. The psoas major originates from the last vertebra and along the lumbar spine to stretch down into the pelvis. The iliacus originates on the iliac fossa on the interior side of the pelvis. The two muscles unite to form the iliopsoas muscle, which is inserted on the lesser trochanter of the femur. The psoas minor, only present in about 50 per cent of subjects, originates above the psoas major to stretch obliquely down to its insertion on the interior side of the major muscle.The posterior dorsal hip muscles are inserted on or directly below the greater trochanter of the femur. The tensor fasciae latae, stretching from the anterior superior iliac spine down into the iliotibial tract, presses the head of the femur into the acetabulum but also flexes, rotates medially, and abducts to hip joint. The piriformis originates on the anterior pelvic surface of the sacrum, passes through the greater sciatic foramen, and inserts on the posterior aspect of the tip of the greater trochanter. In a standing posture it is a lateral rotator, but it also assists extending the thigh. The gluteus maximus has its origin between (and around) the iliac crest and the coccyx, from where one part radiates into the iliotibial tract and the other stretches down to the gluteal tuberosity under the greater trochanter. The gluteus maximus is primarily an extensor and lateral rotator of the hip joint, and it comes into action when climbing stairs or rising from a sitting to a standing posture. Furthermore, the part inserted into the fascia latae abducts and the part inserted into the gluteal tuberosity adducts the hip. The two deep glutei muscles, the gluteus medius and minimus, originate on the lateral side of the pelvis. The medius muscle is shaped like a cap. Its anterior fibers act as a medial rotator and flexor; the posterior fibers as a lateral rotator and extensor; and the entire muscle abducts the hip. The minimus has similar functions and both muscles are inserted onto the greater trochanter. The ventral hip muscles function as lateral rotators and play an important role in the control of the bodys balance. Because they are stronger than the medial rotators, in the normal position of the leg, the apex of the foot is pointing outward to achieve better support. The obturator internus originates on the pelvis on the obturator foramen and its membrane, passes through the lesser sciatic foramen, and is inserted on the trochanteric fossa of the femur. "Bent" over the lesser sciatic notch, which acts as a fulcrum, the muscle forms the strongest lateral rotators of the hip together with the gluteus maximus and quadratus femoris. When sitting with the knees flexed it acts as an abductor. The obturator externus has a parallel course with its origin located on the posterior border of the obturator foramen. It is covered by several muscles and acts as a lateral rotator and a weak adductor. The inferior and superior gemelli muscles represent marginal heads of the obturator internus and assist this muscle. These three muscles form a three-headed muscle (tricipital) known as the triceps coxae. The quadratus femoris originates at the ischial tuberosity and is inserted onto the intertrochanteric crest between the trochanters. This flattened muscle act as a strong lateral rotator and adductor of the thigh. The adductor muscles of the thigh are innervated by the obturator nerve, with the exception of pectineus which receives fibers from the femoral nerve, and the adductor magnus which receives fibers from the tibial nerve. The gracilis arises from near the pubic symphysis and is unique among the adductors in that it reaches past the knee to attach on the medial side of the shaft of the tibia, thus acting on two joints. It share its distal insertion with the sartorius and semitendinosus, all three muscles forming the pes anserinus. It is the most medial muscle of the adductors, and with the thigh abducted its origin can be clearly seen arching under the skin. With the knee extended, it adducts the thigh and flexes the hip. The pectineus has its origin on the iliopubic eminence laterally to the gracilis and, rectangular in shape, extends obliquely to attach immediately behind the lesser trochanter and down the pectineal line and the proximal part of the linea aspera on the femur. It is a flexor of the hip joint, and an adductor and a weak medial rotator of the thigh. The adductor brevis originates on the inferior ramus of the pubis below the gracilis and stretches obliquely below the pectineus down to the upper third of the linea aspera. Except for being an adductor, it is a lateral rotator and weak flexor of the hip joint.The adductor longus has its origin at superior ramus of the pubis and inserts medially on the middle third of the linea aspera. Primarily an adductor, it is also responsible for some flexion. The adductor magnus has its origin just behind the longus and lies deep to it. Its wide belly divides into two parts: One is inserted into the linea aspera and the tendon of the other reaches down to adductor tubercle on the medial side of the femurs distal end where it forms an intermuscular septum that separates the flexors from the extensors. Magnus is a powerful adductor, especially active when crossing legs. Its superior part is a lateral rotator but the inferior part acts as a medial rotator on the flexed leg when rotated outward and also extends the hip joint. The adductor minimus is an incompletely separated subdivision of the adductor magnus. Its origin forms an anterior part of the magnus and distally it is inserted on the linea aspera above the magnus. It acts to adduct and lateral rotate the femur. Thigh The muscles of the thigh can be classified into three groups according to their location: anterior and posterior muscles and the adductors (on the medial side). All the adductors except gracilis insert on the femur and act on the hip joint, and so functionally qualify as hip muscles. The majority of the thigh muscles, the "true" thigh muscles, insert on the leg (either the tibia or the fibula) and act primarily on the knee joint. Generally, the extensors lie on anterior of the thigh and flexors lie on the posterior. Even though the sartorius flexes the knee, it is ontogenetically considered an extensor since its displacement is secondary. Of the anterior thigh muscles the largest are the four muscles of the quadriceps femoris: the central rectus femoris, which is surrounded by the three vasti, the vastus intermedius, medialis, and lateralis. Rectus femoris is attached to the pelvis with two tendons, while the vasti are inserted to the femur. All four muscles unite in a common tendon inserted into the patella from where the patellar ligament extends it down to the tibial tuberosity. Fibers from the medial and lateral vasti form two retinacula that stretch past the patella on either sides down to the condyles of the tibia. The quadriceps is the knee extensor, but the rectus femoris additionally flexes the hip joint, and articular muscle of the knee protects the articular capsule of the knee joint from being nipped during extension. The sartorius runs superficially and obliquely down on the anterior side of the thigh, from the anterior superior iliac spine to the pes anserinus on the medial side of the knee, from where it is further extended into the crural fascia. The sartorius acts as a flexor on both the hip and knee, but, due to its oblique course, also contributes to medial rotation of the leg as one of the pes anserinus muscles (with the knee flexed), and to lateral rotation of the hip joint.There are four posterior thigh muscles. The biceps femoris has two heads: The long head has its origin on the ischial tuberosity together with the semitendinosus and acts on two joints. The short head originates from the middle third of the linea aspera on the shaft of the femur and the lateral intermuscular septum of thigh, and acts on only one joint. These two heads unite to form the biceps which inserts on the head of the fibula. The biceps flexes the knee joint and rotates the flexed leg laterally—it is the only lateral rotator of the knee and thus has to oppose all medial rotator. Additionally, the long head extends the hip joint. The semitendinosus and the semimembranosus share their origin with the long head of the biceps, and both attaches on the medial side of the proximal head of the tibia together with the gracilis and sartorius to form the pes anserinus. The semitendinosus acts on two joints; extension of the hip, flexion of the knee, and medial rotation of the leg. Distally, the semimembranosus tendon is divided into three parts referred to as the pes anserinus profondus. Functionally, the semimembranosus is similar to the semitendinosus, and thus produces extension at the hip joint and flexion and medial rotation at the knee. Posteriorly below the knee joint, the popliteus stretches obliquely from the lateral femoral epicondyle down to the posterior surface of the tibia. The subpopliteal bursa is located deep to the muscle. Popliteus flexes the knee joint and medially rotates the leg. Lower leg and foot With the popliteus (see above) as the single exception, all muscles in the leg are attached to the foot and, based on location, can be classified into an anterior and a posterior group separated from each other by the tibia, the fibula, and the interosseous membrane. In turn, these two groups can be subdivided into subgroups or layers—the anterior group consists of the extensors and the peroneals, and the posterior group of a superficial and a deep layer. Functionally, the muscles of the leg are either extensors, responsible for the dorsiflexion of the foot, or flexors, responsible for the plantar flexion. These muscles can also classified by innervation, muscles supplied by the anterior subdivision of the plexus and those supplied by the posterior subdivision. The leg muscles acting on the foot are called the extrinsic foot muscles whilst the foot muscles located in the foot are called intrinsic.Dorsiflexion (extension) and plantar flexion occur around the transverse axis running through the ankle joint from the tip of the medial malleolus to the tip of the lateral malleolus. Pronation (eversion) and supination (inversion) occur along the oblique axis of the ankle joint. Extrinsic Three of the anterior muscles are extensors. From its origin on the lateral surface of the tibia and the interosseus membrane, the three-sided belly of the tibialis anterior extends down below the superior and inferior extensor retinacula to its insertion on the plantar side of the medial cuneiform bone and the first metatarsal bone. In the non-weight-bearing leg, the anterior tibialis dorsal flexes the foot and lifts the medial edge of the foot. In the weight-bearing leg, it pulls the leg towards the foot. The extensor digitorum longus has a wide origin stretching from the lateral condyle of the tibia down along the anterior side of the fibula, and the interosseus membrane. At the ankle, the tendon divides into four that stretch across the foot to the dorsal aponeuroses of the last phalanges of the four lateral toes. In the non-weight-bearing leg, the muscle extends the digits and dorsiflexes the foot, and in the weight-bearing leg acts similar to the tibialis anterior. The extensor hallucis longus has its origin on the fibula and the interosseus membrane between the two other extensors and is, similarly to the extensor digitorum, is inserted on the last phalanx of big toe ("hallux"). The muscle dorsiflexes the hallux, and acts similar to the tibialis anterior in the weight-bearing leg. Two muscles on the lateral side of the leg form the fibular (peroneal) group. The fibularis (peroneus) longus and fibularis (peroneus) brevis both have their origins on the fibula, and they both pass behind the lateral malleolus where their tendons pass under the fibular retinacula. Under the foot, the fibularis longus stretches from the lateral to the medial side in a groove, thus bracing the transverse arch of the foot. The fibularis brevis is attached on the lateral side to the tuberosity of the fifth metatarsal. Together, these two fibularis muscles form the strongest pronators of the foot. The fibularis muscles are highly variable, and several variants can occasionally be present. Of the posterior muscles three are in the superficial layer. The major plantar flexors, commonly referred to as the triceps surae, are the soleus, which arises on the proximal side of both leg bones, and the gastrocnemius, the two heads of which arises on the distal end of the femur. These muscles unite in a large terminal tendon, the Achilles tendon, which is attached to the posterior tubercle of the calcaneus. The plantaris closely follows the lateral head of the gastrocnemius. Its tendon runs between those of the soleus and gastrocnemius and is embedded in the medial end of the calcaneus tendon.In the deep layer, the tibialis posterior has its origin on the interosseus membrane and the neighbouring bone areas and runs down behind the medial malleolus. Under the foot it splits into a thick medial part attached to the navicular bone and a slightly weaker lateral part inserted to the three cuneiform bones. The muscle produces simultaneous plantar flexion and supination in the non-weight-bearing leg, and approximates the heel to the calf of the leg. The flexor hallucis longus arises distally on the fibula and on the interosseus membrane from where its relatively thick muscle belly extends far distally. Its tendon extends beneath the flexor retinaculum to the sole of the foot and finally attaches on the base of the last phalanx of the hallux. It plantarflexes the hallux and assists in supination. The flexor digitorum longus, finally, has its origin on the upper part of the tibia. Its tendon runs to the sole of the foot where it forks into four terminal tendon attached to the last phalanges of the four lateral toes. It crosses the tendon of the tibialis posterior distally on the tibia, and the tendon of the flexor hallucis longus in the sole. Distally to its division, the quadratus plantae radiates into it and near the middle phalanges its tendons penetrate the tendons of the flexor digitorum brevis. In the non-weight-bearing leg, it plantar flexes the toes and foot and supinates. In the weight-bearing leg it supports the plantar arch. (For the popliteus, see above.) Intrinsic The intrinsic muscles of the foot, muscles whose bellies are located in the foot proper, are either dorsal (top) or plantar (sole). On the dorsal side, two long extrinsic extensor muscles are superficial to the intrinsic muscles, and their tendons form the dorsal aponeurosis of the toes. The short intrinsic extensors and the plantar and dorsal interossei radiates into these aponeuroses. The extensor digitorum brevis and extensor hallucis brevis have a common origin on the anterior side of the calcaneus, from where their tendons extend into the dorsal aponeuroses of digits 1–4. They act to dorsiflex these digits.The plantar muscles can be subdivided into three groups associated with three regions: those of the big digit, the little digit, and the region between these two. All these muscles are covered by the thick and dense plantar aponeurosis, which, together with two tough septa, form the spaces of the three groups. These muscles and their fatty tissue function as cushions that transmit the weight of the body downward. As a whole, the foot is a functional entity. The abductor hallucis stretches along the medial edge of the foot, from the calcaneus to the base of the first phalanx of the first digit and the medial sesamoid bone. It is an abductor and a weak flexor, and also helps maintain the arch of the foot. Lateral to the abductor hallucis is the flexor hallucis brevis, which originates from the medial cuneiform bone and from the tendon of the tibialis posterior. The flexor hallucis has a medial and a lateral head inserted laterally to the abductor hallucis. It is an important plantar flexor which comes into prominent use in classical ballet (i.e. for pointe work). The adductor hallucis has two heads; a stronger oblique head which arises from the cuboid and lateral cuneiform bones and the bases of the second and third metatarsals; and a transverse head which arises from the distal ends of the third-fifth metatarsals. Both heads are inserted on the lateral sesamoid bone of the first digit. The muscle acts as a tensor to the arches of the foot, but can also adduct the first digit and plantar flex its first phalanx.The opponens digiti minimi originates from the long plantar ligament and the plantar tendinous sheath of the fibularis (peroneus) longus and is inserted on the fifth metatarsal. When present, it acts to plantar flex the fifth digit and supports the plantar arch. The flexor digiti minimi arises from the region of base of the fifth metatarsal and is inserted onto the base of the first phalanx of the fifth digit where it is usually merged with the abductor of the first digit. It acts to plantar flex the last digit. The largest and longest muscles of the little toe is the abductor digiti minimi. Stretching from the lateral process of the calcaneus, with a second attachment on the base of the fifth metatarsal, to the base of the fifth digits first phalanx, the muscle forms the lateral edge of the sole. Except for supporting the arch, it plantar flexes the little toe and also acts as an abductor.The four lumbricales have their origin on the tendons of the flexor digitorum longus, from where they extend to the medial side of the bases of the first phalanx of digits two-five. Except for reinforcing the plantar arch, they contribute to plantar flexion and move the four digits toward the big toe. They are, in contrast to the lumbricales of the hand, rather variable, sometimes absent and sometimes more than four are present. The quadratus plantae arises with two slips from margins of the plantar surface of the calcaneus and is inserted into the tendon(s) of the flexor digitorum longus, and is known as the "plantar head" of this latter muscle. The three plantar interossei arise with their single heads on the medial side of the third-fifth metatarsals and are inserted on the bases of the first phalanges of these digits. The two heads of the four dorsal interossei arise on two adjacent metatarsals and merge in the intermediary spaces. Their distal attachment is on the bases of the proximal phalanges of the second-fourth digits. The interossei are organized with the second digit as a longitudinal axis; the plantars act as adductors and pull digits 3–5 towards the second digit; while the dorsals act as abductors. Additionally, the interossei act as plantar flexors at the metatarsophalangeal joints. Lastly, the flexor digitorum brevis arises from underneath the calcaneus to insert its tendons on the middle phalanges of digit 2–4. Because the tendons of the flexor digitorum longus run between these tendons, the brevis is sometimes called perforatus. The tendons of these two muscles are surrounded by a tendinous sheath. The brevis acts to plantar flex the middle phalanges. Flexibility Flexibility can be simply defined as the available range of motion (ROM) provided by a specific joint or group of joints. For the most part, exercises that increase flexibility are performed with intentions to boost overall muscle length, reduce the risks of injury and to potentially improve muscular performance in physical activity. Stretching muscles after engagement in any physical activity can improve muscular strength, increase flexibility, and reduce muscle soreness. If limited movement is present within a joint, the "insufficient extensibility" of the muscle, or muscle group, could be restricting the activity of the affected joint. Stretching Stretching prior to strenuous physical activity has been thought to increase muscular performance by extending the soft tissue past its attainable length in order to increase range of motion. Many physically active individuals practice these techniques as a “warm-up” in order to achieve a certain level of muscular preparation for specific exercise movements. When stretching, muscles should feel somewhat uncomfortable but not physically agonizing. Plantar flexion: One of the most popular lower leg muscle stretches is the step standing heel raises, which mainly involves the gastrocnemius, soleus, and the Achilles tendon. Standing heel raises allow the individual to activate their calf muscles by standing on a step with toes and forefoot, leaving the heel hanging off the step, and plantar flexing the ankle joint by raising the heel. This exercise is easily modified by holding on to a nearby rail for balance and is generally repeated 5–10 times. Dorsiflexion: In order to stretch the anterior muscles of the lower leg, crossover shin stretches work well. This motion will stretch the dorsiflexion muscles, mainly the anterior tibialis, extensor hallucis longus and extensor digitorum longus, by slowly causing the muscles to lengthen as body weight is leaned on the ankle joint by using the floor as resistance against the top of the foot. Crossover shin stretches can vary in intensity depending on the amount of body weight applied on the ankle joint as the individual bends at the knee. This stretch is typically held for 15–30 seconds. Eversion and inversion: Stretching the eversion and inversion muscles allows for better range of motion to the ankle joint. Seated ankle elevations and depressions will stretch the fibularis (peroneus) and tibilalis muscles that are associated with these movements as they lengthen. Eversion muscles are stretched when the ankle becomes depressed from the starting position. In like manner, the inversion muscles are stretched when the ankle joint becomes elevated. Throughout this seated stretch, the ankle joint is to remain supported while depressed and elevated with the ipsilateral (same side) hand in order to sustain the stretch for 10–15 seconds. This stretch will increase overall eversion and inversion muscle group length and provide more flexibility to the ankle joint for larger range of motion during activity. Blood supply The arteries of the leg are divided into a series of segments. In the pelvis area, at the level of the last lumbar vertebra, the abdominal aorta, a continuation the descending aorta, splits into a pair of common iliac arteries. These immediately split into the internal and external iliac arteries, the latter of which descends along the medial border of the psoas major to exits the pelvis area through the vascular lacuna under the inguinal ligament.The artery enters the thigh as the femoral artery which descends the medial side of the thigh to the adductor canal. The canal passes from the anterior to the posterior side of the limb where the artery leaves through the adductor hiatus and becomes the popliteal artery. On the back of the knee the popliteal artery runs through the popliteal fossa to the popliteal muscle where it divides into anterior and posterior tibial arteries.In the lower leg, the anterior tibial enters the extensor compartment near the upper border of the interosseus membrane to descend between the tibialis anterior and the extensor hallucis longus. Distal to the superior and extensor retinacula of the foot it becomes the dorsal artery of the foot. The posterior tibial forms a direct continuation of the popliteal artery which enters the flexor compartment of the lower leg to descend behind the medial malleolus where it divides into the medial and lateral plantar arteries, of which the posterior branch gives rise to the fibular artery.For practical reasons the lower limb is subdivided into somewhat arbitrary regions: The regions of the hip are all located in the thigh: anteriorly, the subinguinal region is bounded by the inguinal ligament, the sartorius, and the pectineus and forms part of the femoral triangle which extends distally to the adductor longus. Posteriorly, the gluteal region corresponds to the gluteus maximus. The anterior region of the thigh extends distally from the femoral triangle to the region of the knee and laterally to the tensor fasciae latae. The posterior region ends distally before the popliteal fossa. The anterior and posterior regions of the knee extend from the proximal regions down to the level of the tuberosity of the tibia. In the lower leg the anterior and posterior regions extend down to the malleoli. Behind the malleoli are the lateral and medial retromalleolar regions and behind these is the region of the heel. Finally, the foot is subdivided into a dorsal region superiorly and a plantar region inferiorly. Veins The veins are subdivided into three systems. The deep veins return approximately 85 percent of the blood and the superficial veins approximately 15 percent. A series of perforator veins interconnect the superficial and deep systems. In the standing posture, the veins of the leg have to handle an exceptional load as they act against gravity when they return the blood to the heart. The venous valves assist in maintaining the superficial to deep direction of the blood flow.Superficial veins: Great saphenous vein Small saphenousDeep veins: Femoral vein, whose segments are the common femoral vein and the subsartorial vein. Popliteal vein Anterior tibial vein Posterior tibial vein Fibular vein Nerve supply The sensory and motor innervation to the lower limb is supplied by the lumbosacral plexus, which is formed by the ventral rami of the lumbar and sacral spinal nerves with additional contributions from the subcostal nerve (T12) and coccygeal nerve (Co1). Based on distribution and topography, the lumbosacral plexus is subdivided into the lumbar plexus (T12-L4) and the Sacral plexus (L5-S4); the latter is often further subdivided into the sciatic and pudendal plexuses:The lumbar plexus is formed lateral to the intervertebral foramina by the ventral rami of the first four lumbar spinal nerves (L1-L4), which all pass through psoas major. The larger branches of the plexus exit the muscle to pass sharply downward to reach the abdominal wall and the thigh (under the inguinal ligament); with the exception of the obturator nerve which pass through the lesser pelvis to reach the medial part of the thigh through the obturator foramen. The nerves of the lumbar plexus pass in front of the hip joint and mainly support the anterior part of the thigh.The iliohypogastric (T12-L1) and ilioinguinal nerves (L1) emerge from the psoas major near the muscles origin, from where they run laterally downward to pass anteriorly above the iliac crest between the transversus abdominis and abdominal internal oblique, and then run above the inguinal ligament. Both nerves give off muscular branches to both these muscles. Iliohypogastric supplies sensory branches to the skin of the lateral hip region, and its terminal branch finally pierces the aponeurosis of the abdominal external oblique above the inguinal ring to supply sensory branches to the skin there. Ilioinguinalis exits through the inguinal ring and supplies sensory branches to the skin above the pubic symphysis and the lateral portion of the scrotum.The genitofemoral nerve (L1, L2) leaves psoas major below the two former nerves, immediately divides into two branches that descends along the muscles anterior side. The sensory femoral branch supplies the skin below the inguinal ligament, while the mixed genital branch supplies the skin and muscles around the sex organ. The lateral femoral cutaneous nerve (L2, L3) leaves psoas major laterally below the previous nerve, runs obliquely and laterally downward above the iliacus, exits the pelvic area near the iliac spine, and supplies the skin of the anterior thigh.The obturator nerve (L2-L4) passes medially behind psoas major to exit the pelvis through the obturator canal, after which it gives off branches to obturator externus and divides into two branches passing behind and in front of adductor brevis to supply motor innervation to all the other adductor muscles. The anterior branch also supplies sensory nerves to the skin on a small area on the distal medial aspect of the thigh. The femoral nerve (L2-L4) is the largest and longest of the nerves of the lumbar plexus. It supplies motor innervation to iliopsoas, pectineus, sartorius, and quadriceps; and sensory branches to the anterior thigh, medial lower leg, and posterior foot.The nerves of the sacral plexus pass behind the hip joint to innervate the posterior part of the thigh, most of the lower leg, and the foot. The superior (L4-S1) and inferior gluteal nerves (L5-S2) innervate the gluteus muscles and the tensor fasciae latae. The posterior femoral cutaneous nerve (S1-S3) contributes sensory branches to the skin on the posterior thigh. The sciatic nerve (L4-S3), the largest and longest nerve in the human body, leaves the pelvis through the greater sciatic foramen. In the posterior thigh it first gives off branches to the short head of the biceps femoris and then divides into the tibial (L4-S3) and common fibular nerves (L4-S2). The fibular nerve continues down on the medial side of biceps femoris, winds around the fibular neck and enters the front of the lower leg. There it divides into a deep and a superficial terminal branch. The superficial branch supplies the fibularis muscles and the deep branch enters the extensor compartment; both branches reaches into the dorsal foot. In the thigh, the tibial nerve gives off branches to semitendinosus, semimembranosus, adductor magnus, and the long head of the biceps femoris. The nerve then runs straight down the back of the leg, through the popliteal fossa to supply the ankle flexors on the back of the lower leg and then continues down to supply all the muscles in the sole of the foot. The pudendal (S2-S4) and coccygeal nerves (S5-Co2) supply the muscles of the pelvic floor and the surrounding skin.The lumbosacral trunk is a communicating branch passing between the sacral and lumbar plexuses containing ventral fibers from L4. The coccygeal nerve, the last spinal nerve, emerges from the sacral hiatus, unites with the ventral rami of the two last sacral nerves, and forms the coccygeal plexus. Lower leg and foot The lower leg and ankle need to keep exercised and moving well as they are the base of the whole body. The lower extremities must be strong in order to balance the weight of the rest of the body, and the gastrocnemius muscles take part in much of the blood circulation. Exercises Isometric and standard There are a number of exercises that can be done to strengthen the lower leg. For example, in order to activate plantar flexors in the deep plantar flexors one can sit on the floor with the hips flexed, the ankle neutral with knees fully extended as they alternate pushing their foot against a wall or platform. This kind of exercise is beneficial as it hardly causes any fatigue. Another form of isometric exercise for the gastrocnemius would be seated calf raises which can be done with or without equipment. One can be seated at a table with their feet flat on the ground, and then plantar flex both ankles so that the heels are raised off the floor and the gastrocnemius flexed. An alternate movement could be heel drop exercises with the toes being propped on an elevated surface—as an opposing movement this would improve the range of motion. One-legged toe raises for the gastrocnemius muscle can be performed by holding one dumbbell in one hand while using the other for balance, and then standing with one foot on a plate. The next step would be to plantar flex and keep the knee joint straight or flexed slightly. The triceps surae is contracted during this exercise. Stabilization exercises like the BOSU ball squat are also important especially as they assist in the ankles having to adjust to the balls form in order to balance. Clinical significance Lower leg injury Lower leg injuries are common while running or playing sports. About 10% of all injuries in athletes involve the lower extremities. The majority of athletes sprain their ankles; this is mainly caused by the increased loads onto the feet when they move into the foot down or in an outer ankle position. All areas of the foot, which are the forefoot, midfoot, and rearfoot, absorb various forces while running and this can also lead to injuries. Running and various activities can cause stress fractures, tendinitis, musculotendinous injuries, or any chronic pain to our lower extremities such as the tibia. Types of activities Injuries to quadriceps or hamstrings are caused by the constant impact loads to the legs during activities, such as kicking a ball. While doing this type of motion, 85% of that shock is absorbed to the hamstrings; this can cause strain to those muscles. Jumping – is another risk because if the legs do not land properly after an initial jump, there may be damage to the meniscus in the knees, sprain to the ankle by everting or inverting the foot, or damage to the Achilles tendon and gastrocnemius if there is too much force while plantar flexing. Weight lifting – such as the improperly performed deep squat, is also dangerous to the lower limbs, because the exercise can lead to an overextension, or an outstretch, of our ligaments in the knee and can cause pain over time. Running – the most common activity associated with lower leg injury. There is constant pressure and stress being put on the feet, knees, and legs while running by gravitational force. Muscle tears in our legs or pain in various areas of the feet can be a result of poor biomechanics of running. Running The most common injuries in running involve the knees and the feet. Various studies have focused on the initial cause of these running related injuries and found that there are many factors that correlate to these injuries. Female distance runners who had a history of stress fracture injuries had higher vertical impact forces than non-injured subjects. The large forces onto the lower legs were associated with gravitational forces, and this correlated with patellofemoral pain or potential knee injuries. Researchers have also found that these running-related injuries affect the feet as well, because runners with previous injuries showed more foot eversion and over-pronation while running than non-injured runners. This causes more loads and forces on the medial side of the foot, causing more stress on the tendons of the foot and ankle. Most of these running injuries are caused by overuse: running longer distances weekly for a long duration is a risk for injuring the lower legs. Prevention tools Voluntary stretches to the legs, such as the wall stretch, condition the hamstrings and the calf muscle to various movements before vigorously working them. The environment and surroundings, such as uneven terrain, can cause the feet to position in an unnatural way, so wearing shoes that can absorb forces from the grounds impact and allow for stabilizing the feet can prevent some injuries while running as well. Shoes should be structured to allow friction-traction at the shoe surface, space for different foot-strike stresses, and for comfortable, regular arches for the feet. Summary The chance of damaging our lower extremities will be reduced by having knowledge about some activities associated with lower leg injury and developing a correct form of running, such as not over-pronating the foot or overusing the legs. Preventative measures, such as various stretches, and wearing appropriate footwear, will also reduce injuries. Fracture A fracture of the leg can be classified according to the involved bone into: Femoral fracture (in the upper leg) Crus fracture (in the lower leg) Pain management Lower leg and foot pain management is critical in reducing the progression of further injuries, uncomfortable sensations and limiting alterations while walking and running. Most individuals suffer from various pains in their lower leg and foot due to different factors. Muscle inflammation, strain, tenderness, swelling and muscle tear from muscle overuse or incorrect movement are several conditions often experienced by athletes and the common public during and after high impact physical activities. Therefore, suggested pain management mechanisms are provided to reduce pain and prevent the progression of injury. Plantar fasciitis A plantar fasciitis foot stretch is one of the recommended methods to reduce pain caused by plantar fasciitis (Figure 1). To do the plantar fascia stretch, while sitting in a chair place the ankle on the opposite knee and hold the toes of the impaired foot, slowly pulling back. The stretch should be held for approximately ten seconds, three times per day. Medial tibial stress syndrome (shin splint) Several methods can be utilized to help control pain caused by shin splints. Placing ice on the affected area prior to and after running will aid in reducing pain. In addition, wearing orthotic devices including a neoprene sleeve (Figure 2) and wearing appropriate footwear such as a foot arch can help to eliminate the condition. Stretching and strengthening of the anterior tibia or medial tibia by performing exercises of plantar and dorsi flexors such as calf stretch can also help in easing the pain. Achilles tendinopathy There are numerous appropriate approaches to handling pain resulting from Achilles tendinitis. The primary action is to rest. Activities that do not provide additional stress to the affected tendon are also recommended. Wearing orthothics or prostheses will provide cushion and will prevent the affected Achilles tendon from experiencing further stress when walking and performing therapeutic stretches. A few stretch modalities or eccentric exercises such as toe extension and flexion and calf and heel stretch are beneficial in lowering pain with Achilles tendinopathy patients (Figure 4) Society and culture Adolescent and adult women in many Western cultures often remove the hair from their legs. Toned, tanned, shaved legs are sometimes perceived as a sign of youthfulness and are often considered attractive in these cultures. Men generally do not shave their legs in any culture. However, leg-shaving is a generally accepted practice in modeling. It is also fairly common in sports where the hair removal makes the athlete appreciably faster by reducing drag; the most common case of this is competitive swimming. Image gallery See also Distraction osteogenesis (leg lengthening) References Literature specified by multiple pages above: Chaitow, Leon; Walker DeLany, Judith (2000). Clinical Application of Neuromuscular Techniques: The Lower Body. Elsevier Health Sciences. ISBN 0-443-06284-6. Archived from the original on 22 September 2014. consulting editors, Lawrence M. Ross, Edward D. Lamperti; authors, Michael Schuenke, Erik Schulte, Udo Schumacher. (2006). Thieme Atlas of Anatomy: General Anatomy and Musculoskeletal System. Thieme. ISBN 1-58890-419-9. {{cite book}}: |author= has generic name (help)CS1 maint: multiple names: authors list (link) Platzer, Werner (2004). Color Atlas of Human Anatomy, Vol. 1: Locomotor System (5th ed.). Thieme. ISBN 3-13-533305-1. External links Interactive images at InnerBody

Can you describe Fibrothorax, to me Aarogya

Fibrothorax

Fibrothorax is a medical condition characterised by severe scarring (fibrosis) and fusion of the layers of the pleural space surrounding the lungs resulting in decreased movement of the lung and ribcage. The main symptom of fibrothorax is shortness of breath. There also may be recurrent fluid collections surrounding the lungs. Fibrothorax may occur as a complication of many diseases, including infection of the pleural space known as an empyema or bleeding into the pleural space known as a haemothorax.Fibrosis in the pleura may be produced intentionally using a technique called pleurodesis to prevent recurrent punctured lung (pneumothorax), and the usually limited fibrosis that this produces can rarely be extensive enough to lead to fibrothorax. The condition is most often diagnosed using an X-ray or CT scan, the latter more readily detecting mild cases. Fibrothorax is often treated conservatively with watchful waiting but may require surgery. The outlook is usually good as long as there is no underlying pulmonary fibrosis or complications following surgery. The disease is highly uncommon. Signs and symptoms Signs Reduced movement of the ribcage during breathing, reduced breath sounds on the affected side(s), and a dull feeling when the chest is pressed are common signs observed during examination for fibrothorax. Sharp chest pain with deep breaths or coughing may be seen in some cases. Severe cases of fibrothorax can lead to respiratory failure due to inadequate ventilation and cause abnormally high levels of carbon dioxide in the bloodstream. Symptoms The condition only causes symptoms if the visceral pleura is affected. Although fibrothorax may not cause any symptoms, people affected by the disorder may report shortness of breath. Persistent, recurrent pleural effusions are a possible symptom, caused by the persistent cavity formed by the hardening pleura around the original fluid collection. Shortness of breath tends to develop gradually and may worsen over time. Less commonly, fibrothorax may cause chest discomfort or a dry cough. Fibrothorax may occur as a complication of other diseases. Symptoms of the underlying problem are sometimes seen, for example, fever in cases of empyema. Causes Fibrothorax is often a complication of other diseases that cause inflammation of the pleura. These include infections such as an empyema or tuberculosis, or bleeding within the pleural space known as a haemothorax. Exposure to certain substances, such as asbestos, can cause generalised fibrosis of the lungs, which may involve the pleura and lead to fibrothorax. Less common causes of fibrothorax include collagen vascular diseases such as systemic lupus erythematosus, sarcoidosis, and rheumatoid arthritis; kidney failure leading to uraemia; and side effects of certain medications. The medications most commonly associated with pleural fibrosis are the ergot alkaloids bromocriptine, pergolide, and methysergide. Fibrothorax may also occur without a clear underlying cause, in which case it is known as idiopathic fibrothorax. A technique called pleurodesis can be used to intentionally create scar tissue within the pleural space, usually as a treatment for repeated episodes of a punctured lung, known as a pneumothorax, or for pleural effusions caused by cancer. While this procedure usually generates only limited scar tissue, in rare cases a fibrothorax can develop. Mechanism Fibrosis can affect one or both of the two layers of tissue forming the pleura—the visceral pleura adjacent to the lung and the parietal pleura adjacent to the ribcage. The term fibrothorax implies severe fibrosis affecting both the visceral and the outer (parietal) pleura, fusing the lung to the chest wall. The condition starts as an undrained pleural effusion. Over time, the undrained pleural effusion causes sustained inflammation of the pleura, which can then lead to deposition of fibrin in the pleura and the development of a fibrotic scar. Eventually, a "peel" that is rich in collagen forms around the fluid collection. From this point, the illness can no longer be treated with thoracentesis, since the fluid will return to the cavity maintained by the peel.Over time, generally over the years, the fibrotic scar tissue slowly tightens and thickens, contracting the contents of one or both halves of the chest and reducing the mobility of the ribs. The peel can become deeper than 2 cm. Within the chest, the lung is compressed and unable to expand (trapped lung), making it vulnerable to collapse and causing breathlessness. Restrictive lung disease from fibrothorax may occur when pleural fibrosis is so severe that it involves the diaphragm and ribcage and results primarily from decreased rib movement. Microscopic At the microscopic level, collagen fibres deposit in a basket weave pattern and form scar tissue. Usually, the underlying condition has to cause intense inflammation of the pleura, though it is unclear exactly how this results in fibrosis. The precise mechanisms producing the fibrosis are not entirely clear. However, research indicates a protein called Transforming Growth Factor beta (TGF-β) plays a central role in producing fibrothorax. Anti-TGF-β antibodies prevent fibrothorax in empyema in animal models. Diagnosis A fibrothorax can typically be diagnosed by taking an appropriate medical history in combination with the use of appropriate imaging techniques such as a plain chest X-ray or CT scan. These imaging techniques can detect fibrothorax and pleural thickening that surround the lungs. The presence of a thickened peel with or without calcification are common features of fibrothorax when imaged. CT scans can more readily differentiate whether pleural thickening is due to extra fat deposition or true pleural thickening than X-rays.If a fibrothorax is severe, the thickening may restrict the lung on the affected side causing a loss of lung volume. Additionally, the mediastinum may be physically shifted toward the affected side. A reduction in the size of one side of the chest (hemithorax) on an X-ray or CT scan of the chest suggests chronic scarring. Signs of the underlying disease causing the fibrothorax are also occasionally seen on the X-ray. A CT scan may show features similar to those seen on a plain X-ray. Lung function testing typically demonstrates findings consistent with restrictive lung disease. Treatment Non-surgical Conservative non-surgical treatment of fibrothorax is generally done by treating its underlying cause and is reserved for milder cases. Tobacco smoking cessation is strongly recommended since tobacco smoke exposure can worsen fibrosis. Severe cases of fibrothorax may require supportive mechanical ventilation if the affected person is unable to breathe adequately on their own.In cases of fibrothorax caused by medication, it is recommended that the offending medications be stopped. Ergot alkaloid medications, which can worsen pleural fibrosis, are typically avoided. Cases of fibrothorax attributable to medication typically stop worsening if the provoking medication is stopped. In some situations, medication-induced fibrothorax improves after stopping the causative medication but fibrothorax usually does not completely resolve.Watchful waiting is appropriate for milder cases of fibrothorax in certain situations. Fibrothorax caused by tuberculosis, empyema, or haemothorax often improves spontaneously 3–6 months after the precipitating illness. Corticosteroids are commonly used to treat fibrothorax but are not well-supported by available evidence. Surgical In severe cases of fibrothorax that are compromising a persons ability to breathe, the scar tissue (fibrous peel) causing fibrothorax can be surgically removed using a technique called decortication. However, surgical decortication is an invasive procedure which carries the risk of complications including a small risk of death, and is therefore generally only considered if severe symptoms are present and have been for many months. Surgical decortication is generally considered for people with fibrothoraces that are severe, causing significant shortness of breath, and have otherwise relatively healthy lungs since this enhances the likelihood of a better outcome. Surgical removal of the pleura (pleurectomy) may be performed in refractory cases, as often happens when asbestosis is the cause. Prognosis Fibrothorax complicating another condition, such as tuberculous pleuritis, empyema, or acute haemothorax often spontaneously resolves in 3-6 months.The prognosis after surgical decortication is variable and depends on the health of the underlying lung before the procedure takes place. If the lung was otherwise healthy, then certain aspects of lung function, such as vital capacity, may improve after decortication. If, however, the lung had significant disease, then lung function often does not improve and may even deteriorate after such intervention. The duration of fibrothorax does not affect prognosis.The mortality of surgery is less than 1% overall, but rises to 4-6% in the elderly. Other factors predicting poorer surgical outcomes include intraoperative complications, incomplete surgery, lung disease beyond the fibrothorax being treated, and specific causes of fibrothorax such as asbestosis. Epidemiology Sporadic cases are rarely reported in the medical literature, for example, due to iatrogenic or postoperative complications. Fibrothorax is rare in developed countries, mainly due to a lower incidence of tuberculosis. The condition is far more common in workers exposed to asbestos, with 5–13.5% of those exposed subsequently developing some degree of pleural fibrosis, sometimes not diagnosed until decades after the initial exposure. == References ==

Hey Aarogya , Do you know what is Hypergammaglobulinemia,

Hypergammaglobulinemia

Hypergammaglobulinemia is a medical condition with elevated levels of gamma globulin. It is a type of immunoproliferative disorder. Types Hypergammaglobulinemia is a condition that is characterized by the increased levels of a certain immunoglobulin in the blood serum. The name of the disorder refers to an excess of proteins after serum protein electrophoresis (found in the gammaglobulin region).Most hypergammaglobulinemias are caused by an excess of immunoglobulin M (IgM), because this is the default immunoglobulin type prior to class switching. Some types of hypergammaglobulinemia are actually caused by a deficiency in the other major types of immunoglobulins, which are IgA, IgE and IgG. There are 5 types of hypergammaglobulinemias associated with hyper IgM.MeSH considers hyper IgM syndrome to be a form of dysgammaglobulinemia, not a form of hypergammaglobulinemia. Type 1 X-linked immunodeficiency with hyper–immunoglobulin M, which is also called type 1 hyper IgM, is a rare form of primary immunodeficiency disease caused by a mutation in the Tumor Necrosis Factor Super Family member 5 (TNFSF5) gene, which codes for CD40 ligand. This gene is located on the long arm of the X chromosome at position 26, denoted Xq26. Normally, CD40 ligand is expressed on activated T cells, and is necessary to induce immunoglobulin class switching from IgM to the other immunoglobulin types. It does this by binding to its ligand, CD40, which is found expressed on the surface of B cells. The mutation in the TNFSF5 gene causes there to be no recognition of CD40 by CD40 ligand, and thus the T cells do not induce Ig class switching in B cells, so there are markedly reduced levels of IgG, IgA, and IgE, but have normal or elevated levels of IgM. CD40 ligand is also required in the functional maturation of T lymphocytes and macrophages, so patients with this disorder have a variable defect in T-lymphocyte and macrophage effector function, as well as hyper IgM. Type 2 Immunodeficiency with hyper IgM type 2 is caused by a mutation in the Activation-Induced Cytidine Deaminase (AICDA) gene, which is located on the short arm of chromosome 12. The protein that is encoded by this gene is called Activation-Induced Cytidine Deaminase (AICDA) and functions as a DNA-editing deaminase that induces somatic hypermutation, class switch recombination, and immunoglobulin gene conversion in B cells. When a person is homozygous for the mutation in the AICDA gene, the protein fails to function, and thus somatic hypermutation, class switch recombination, and immunoglobulin gene conversion cannot occur, which creates an excess of IgM. Type 3 Immunodeficiency with hyper IgM type 3 is caused by a mutation in the gene that codes for CD40. As mentioned above, CD40 is expressed on the surface of B cells, and its binding to CD40 ligand on activated T cells induces Ig class switching. When the mutation is present, there is no signal for B cells to undergo class switching, so there is an excess of IgM and little to no other immunoglobulin types produced. Type 4 Immunodeficiency with hyper IgM type 4 is poorly characterized. All that is known is that there is an excess of IgM in the blood, with normal levels of the other immunoglobulins. The exact cause is yet to be determined. Type 5 Immunodeficiency with hyper IgM type 5 is caused by a mutation in the Uracil-DNA glycosylase (UNG) gene, which, like AICDA, is located on chromosome 12. This codes for Uracil DNA Glycosylase, which is responsible for excising previous uracil bases that are due to cytosine deamination, or previous uracil misincorporation from double-stranded previous DNA substrates. This enzyme is also responsible for helping with gene conversion during somatic recombination in B cells. The mutation in the gene causes an enzyme that does not function properly, thus gene conversion does not proceed and class switching cannot occur. See also Monoclonal gammopathy of undetermined significance References == External links ==

Hey Aarogya , Do you know what is Femur,

Femur

The femur (; pl. femurs or femora ), or thigh bone, is the proximal bone of the hindlimb in tetrapod vertebrates. The head of the femur articulates with the acetabulum in the pelvic bone forming the hip joint, while the distal part of the femur articulates with the tibia (shinbone) and patella (kneecap), forming the knee joint. By most measures the two (left and right) femurs are the strongest bones of the body, and in humans, the largest and thickest. Structure The femur is the only bone in the upper leg. The two femurs converge medially toward the knees, where they articulate with the proximal ends of the tibiae. The angle of convergence of the femora is a major factor in determining the femoral-tibial angle. Human females have thicker pelvic bones, causing their femora to converge more than in males. In the condition genu valgum (knock knee) the femurs converge so much that the knees touch one another. The opposite extreme is genu varum (bow-leggedness). In the general population of people without either genu valgum or genu varum, the femoral-tibial angle is about 175 degrees.The femur is the largest and thickest bone in the human body. By some measures, it is also the strongest bone in the human body. This depends on the type of measurement taken to calculate strength. Some strength tests show the temporal bone in the skull to be the strongest bone. The femur length on average is 26.74% of a persons height, a ratio found in both men and women and most ethnic groups with only restricted variation, and is useful in anthropology because it offers a basis for a reasonable estimate of a subjects height from an incomplete skeleton. The femur is categorised as a long bone and comprises a diaphysis (shaft or body) and two epiphyses (extremities) that articulate with adjacent bones in the hip and knee. Upper part The upper or proximal extremity (close to the torso) contains the head, neck, the two trochanters and adjacent structures. The upper extremity is the shortest femoral extremity, the lower extremity is the thickest femoral extremity. The head of the femur, which articulates with the acetabulum of the pelvic bone, comprises two-thirds of a sphere. It has a small groove, or fovea, connected through the round ligament to the sides of the acetabular notch. The head of the femur is connected to the shaft through the neck or collum. The neck is 4–5 cm. long and the diameter is smallest front to back and compressed at its middle. The collum forms an angle with the shaft in about 130 degrees. This angle is highly variant. In the infant it is about 150 degrees and in old age reduced to 120 degrees on average. An abnormal increase in the angle is known as coxa valga and an abnormal reduction is called coxa vara. Both the head and neck of the femur is vastly embedded in the hip musculature and can not be directly palpated. In skinny people with the thigh laterally rotated, the head of the femur can be felt deep as a resistance profound (deep) for the femoral artery.The transition area between the head and neck is quite rough due to attachment of muscles and the hip joint capsule. Here the two trochanters, greater and lesser trochanter, are found. The greater trochanter is almost box-shaped and is the most lateral prominent of the femur. The highest point of the greater trochanter is located higher than the collum and reaches the midpoint of the hip joint. The greater trochanter can easily be felt. The trochanteric fossa is a deep depression bounded posteriorly by the intertrochanteric crest on the medial surface of the greater trochanter. The lesser trochanter is a cone-shaped extension of the lowest part of the femur neck. The two trochanters are joined by the intertrochanteric crest on the back side and by the intertrochanteric line on the front.A slight ridge is sometimes seen commencing about the middle of the intertrochanteric crest, and reaching vertically downward for about 5 cm. along the back part of the body: it is called the linea quadrata (or quadrate line). About the junction of the upper one-third and lower two-thirds on the intertrochanteric crest is the quadrate tubercle located. The size of the tubercle varies and it is not always located on the intertrochanteric crest and that also adjacent areas can be part of the quadrate tubercle, such as the posterior surface of the greater trochanter or the neck of the femur. In a small anatomical study it was shown that the epiphyseal line passes directly through the quadrate tubercle. Body The body of the femur (or shaft) is large, thick and almost cylindrical in form. It is a little broader above than in the center, broadest and somewhat flattened from before backward below. It is slightly arched, so as to be convex in front, and concave behind, where it is strengthened by a prominent longitudinal ridge, the linea aspera which diverges proximally and distal as the medial and lateral ridge. Proximally the lateral ridge of the linea aspera becomes the gluteal tuberosity while the medial ridge continues as the pectineal line. Besides the linea aspera the shaft has two other bordes; a lateral and medial border. These three bordes separates the shaft into three surfaces: One anterior, one medial and one lateral. Due to the vast musculature of the thigh the shaft can not be palpated.The third trochanter is a bony projection occasionally present on the proximal femur near the superior border of the gluteal tuberosity. When present, it is oblong, rounded, or conical in shape and sometimes continuous with the gluteal ridge. A structure of minor importance in humans, the incidence of the third trochanter varies from 17–72% between ethnic groups and it is frequently reported as more common in females than in males. Lower part The lower extremity of the femur (or distal extremity) is the thickest femoral extremity, the upper extremity is the shortest femoral extremity. It is somewhat cuboid in form, but its transverse diameter is greater than its antero-posterior (front to back). It consists of two oblong eminences known as the condyles.Anteriorly, the condyles are slightly prominent and are separated by a smooth shallow articular depression called the patellar surface. Posteriorly, they project considerably and a deep notch, the Intercondylar fossa of femur, is present between them. The lateral condyle is the more prominent and is the broader both in its antero-posterior and transverse diameters. The medial condyle is the longer and, when the femur is held with its body perpendicular, projects to a lower level. When, however, the femur is in its natural oblique position the lower surfaces of the two condyles lie practically in the same horizontal plane. The condyles are not quite parallel with one another; the long axis of the lateral is almost directly antero-posterior, but that of the medial runs backward and medialward. Their opposed surfaces are small, rough, and concave, and form the walls of the intercondyloid fossa. This fossa is limited above by a ridge, the intercondyloid line, and below by the central part of the posterior margin of the patellar surface. The posterior cruciate ligament of the knee joint is attached to the lower and front part of the medial wall of the fossa and the anterior cruciate ligament to an impression on the upper and back part of its lateral wall.The articular surface of the lower end of the femur occupies the anterior, inferior, and posterior surfaces of the condyles. Its front part is named the patellar surface and articulates with the patella; it presents a median groove which extends downward to the intercondyloid fossa and two convexities, the lateral of which is broader, more prominent, and extends farther upward than the medial.Each condyle is surmounted by an elevation, the epicondyle. The medial epicondyle is a large convex eminence to which the tibial collateral ligament of the knee-joint is attached. At its upper part is the adductor tubercle and behind it is a rough impression which gives origin to the medial head of the gastrocnemius. The lateral epicondyle which is smaller and less prominent than the medial, gives attachment to the fibular collateral ligament of the knee-joint. Development The femur develops from the limb buds as a result of interactions between the ectoderm and the underlying mesoderm, formation occurs roughly around the fourth week of development.By the sixth week of development, the first hyaline cartilage model of the femur is formed by chondrocytes. Endochondral ossification begins by the end of the embryonic period and primary ossification centers are present in all long bones of the limbs, including the femur, by the 12th week of development. The hindlimb development lags behind forelimb development by 1–2 days. Function As the femur is the only bone in the thigh, it serves as an attachment point for all the muscles that exert their force over the hip and knee joints. Some biarticular muscles – which cross two joints, like the gastrocnemius and plantaris muscles – also originate from the femur. In all, 23 individual muscles either originate from or insert onto the femur. In cross-section, the thigh is divided up into three separate fascial compartments divided by fascia, each containing muscles. These compartments use the femur as an axis, and are separated by tough connective tissue membranes (or septa). Each of these compartments has its own blood and nerve supply, and contains a different group of muscles. These compartments are named the anterior, medial and posterior fascial compartments. Muscle attachments Clinical significance Fractures A femoral fracture that involves the femoral head, femoral neck or the shaft of the femur immediately below the lesser trochanter may be classified as a hip fracture, especially when associated with osteoporosis. Femur fractures can be managed in a pre-hospital setting with the use of a traction splint. Diversity among animals In primitive tetrapods, the main points of muscle attachment along the femur are the internal trochanter and third trochanter, and a ridge along the ventral surface of the femoral shaft referred to as the adductor crest. The neck of the femur is generally minimal or absent in the most primitive forms, reflecting a simple attachment to the acetabulum. The greater trochanter was present in the extinct archosaurs, as well as in modern birds and mammals, being associated with the loss of the primitive sprawling gait. The lesser trochanter is a unique development of mammals, which lack both the internal and fourth trochanters. The adductor crest is also often absent in mammals or alternatively reduced to a series of creases along the surface of the bone. Structures analogous to the third trochanter are present in mammals, including some primates.Some species of whales, snakes, and other non-walking vertebrates have vestigial femurs. In some snakes the protruding end of a pelvic spur, a vestigial pelvis and femur remnant which is not connected to the rest of the skeleton, plays a role in mating. This role in mating is hypothesized to have possibly occurred in Basilosauridae, an extinct family of whales with well-defined femurs, lower legs and feet. Occasionally, the genes that code for longer extremities cause a modern whale to develop miniature legs (atavism).One of the earliest known vertebrates to have a femur is the eusthenopteron, a prehistoric lobe-finned fish from the Late Devonian period. Viral metagenomics A recent study revealed that bone is a much richer source of persistent DNA viruses than earlier perceived. Besides Parvovirus 19 and hepatitis B virus, ten additional ones were discovered, namely several members of the herpes- and polyomavirus families, as well as human papillomavirus 31 and torque teno virus. Invertebrates In invertebrate zoology the name femur appears in arthropodology. The usage is not homologous with that of vertebrate anatomy; the term "femur" simply has been adopted by analogy and refers, where applicable, to the most proximal of (usually) the two longest jointed segments of the legs of the arthropoda. The two basal segments preceding the femur are the coxa and trochanter. This convention is not followed in carcinology but it applies in arachnology and entomology. In myriapodology another segment, the prefemur, connects the trochanter and femur. Additional media References External links Media related to Femur at Wikimedia Commons The dictionary definition of Femur at Wiktionary The dictionary definition of thighbone at Wiktionary

Aarogya, elaborate on Histiocytic sarcoma

Histiocytic sarcoma

Histiocytic sarcoma is a tumor derived from histiocytes. The tumor is often positive for CD163 and can appear in the thyroid. However, in some cases it can also appear in the brain. References == External links ==

Please give me a short description about MELAS syndrome , Aarogya

MELAS syndrome

Mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) is one of the family of mitochondrial diseases, which also include MIDD (maternally inherited diabetes and deafness, MERRF syndrome, and Lebers hereditary optic neuropathy. It was first characterized under this name in 1984. A feature of these diseases is that they are caused by defects in the mitochondrial genome which is inherited purely from the female parent. The most common MELAS mutation is mitochondrial mutation, mtDNA, referred to as m.3243A>G. Signs and symptoms MELAS is a condition that affects many of the bodys systems, particularly the brain and nervous system (encephalo-) and muscles (myopathy). In most cases, the signs and symptoms of this disorder appear in childhood following a period of normal development. Children with MELAS often have normal early psychomotor development until the onset of symptoms between 2 and 10 years old. Though less common, infantile onset may occur and may present as failure to thrive, growth retardation and progressive deafness. Onset in older children typically presents as recurrent attacks of a migraine-like headache, anorexia, vomiting, and seizures. Children with MELAS are also frequently found to have short stature.Most people with MELAS have a buildup of lactic acid in their bodies, a condition called lactic acidosis. Increased acidity in the blood can lead to vomiting, abdominal pain, extreme tiredness (fatigue), muscle weakness, loss of bowel control, and difficulty breathing. Less commonly, people with MELAS may experience involuntary muscle spasms (myoclonus), impaired muscle coordination (ataxia), hearing loss, heart and kidney problems, diabetes, epilepsy, and hormonal imbalances. Differential diagnosis The presentation of some cases is similar to that of Kearns–Sayre syndrome.Myoclonus epilepsy associated with ragged red fibers (MERRF) may be confused with MELAS as they both involve seizures, mental deterioration, and myopathy with ragged red fibers on biopsy. MERRF patients may also have hearing loss, visual disturbance secondary to optic atrophy, and short stature. The characteristic myoclonic seizure in MERRF may help to narrow diagnosis, but genetic testing should be considered to distinguish the two conditions.Leigh syndrome may also present with progressive neurological deterioration, seizures, and vomiting mainly in young children. Genetics MELAS is mostly caused by mutations in the genes in mitochondrial DNA, but it can also be caused by mutations in the nuclear DNA. NADH dehydrogenase Some of the genes (MT-ND1, MT-ND5) affected in MELAS encode proteins that are part of NADH dehydrogenase (also called complex I) in mitochondria, that helps convert oxygen and simple sugars to energy. Transfer RNAs Other genes (MT-TH, MT-TL1, and MT-TV) encode mitochondrial specific transfer RNAs (tRNAs).Mutations in MT-TL1 cause more than 80 percent of all cases of MELAS. They impair the ability of mitochondria to make proteins, use oxygen, and produce energy. Researchers have not determined how changes in mitochondrial DNA lead to the specific signs and symptoms of MELAS. They continue to investigate the effects of mitochondrial gene mutations in different tissues, particularly in the brain. Inheritance This condition is inherited in a mitochondrial pattern, which is also known as maternal inheritance and heteroplasmy. This pattern of inheritance applies to genes contained in mitochondrial DNA. Because egg cells, but not sperm cells, contribute mitochondria to the developing embryo, only females pass mitochondrial conditions to their children. Mitochondrial disorders can appear in every generation of a family and can affect both males and females, but fathers do not pass mitochondrial traits to their children. In most cases, people with MELAS inherit an altered mitochondrial gene from their mother. Less commonly, the disorder results from a new mutation in a mitochondrial gene and occurs in people with no family history of MELAS. Diagnosis MRI: Multifocal infarct-like cortical areas in different stages of ischemic evolution, areas that do not conform to any known vascular territory. Initial lesions often occur in the occipital or parietal lobes with eventual involvement of the cerebellum, cerebral cortex, basal ganglia, and thalamus.Lactate levels are often elevated in serum and cerebrospinal fluid. MR spectroscopy may show an elevated lactate peak in affected and even unaffected brain areas. Muscle biopsy shows ragged red fibers. However, genetic evaluation should be done first, which eliminates the need for muscle biopsy in most cases. Diagnosis may be molecular or clinical: Stroke-like episodes before or after 40 years old Encephalopathy with seizures or dementia Blood lactic acidosis* or ragged red fibers on muscle biopsyDue to mitochondrial heteroplasmy, urine and blood testing is preferable to blood alone. PCR and ARMS-PCR are commonly used, reliable, rapid, and cost-effective techniques for the diagnosis of MELAS.Hearing loss and mitochondrial diabetes are common features. Eyes may have a distinctive speckled pigment in the retina, referred to as a maculopathy. Family members may present differently. Treatment There is no curative treatment. The disease remains progressive and fatal.Patients are managed according to what areas of the body are affected at a particular time. Enzymes, amino acids, antioxidants and vitamins have been used. Treatment for MELAS currently is 1. support the good mitochondria that is left with a mito cocktail and 2. avoid known mito toxins. Also the following supplements may help: CoQ10 has been helpful for some MELAS patients. B complex 100 is recommended as the B vitamins are the energy vitamins. Nicotinamide has been used because complex l accepts electrons from NADH and ultimately transfers electrons to CoQ10. Riboflavin has been reported to improve the function of a patient with complex l deficiency and the 3250T-C mutation. The administration of L-arginine during the acute and interictal periods may represent a potential new therapy for this syndrome to reduce brain damage due to impairment of vasodilation in intracerebral arteries due to nitric oxide depletion. Citrulline is also used as citrulline makes the plasma arginine higher, these doses are being studied at Baylor. Treatment with IV arginine is thought to relax the blood vessels to the brain, via nitric oxide. https://jamanetwork.com/journals/jamaneurology/article-abstract/2499460 Epidemiology The exact incidence of MELAS is unknown. It is one of the more common conditions in a group known as mitochondrial diseases. Together, mitochondrial diseases occur in about 1 in 4,000 people. See also Mitochondrial myopathy References External links melas at NIH/UW GeneTests

Aarogya, share information about a health condition involving Procedure

Procedure

Procedure may refer to: Medical procedure Instructions or recipes, a set of commands that show how to achieve some result, such as to prepare or make something Procedure (business), specifying parts of a business process Standard operating procedure, a step-by-step instruction to achieve some result, used in industry and military Legal procedure, the body of law and rules used in the administration of justice in the court system, including: Civil procedure Criminal procedure Administrative procedure Parliamentary procedure, a set of rules governing meetings Procedure (computer science), also termed a subroutine, function, or subprogram Stored procedure, a subroutine in the data dictionary of a relational database The Procedure, an American hardcore band See also Procedural (disambiguation)

Hello Aarogya, what is Browns syndrome

Browns syndrome

Browns syndrome is a rare form of strabismus characterized by limited elevation of the affected eye. The disorder may be congenital (existing at or before birth), or acquired. Brown syndrome is caused by a malfunction of the superior oblique muscle, causing the eye to have difficulty moving up, particularly during adduction (when eye turns towards the nose). Harold W. Brown first described the disorder in 1950 and initially named it the "superior oblique tendon sheath syndrome". Presentation A simple definition of the syndrome is "limited elevation in adduction from mechanical causes around the superior oblique". This definition indicates that when the head is upright, the eye is restricted in movement due to problems with muscles and tendons that surround the eye.Harold W. Brown characterized the syndrome in many ways such as: Limited elevation in the eye when head is straight up Eyes point out in a straight up gaze (divergence in up gaze) Widening of the eyelids in the affected eye on adduction Head tilts backwards (compensatory chin elevation to avoid double vision) Near normal elevation in abductionHe concluded that all of these features of Brown syndrome were due to the shortening or tightening of the anterior superior oblique tendon. Because this syndrome can be acquired or occur at random and has spontaneous resolution, Brown hypothesized one major truth for this disorder — that the short tendon sheath was due to a complete separation, congenital paresis, of the ipsilateral (on the same side) inferior oblique muscle and secondary to a permanent shortening.After further research, he redefined the sheath syndrome into the following divisions: true sheath syndrome, which categorized only the cases that had a congenital short anterior sheath of the superior oblique tendon, and simulated sheath syndrome, which characterized all cases in which the clinical features of a sheath syndrome caused by something different other than a congenital short anterior sheath of the tendon. The clinical features of the two categories are correct but true sheath syndrome is always congenital. However, in 1970 it was discovered that a tight sheath tendon was not the cause of Browns Syndrome. The real cause was a tight or short superior oblique tendon; studies have confirmed this and have labeled the tendon inelastic. Causes Browns syndrome can be divided in two categories based on the restriction of movement on the eye itself and how it affects the eye excluding the movement: Congenital (present at birth) Browns syndrome results from structural anomalies other than a short tendon sheath but other fibrous adhesions may be present around the trochlear area. Acquired cases arise from trauma, surgery, sinusitis and inflammation of the superior oblique tendon sheath in rheumatoid arthritis. Orbital floor fractures may trap the orbital tissue in such a way as to simulate Browns syndrome. Intermittent forms of vertical retraction syndrome have been associated with click, which occurs as the restriction is released (superior oblique click syndrome). Diagnosis Diagnosis of Browns syndrome usually happens during a routine ophthalmologic appointment. Treatments If binocular vision is present and head position is correct, treatment is not obligatory. Treatment is required for: visual symptoms, strabismus, or incorrect head position.Acquired cases that have active inflammation of the superior oblique tendon may benefit from local corticosteroid injections in the region of the trochlea. The goal of surgery is to restore free ocular rotations. Various surgical techniques have been used: Harold Brown advocated that the superior oblique tendon be stripped. A procedure named sheathotomy. The results of such a procedure are frequently unsatisfactory because of reformation of scar tissue. Tenotomy of the superior oblique tendon (with or without a tendon spacer) has also been advocated. This has the disadvantage that it frequently produces a superior oblique paresis. Weakening of the inferior oblique muscle of the affected eye may be needed to compensate for iatrogenic fourth nerve palsy.During surgery, a traction test is repeated until the eye rotations are free and the eye is anchored in an elevated adducted position for about two weeks after the surgery. This maneuver is intended to prevent the reformation of scar tissue in the same places. Normalization of head position may occur but restoration of full motility is seldom achieved. A second procedure may be required. Epidemiology In Browns original series there was a 3:2 predominance of women to men and nearly twice as many cases involved the right eye as the left. 10% of cases showed bilaterality. Familial occurrence of Browns syndrome has been reported. See also Strabismus Strabismus surgery Pediatric ophthalmology Duane syndrome References == External links ==

Give me a short description about Headache , Aarogya

Headache

Headache is the symptom of pain in the face, head, or neck. It can occur as a migraine, tension-type headache, or cluster headache. There is an increased risk of depression in those with severe headaches.Headaches can occur as a result of many conditions. There are a number of different classification systems for headaches. The most well-recognized is that of the International Headache Society, which classifies it into more than 150 types of primary and secondary headaches. Causes of headaches may include dehydration; fatigue; sleep deprivation; stress; the effects of medications (overuse) and recreational drugs, including withdrawal; viral infections; loud noises; head injury; rapid ingestion of a very cold food or beverage; and dental or sinus issues (such as sinusitis).Treatment of a headache depends on the underlying cause, but commonly involves pain medication (especially in case of migraine or cluster headache). A headache is one of the most commonly experienced of all physical discomforts.About half of adults have a headache in a given year. Tension headaches are the most common, affecting about 1.6 billion people (21.8% of the population) followed by migraine headaches which affect about 848 million (11.7%). Causes There are more than 200 types of headaches. Some are harmless and some are life-threatening. The description of the headache and findings on neurological examination, determine whether additional tests are needed and what treatment is best.Headaches are broadly classified as "primary" or "secondary". Primary headaches are benign, recurrent headaches not caused by underlying disease or structural problems. For example, migraine is a type of primary headache. While primary headaches may cause significant daily pain and disability, they are not dangerous from a physiological point of view. Secondary headaches are caused by an underlying disease, like an infection, head injury, vascular disorders, brain bleed, stomach irritation, or tumors. Secondary headaches can be dangerous. Certain "red flags" or warning signs indicate a secondary headache may be dangerous. Primary Ninety percent of all headaches are primary headaches. Primary headaches usually first start when people are between 20 and 40 years old. The most common types of primary headaches are migraines and tension-type headaches. They have different characteristics. Migraines typically present with pulsing head pain, nausea, photophobia (sensitivity to light) and phonophobia (sensitivity to sound). Tension-type headaches usually present with non-pulsing "bandlike" pressure on both sides of the head, not accompanied by other symptoms. Such kind of headaches maybe further classified into-episodic and chronic tension type headaches Other very rare types of primary headaches include: cluster headaches: short episodes (15–180 minutes) of severe pain, usually around one eye, with autonomic symptoms (tearing, red eye, nasal congestion) which occur at the same time every day. Cluster headaches can be treated with triptans and prevented with prednisone, ergotamine or lithium. trigeminal neuralgia or occipital neuralgia: shooting face pain hemicrania continua: continuous unilateral pain with episodes of severe pain. Hemicrania continua can be relieved by the medication indomethacin. primary stabbing headache: recurrent episodes of stabbing "ice pick pain" or "jabs and jolts" for 1 second to several minutes without autonomic symptoms (tearing, red eye, nasal congestion). These headaches can be treated with indomethacin. primary cough headache: starts suddenly and lasts for several minutes after coughing, sneezing or straining (anything that may increase pressure in the head). Serious causes (see secondary headaches red flag section) must be ruled out before a diagnosis of "benign" primary cough headache can be made. primary exertional headache: throbbing, pulsatile pain which starts during or after exercising, lasting for 5 minutes to 24 hours. The mechanism behind these headaches is unclear, possibly due to straining causing veins in the head to dilate, causing pain. These headaches can be prevented by not exercising too strenuously and can be treated with medications such as indomethacin. primary sex headache: dull, bilateral headache that starts during sexual activity and becomes much worse during orgasm. These headaches are thought to be due to lower pressure in the head during sex. It is important to realize that headaches that begin during orgasm may be due to a subarachnoid hemorrhage, so serious causes must be ruled out first. These headaches are treated by advising the person to stop sex if they develop a headache. Medications such as propranolol and diltiazem can also be helpful. hypnic headache: a moderate-severe headache that starts a few hours after falling asleep and lasts 15–30 minutes. The headache may recur several times during the night. Hypnic headaches are usually in older women. They may be treated with lithium. Secondary Headaches may be caused by problems elsewhere in the head or neck. Some of these are not harmful, such as cervicogenic headache (pain arising from the neck muscles). The excessive use of painkillers can paradoxically cause worsening painkiller headaches.More serious causes of secondary headaches include the following: meningitis: inflammation of the meninges which presents with fever and meningismus, or stiff neck bleeding inside the brain (intracranial hemorrhage) subarachnoid hemorrhage (acute, severe headache, stiff neck without fever) ruptured aneurysm, arteriovenous malformation, intraparenchymal hemorrhage (headache only) brain tumor: dull headache, worse with exertion and change in position, accompanied by nausea and vomiting. Often, the person will have nausea and vomiting for weeks before the headache starts. temporal arteritis: inflammatory disease of arteries common in the elderly (average age 70) with fever, headache, weight loss, jaw claudication, tender vessels by the temples, polymyalgia rheumatica acute closed-angle glaucoma (increased pressure in the eyeball): a headache that starts with eye pain, blurry vision, associated with nausea and vomiting. On physical exam, the person will have red eyes and a fixed, mid-dilated pupil. Post-ictal headaches: Headaches that happen after a convulsion or other type of seizure, as part of the period after the seizure (the post-ictal state)Gastrointestinal disorders may cause headaches, including Helicobacter pylori infection, celiac disease, non-celiac gluten sensitivity, irritable bowel syndrome, inflammatory bowel disease, gastroparesis, and hepatobiliary disorders. The treatment of the gastrointestinal disorders may lead to a remission or improvement of headaches.Migraine headaches are also associated with Cyclic Vomiting Syndrome (CVS). CVS is characterized by episodes of severe vomiting, and often occur alongside symptoms similar to those of migraine headaches (photophobia, abdominal pain, etc.). Pathophysiology The brain itself is not sensitive to pain, because it lacks pain receptors. However, several areas of the head and neck do have pain receptors and can thus sense pain. These include the extracranial arteries, middle meningeal artery, large veins, venous sinuses, cranial and spinal nerves, head and neck muscles, the meninges, falx cerebri, parts of the brainstem, eyes, ears, teeth, and lining of the mouth. Pial arteries, rather than pial veins are responsible for pain production.Headaches often result from traction to or irritation of the meninges and blood vessels. The pain receptors may be stimulated by head trauma or tumors and cause headaches. Blood vessel spasms, dilated blood vessels, inflammation or infection of meninges and muscular tension can also stimulate pain receptors. Once stimulated, a nociceptor sends a message up the length of the nerve fiber to the nerve cells in the brain, signalling that a part of the body hurts.Primary headaches are more difficult to understand than secondary headaches. The exact mechanisms which cause migraines, tension headaches and cluster headaches are not known. There have been different hypotheses over time that attempt to explain what happens in the brain to cause these headaches.Migraines are currently thought to be caused by dysfunction of the nerves in the brain. Previously, migraines were thought to be caused by a primary problem with the blood vessels in the brain. This vascular theory, which was developed in the 20th century by Wolff, suggested that the aura in migraines is caused by constriction of intracranial vessels (vessels inside the brain), and the headache itself is caused by rebound dilation of extracranial vessels (vessels just outside the brain). Dilation of these extracranial blood vessels activates the pain receptors in the surrounding nerves, causing a headache. The vascular theory is no longer accepted. Studies have shown migraine head pain is not accompanied by extracranial vasodilation, but rather only has some mild intracranial vasodilation.Currently, most specialists think migraines are due to a primary problem with the nerves in the brain. Auras are thought to be caused by a wave of increased activity of neurons in the cerebral cortex (a part of the brain) known as cortical spreading depression followed by a period of depressed activity. Some people think headaches are caused by the activation of sensory nerves which release peptides or serotonin, causing inflammation in arteries, dura and meninges and also cause some vasodilation. Triptans, medications that treat migraines, block serotonin receptors and constrict blood vessels.People who are more susceptible to experiencing migraines without headache are those who have a family history of migraines, women, and women who are experiencing hormonal changes or are taking birth control pills or are prescribed hormone replacement therapy.Tension headaches are thought to be caused by activation of peripheral nerves in the head and neck muscles.Cluster headaches involve overactivation of the trigeminal nerve and hypothalamus in the brain, but the exact cause is unknown. Diagnosis Most headaches can be diagnosed by the clinical history alone. If the symptoms described by the person sound dangerous, further testing with neuroimaging or lumbar puncture may be necessary. Electroencephalography (EEG) is not useful for headache diagnosis.The first step to diagnosing a headache is to determine if the headache is old or new. A "new headache" can be a headache that has started recently, or a chronic headache that has changed character. For example, if a person has chronic weekly headaches with pressure on both sides of his head, and then develops a sudden severe throbbing headache on one side of his head, they have a new headache. Red flags It can be challenging to differentiate between low-risk, benign headaches and high-risk, dangerous headaches since symptoms are often similar. Headaches that are possibly dangerous require further lab tests and imaging to diagnose.The American College for Emergency Physicians published criteria for low-risk headaches. They are as follows: age younger than 30 years features typical of primary headache history of similar headache no abnormal findings on neurologic exam no concerning change in normal headache pattern no high-risk comorbid conditions (for example, HIV) no new concerning history or physical examination findingsA number of characteristics make it more likely that the headache is due to potentially dangerous secondary causes which may be life-threatening or cause long-term damage. These "red flag" symptoms mean that a headache warrants further investigation with neuroimaging and lab tests.In general, people complaining of their "first" or "worst" headache warrant imaging and further workup. People with progressively worsening headache also warrant imaging, as they may have a mass or a bleed that is gradually growing, pressing on surrounding structures and causing worsening pain. People with neurological findings on exam, such as weakness, also need further workup.The American Headache Society recommends using "SSNOOP", a mnemonic to remember the red flags for identifying a secondary headache: Systemic symptoms (fever or weight loss) Systemic disease (HIV infection, malignancy) Neurologic symptoms or signs Onset sudden (thunderclap headache) Onset after age 40 years Previous headache history (first, worst, or different headache)Other red flag symptoms include: Old headaches Old headaches are usually primary headaches and are not dangerous. They are most often caused by migraines or tension headaches. Migraines are often unilateral, pulsing headaches accompanied by nausea or vomiting. There may be an aura (visual symptoms, numbness or tingling) 30–60 minutes before the headache, warning the person of a headache. Migraines may also not have auras. Tension-type headaches usually have bilateral "bandlike" pressure on both sides of the head usually without nausea or vomiting. However, some symptoms from both headache groups may overlap. It is important to distinguish between the two because the treatments are different. The mnemonic POUND helps distinguish between migraines and tension-type headaches. POUND stands for: One review article found that if 4–5 of the POUND characteristics are present, a migraine is 24 times as likely a diagnosis than a tension-type headache (likelihood ratio 24). If 3 characteristics of POUND are present, migraine is 3 times more likely a diagnosis than tension type headache (likelihood ratio 3). If only 2 POUND characteristics are present, tension-type headaches are 60% more likely (likelihood ratio 0.41). Another study found the following factors independently each increase the chance of migraine over tension-type headache: nausea, photophobia, phonophobia, exacerbation by physical activity, unilateral, throbbing quality, chocolate as a headache trigger, and cheese as a headache trigger.Cluster headaches are relatively rare (1 in 1000 people) and are more common in men than women. They present with sudden onset explosive pain around one eye and are accompanied by autonomic symptoms (tearing, runny nose and red eye).Temporomandibular jaw pain (chronic pain in the jaw joint), and cervicogenic headache (headache caused by pain in muscles of the neck) are also possible diagnoses.For chronic, unexplained headaches, keeping a headache diary can be useful for tracking symptoms and identifying triggers, such as association with menstrual cycle, exercise and food. While mobile electronic diaries for smartphones are becoming increasingly common, a recent review found most are developed with a lack of evidence base and scientific expertise. New headaches New headaches are more likely to be dangerous secondary headaches. They can, however, simply be the first presentation of a chronic headache syndrome, like migraine or tension-type headaches.One recommended diagnostic approach is as follows. If any urgent red flags are present such as visual loss, new seizures, new weakness, new confusion, further workup with imaging and possibly a lumbar puncture should be done (see red flags section for more details). If the headache is sudden onset (thunderclap headache), a computed tomography test to look for a brain bleed (subarachnoid hemorrhage) should be done. If the CT scan does not show a bleed, a lumbar puncture should be done to look for blood in the CSF, as the CT scan can be falsely negative and subarachnoid hemorrhages can be fatal. If there are signs of infection such as fever, rash, or stiff neck, a lumbar puncture to look for meningitis should be considered. If there is jaw claudication and scalp tenderness in an older person, a temporal artery biopsy to look for temporal arteritis should be performed and immediate treatment should be started. Neuroimaging Old headaches The US Headache Consortium has guidelines for neuroimaging of non-acute headaches. Most old, chronic headaches do not require neuroimaging. If a person has the characteristic symptoms of a migraine, neuroimaging is not needed as it is very unlikely the person has an intracranial abnormality. If the person has neurological findings, such as weakness, on exam, neuroimaging may be considered. New headaches All people who present with red flags indicating a dangerous secondary headache should receive neuroimaging. The best form of neuroimaging for these headaches is controversial. Non-contrast computerized tomography (CT) scan is usually the first step in head imaging as it is readily available in Emergency Departments and hospitals and is cheaper than MRI. Non-contrast CT is best for identifying an acute head bleed. Magnetic Resonance Imaging (MRI) is best for brain tumors and problems in the posterior fossa, or back of the brain. MRI is more sensitive for identifying intracranial problems, however it can pick up brain abnormalities that are not relevant to the persons headaches.The American College of Radiology recommends the following imaging tests for different specific situations: Lumbar puncture A lumbar puncture is a procedure in which cerebral spinal fluid is removed from the spine with a needle. A lumbar puncture is necessary to look for infection or blood in the spinal fluid. A lumbar puncture can also evaluate the pressure in the spinal column, which can be useful for people with idiopathic intracranial hypertension (usually young, obese women who have increased intracranial pressure), or other causes of increased intracranial pressure. In most cases, a CT scan should be done first. Classification Headaches are most thoroughly classified by the International Headache Societys International Classification of Headache Disorders (ICHD), which published the second edition in 2004. The third edition of the International Headache Classification was published in 2013 in a beta version ahead of the final version. This classification is accepted by the WHO.Other classification systems exist. One of the first published attempts was in 1951. The US National Institutes of Health developed a classification system in 1962. ICHD-2 The International Classification of Headache Disorders (ICHD) is an in-depth hierarchical classification of headaches published by the International Headache Society. It contains explicit (operational) diagnostic criteria for headache disorders. The first version of the classification, ICHD-1, was published in 1988. The current revision, ICHD-2, was published in 2004. The classification uses numeric codes. The top, one-digit diagnostic level includes 14 headache groups. The first four of these are classified as primary headaches, groups 5-12 as secondary headaches, cranial neuralgia, central and primary facial pain and other headaches for the last two groups.The ICHD-2 classification defines migraines, tension-types headaches, cluster headache and other trigeminal autonomic headache as the main types of primary headaches. Also, according to the same classification, stabbing headaches and headaches due to cough, exertion and sexual activity (sexual headache) are classified as primary headaches. The daily-persistent headaches along with the hypnic headache and thunderclap headaches are considered primary headaches as well.Secondary headaches are classified based on their cause and not on their symptoms. According to the ICHD-2 classification, the main types of secondary headaches include those that are due to head or neck trauma such as whiplash injury, intracranial hematoma, post craniotomy or other head or neck injury. Headaches caused by cranial or cervical vascular disorders such as ischemic stroke and transient ischemic attack, non-traumatic intracranial hemorrhage, vascular malformations or arteritis are also defined as secondary headaches. This type of headache may also be caused by cerebral venous thrombosis or different intracranial vascular disorders. Other secondary headaches are those due to intracranial disorders that are not vascular such as low or high pressure of the cerebrospinal fluid pressure, non-infectious inflammatory disease, intracranial neoplasm, epileptic seizure or other types of disorders or diseases that are intracranial but that are not associated with the vasculature of the central nervous system.ICHD-2 classifies headaches that are caused by the ingestion of a certain substance or by its withdrawal as secondary headaches as well. This type of headache may result from the overuse of some medications or exposure to some substances. HIV/AIDS, intracranial infections and systemic infections may also cause secondary headaches. The ICHD-2 system of classification includes the headaches associated with homeostasis disorders in the category of secondary headaches. This means that headaches caused by dialysis, high blood pressure, hypothyroidism, cephalalgia and even fasting are considered secondary headaches. Secondary headaches, according to the same classification system, can also be due to the injury of any of the facial structures including teeth, jaws, or temporomandibular joint. Headaches caused by psychiatric disorders such as somatization or psychotic disorders are also classified as secondary headaches.The ICHD-2 classification puts cranial neuralgias and other types of neuralgia in a different category. According to this system, there are 19 types of neuralgias and headaches due to different central causes of facial pain. Moreover, the ICHD-2 includes a category that contains all the headaches that cannot be classified.Although the ICHD-2 is the most complete headache classification there is and it includes frequency in the diagnostic criteria of some types of headaches (primarily primary headaches), it does not specifically code frequency or severity which are left at the discretion of the examiner. NIH The NIH classification consists of brief definitions of a limited number of headaches.The NIH system of classification is more succinct and only describes five categories of headaches. In this case, primary headaches are those that do not show organic or structural causes. According to this classification, primary headaches can only be vascular, myogenic, cervicogenic, traction, and inflammatory. Management Primary headache syndromes have many different possible treatments. In those with chronic headaches the long term use of opioids appears to result in greater harm than benefit. Migraines Migraine can be somewhat improved by lifestyle changes, but most people require medicines to control their symptoms. Medications are either to prevent getting migraines, or to reduce symptoms once a migraine starts.Preventive medications are generally recommended when people have more than four attacks of migraine per month, headaches last longer than 12 hours or the headaches are very disabling. Possible therapies include beta blockers, antidepressants, anticonvulsants and NSAIDs. The type of preventive medicine is usually chosen based on the other symptoms the person has. For example, if the person also has depression, an antidepressant is a good choice.Abortive therapies for migraines may be oral, if the migraine is mild to moderate, or may require stronger medicine given intravenously or intramuscularly. Mild to moderate headaches should first be treated with acetaminophen (paracetamol) or NSAIDs, like ibuprofen. If accompanied by nausea or vomiting, an antiemetic such as metoclopramide (Reglan) can be given orally or rectally. Moderate to severe attacks should be treated first with an oral triptan, a medication that mimics serotonin (an agonist) and causes mild vasoconstriction. If accompanied by nausea and vomiting, parenteral (through a needle in the skin) triptans and antiemetics can be given.Sphenopalatine ganglion block (SPG block, also known nasal ganglion block or pterygopalatine ganglion blocks) can abort and prevent migraines, tension headaches and cluster headaches. It was originally described by American ENT surgeon Greenfield Sluder in 1908. Both blocks and neurostimulation have been studied as treatment for headaches.Several complementary and alternative strategies can help with migraines. The American Academy of Neurology guidelines for migraine treatment in 2000 stated relaxation training, electromyographic feedback and cognitive behavioral therapy may be considered for migraine treatment, along with medications. Tension-type headaches Tension-type headaches can usually be managed with NSAIDs (ibuprofen, naproxen, aspirin), or acetaminophen. Triptans are not helpful in tension-type headaches unless the person also has migraines. For chronic tension type headaches, amitriptyline is the only medication proven to help. Amitriptyline is a medication which treats depression and also independently treats pain. It works by blocking the reuptake of serotonin and norepinephrine, and also reduces muscle tenderness by a separate mechanism. Studies evaluating acupuncture for tension-type headaches have been mixed. Overall, they show that acupuncture is probably not helpful for tension-type headaches. Cluster headaches Abortive therapy for cluster headaches includes subcutaneous sumatriptan (injected under the skin) and triptan nasal sprays. High flow oxygen therapy also helps with relief.For people with extended periods of cluster headaches, preventive therapy can be necessary. Verapamil is recommended as first line treatment. Lithium can also be useful. For people with shorter bouts, a short course of prednisone (10 days) can be helpful. Ergotamine is useful if given 1–2 hours before an attack. Secondary headaches Treatment of secondary headaches involves treating the underlying cause. For example, a person with meningitis will require antibiotics. A person with a brain tumor may require surgery, chemotherapy or brain radiation. Neuromodulation Peripheral neuromodulation has tentative benefits in primary headaches including cluster headaches and chronic migraine. How it may work is still being looked into. Epidemiology Literature reviews find that approximately 64–77% of adults have had a headache at some point in their lives. During each year, on average, 46–53% of people have headaches. However, the prevalence of headache varies widely depending on how the survey was conducted, with studies finding lifetime prevalence of as low as 8% to as high as 96%. Most of these headaches are not dangerous. Only approximately 1–5% of people who seek emergency treatment for headaches have a serious underlying cause.More than 90% of headaches are primary headaches. Most of these primary headaches are tension headaches. Most people with tension headaches have "episodic" tension headaches that come and go. Only 3.3% of adults have chronic tension headaches, with headaches for more than 15 days in a month.Approximately 12–18% of people in the world have migraines. More women than men experience migraines. In Europe and North America, 5–9% of men experience migraines, while 12–25% of women experience migraines.Cluster headaches are relatively uncommon. They affect only 1–3 per thousand people in the world. Cluster headaches affect approximately three times as many men as women. History The first recorded classification system was published by Aretaeus of Cappadocia, a medical scholar of Greco-Roman antiquity. He made a distinction between three different types of headache: i) cephalalgia, by which he indicates a shortlisting, mild headache; ii) cephalea, referring to a chronic type of headache; and iii) heterochromia, a paroxysmal headache on one side of the head. Another classification system that resembles the modern ones was published by Thomas Willis, in De Cephalalgia in 1672. In 1787 Christian Baur generally divided headaches into idiopathic (primary headaches) and symptomatic (secondary ones), and defined 84 categories. Children In general, children experience the same types of headaches as adults do, but their symptoms may be slightly different. The diagnostic approach to headaches in children is similar to that of adults. However, young children may not be able to verbalize pain well. If a young child is fussy, they may have a headache.Approximately 1% of emergency department visits for children are for headache. Most of these headaches are not dangerous. The most common type of headache seen in pediatric emergency rooms is headache caused by a cold (28.5%). Other headaches diagnosed in the emergency department include post-traumatic headache (20%), headache related to a problem with a ventriculoperitoneal shunt (a device put into the brain to remove excess CSF and reduce pressure in the brain) (11.5%) and migraine (8.5%). The most common serious headaches found in children include brain bleeds (subdural hematoma, epidural hematoma), brain abscesses, meningitis and ventriculoperitoneal shunt malfunction. Only 4–6.9% of kids with a headache have a serious cause.Just as in adults, most headaches are benign, but when head pain is accompanied with other symptoms such as speech problems, muscle weakness, and loss of vision, a more serious underlying cause may exist: hydrocephalus, meningitis, encephalitis, abscess, hemorrhage, tumor, blood clots, or head trauma. In these cases, the headache evaluation may include CT scan or MRI in order to look for possible structural disorders of the central nervous system. If a child with a recurrent headache has a normal physical exam, neuroimaging is not recommended. Guidelines state children with abnormal neurologic exams, confusion, seizures and recent onset of worst headache of life, change in headache type or anything suggesting neurologic problems should receive neuroimaging.When children complain of headaches, many parents are concerned about a brain tumor. Generally, headaches caused by brain masses are incapacitating and accompanied by vomiting. One study found characteristics associated with brain tumor in children are: headache for greater than 6 months, headache related to sleep, vomiting, confusion, no visual symptoms, no family history of migraine and abnormal neurologic exam.Some measures can help prevent headaches in children. Drinking plenty of water throughout the day, avoiding caffeine, getting enough and regular sleep, eating balanced meals at the proper times, and reducing stress and excess of activities may prevent headaches. Treatments for children are similar to those for adults, however certain medications such as narcotics should not be given to children.Children who have headaches will not necessarily have headaches as adults. In one study of 100 children with headache, eight years later 44% of those with tension headache and 28% of those with migraines were headache free. In another study of people with chronic daily headache, 75% did not have chronic daily headaches two years later, and 88% did not have chronic daily headaches eight years later. See also Eye strain References External links Headache at Curlie

Hello Aarogya, could you help me understand about Viral cardiomyopathy

Viral cardiomyopathy

Viral cardiomyopathy occurs when viral infections cause myocarditis with a resulting thickening of the myocardium and dilation of the ventricles. These viruses include Coxsackie B and adenovirus, echoviruses, influenza H1N1, Epstein–Barr virus, rubella (German measles virus), varicella (chickenpox virus), mumps, measles, parvoviruses, yellow fever, dengue fever, polio, rabies and the viruses that cause hepatitis A and C, as well as COVID-19, which has been seen to cause this in persons otherwise thought to have a "low risk" of the viruss effects. COVID-19 Cardiomyopathy Patients with Covid-19 frequently experience heart issues. According to studies, people who have had previous cardiovascular conditions like cardiomyopathy, hypertension, coronary heart disease, or arrhythmia are more likely to become critically ill from SARS-CoV-2 infection. Myocarditis may result from a direct viral infection of the myocardium. Cardiovascular biomarkers like troponin, lactate dehydrogenase, high sensitivity amino-terminal B-type natriuretic peptide, creatinine kinase, and creatinine kinase myocardial band, which indicate myocardial damage, increase in concentration in response to covid-19. Hundreds of studies have reported myocarditis/myopericarditis caused by Covid-19 infection in living patients, with a male predominance (58%), and a median age of 50 years. See also Coxsackievirus-induced cardiomyopathy Myocarditis Pericarditis Vaccine adverse event References External links Myocarditis on emedicine

Hello Aarogya, explain a situation where Argyll Robertson pupil occurs

Argyll Robertson pupil

Argyll Robertson pupils (AR pupils) are bilateral small pupils that reduce in size on a near object (i.e., they accommodate), but do not constrict when exposed to bright light (i.e., they do not react). They are a highly specific sign of neurosyphilis; however, Argyll Robertson pupils may also be a sign of diabetic neuropathy. In general, pupils that accommodate but do not react are said to show light-near dissociation (i.e., it is the absence of a miotic reaction to light, both direct and consensual, with the preservation of a miotic reaction to near stimulus (accommodation/convergence).AR pupils are extremely uncommon in the developed world. There is continued interest in the underlying pathophysiology, but the scarcity of cases makes ongoing research difficult. Pathophysiology The two different types of near response are caused by different underlying disease processes. Adies pupil is caused by damage to peripheral pathways to the pupil (parasympathetic neurons in the ciliary ganglion that cause pupillary constriction to bright light and with near vision). The pathophysiologic mechanism which produces an Argyll Robertson pupil is unclear, but is believed to be the result of bilateral damage to the pretectal nuclei in the midbrain. Studies have failed to demonstrate a focal localising lesion. Research has implicated the rostral midbrain in the vicinity of the cerebral aqueduct of the third ventricle as the most likely region of damage. A lesion in this area would involve efferent pupillary fibres on the dorsal aspect of the Edinger-Westphal nucleus (associated with the response to light) while sparing the fibres associated with the response to near, which lie slightly more ventrally. The exact relationship between syphilis and the two types of pupils (AR pupils and tonic pupils) is not known at the present time. The older literature on AR pupils did not report the details of pupillary constriction (brisk vs. tonic) that are necessary to distinguish AR pupils from tonic pupils. Tonic pupils can occur in neurosyphilis. It is not known whether neurosyphilis itself (infection by Treponema pallidum) can cause tonic pupils, or whether tonic pupils in syphilis simply reflect a coexisting peripheral neuropathy. Thompson and Kardon summarize the present view: The evidence supports a midbrain cause of the AR pupil, provided one follows Loewenfeld’s definition of the AR pupil as small pupils that react very poorly to light and yet seem to retain a normal pupillary near response that is definitely not tonic.To settle the question of whether the AR pupil is of central or peripheral origin, it will be necessary to perform iris transillumination (or a magnified slit-lamp examination) in a substantial number of patients who have a pupillary light-near dissociation (with and without tonicity of the near reaction), perhaps in many parts of the world. Parinaud syndrome A third cause of light-near dissociation is Parinaud syndrome, also called dorsal midbrain syndrome. This uncommon syndrome involves vertical gaze palsy associated with pupils that “accommodate but do not react." The causes of Parinaud syndrome include brain tumors (pinealomas), multiple sclerosis and brainstem infarction. Due to the lack of detail in the older literature and the scarcity of AR pupils at the present time, it is not known whether syphilis can cause Parinaud syndrome. It is not known whether AR pupils are any different from the pupils seen in other dorsal midbrain lesions. The condition is diagnosed clinically by a physician. Treatment There is no definite treatment, but, because syphilis may be an underlying cause, it should be treated. However, because this sign is associated with neurosyphilis, it should be treated with crystalline penicillin 24 mU intravenous per day for 10 to 14 days. If the patient is allergic to penicillin, they should undergo desensitization and then be treated. History Argyll Robertson pupils were named after Douglas Argyll Robertson (1837–1909), a Scottish ophthalmologist and surgeon who described the condition in the mid-1860s in the context of neurosyphilis. In the early 20th century, William John Adie described a second type of pupil that could "accommodate but not react". Adies tonic pupil is usually associated with a benign peripheral neuropathy (Adie syndrome), not with syphilis.When penicillin became widely available in the 1940s, the prevalence of AR pupils (which develop only after decades of untreated infection) decreased dramatically. AR pupils are now quite rare. A patient whose pupil “accommodates but does not react” almost always has a tonic pupil, not an AR pupil. In the 1950s, Loewenfeld distinguished between the two types of pupils by carefully observing the exact way in which the pupils constrict with near vision. The near response in AR pupils is brisk and immediate. The near response in tonic pupils is slow and prolonged. See also References Further reading Pearce JM (2004). "The Argyll Robertson pupil". J. Neurol. Neurosurg. Psychiatry. 75 (9): 1345. doi:10.1136/jnnp.2003.014225. PMC 1739227. PMID 15314131. == External links ==

Aarogya, elaborate on Hypernasal speech

Hypernasal speech

Hypernasal speech is a disorder that causes abnormal resonance in a humans voice due to increased airflow through the nose during speech. It is caused by an open nasal cavity resulting from an incomplete closure of the soft palate and/or velopharyngeal sphincter. In normal speech, nasality is referred to as nasalization and is a linguistic category that can apply to vowels or consonants in a specific language. The primary underlying physical variable determining the degree of nasality in normal speech is the opening and closing of a velopharyngeal passage way between the oral vocal tract and the nasal vocal tract. In the normal vocal tract anatomy, this opening is controlled by lowering and raising the velum or soft palate, to open or close, respectively, the velopharyngeal passageway. Anatomy The palate comprises two parts, the hard palate (palatum durum) and the soft palate (palatum molle), which is connected to the uvula. The movements of the soft palate and the uvula are made possible by the velopharyngeal sphincter. During speech or swallowing, the soft palate lifts against the back throat wall to close the nasal cavity. When producing nasal consonants (such as "m", "n", and "ng"), the soft palate remains relaxed, thereby enabling the air to go through the nose. The Eustachian tube, which opens near the velopharyngeal sphincter, connects the middle ear and nasal pharynx. Normally, the tube ensures aeration and drainage (of secretions) of the middle ear. Narrow and closed at rest, it opens during swallowing and yawning, controlled by the tensor veli palatini and the levator veli palatini (muscles of the soft palate). Children with a cleft palate have difficulties controlling these muscles and thus are unable to open the Eustachian tube. Secretions accumulate in the middle ear when the tube remains dysfunctional over a long period of time, which cause hearing loss and middle ear infections. Ultimately, hearing loss can lead to impaired speech and language development. Causes The general term for disorders of the velopharyngeal valve is velopharyngeal dysfunction (VPD). It includes three subterms: velopharyngeal insufficiency, velopharyngeal inadequacy, and velopharyngeal mislearning. Velopharyngeal insufficiency can be caused by an anatomical abnormality of the throat. It occurs in children with a history of cleft palate or submucous cleft, who have short or otherwise abnormal vela. Velopharyngeal insufficiency can also occur after adenoidectomy. Velopharyngeal incompetence is a defective closure of the velopharyngeal valve due to its lack of speed and precision. It is caused by a neurologic disorder or injury (e.g. cerebral palsy or traumatic brain injury). Sometimes children present no abnormalities yet still have hypernasal speech: this can be due to velopharyngeal mislearning, indicating that the child has been imitating or has never learned how to use the valve correctly. Diagnosis There are several methods for diagnosing hypernasality. A speech therapist listens to and records the child while analysing perceptual speech. In hypernasality, the child cannot produce oral sounds (vowels and consonants) correctly. Only the nasal sounds can be correctly produced. A hearing test is also desirable. A mirror is held beneath the nose while the child pronounces the vowels. Nasal air escape, and thus hypernasality, is indicated if the mirror fogs up. A pressure-flow technique is used to measure velopharyngeal orifice area during the speech. The patient must be at least three to four years old. A video nasopharyngeal endoscopy observes velopharyngeal function, movements of the soft palate, and pharyngeal walls. It utilises a very small scope placed in the back of the nasal cavity. The doctor will then ask the child to say a few words. The patient must be at least three to four years old to ensure cooperation. A cinefluoroscopy gives dynamic visualisation and can easier be applied to younger children, though it has the disadvantage of exposing the patient to radiation. A nasometer calculates the ratio of nasality. The patient wears a headset, where the oral and nasal cavities are separated by a plate. On both sides of the plate are microphones. The ratio calculated by the nasometer indicates the amount of nasality, with a higher ratio indicating more nasality. Effects on Speech Hypernasality is generally segmented into so-called resonance effects in vowels and some voiced or sonorant consonants and the effects of excess nasal airflow during those consonants requiring a buildup of oral air pressure, such as stop consonants (as /p/) or sibilants (as /s/). The latter nasal airflow problem is termed nasal emission, and acts to prevent the buildup of air pressure and thus prevent the normal production of the consonant. In testing for resonance effects without the aid of technology, speech pathologists are asked to rate the speech by listening to a recorded sentence or paragraph, though there is much variability in such subjective ratings, for at least two reasons. First, the acoustic effect of a given velopharyngeal opening varies greatly depending on the degree of occlusion of the nasal passageways. (This is the reason why a stuffy nose from an allergy or cold will sound more nasal than when the nose is clear.) Secondly, for many persons with hypernasal speech, especially hearing impaired, there are also mispronunciations of the articulation of the vowels. It is extremely difficult to separate the acoustic effects of hypernasality from the acoustic effects of mispronounced vowels (examples). Of course, in speech training of the hearing impaired, there is little possibility of making nasality judgments aurally, and holding a finger to the side of the nose, to feel voice frequency vibration, is sometimes recommended. Treatment Speech therapy In cases of muscle weakness or cleft palate, special exercises can help to strengthen the soft palate muscles with the ultimate aim of decreasing airflow through the nose and thereby increasing intelligibility. Intelligibility requires the ability to close the nasal cavity, as all English sounds, except the nasal sounds "m" [m], "n" [n], and "ng" [ŋ], have airflow only through the mouth. Normally, by age three, a child can raise the muscles of the soft palate to close to nasal cavity. Without the use of a technological aid, nasal emission is sometimes judged by listening for any turbulence that may be produced by the nasal airflow, as when there is a small velopharyngeal opening and there is some degree of mucous in the opening. More directly, methods recommended include looking for the fogging of a mirror held near the nares or listening through a tube, the other end of which is held in or near a nares opening.There have been many attempts to use technological augmentation more than a mirror or tube to aid the speech pathologist or provide meaningful feedback to the person attempting to correct their hypernasality. Among the more successful of these attempts, the incompleteness of velopharyngeal closure during vowels and sonorants that causes nasal resonance can be estimated and displayed for evaluation or biofeedback in speech training through the nasalance of the voice, with nasalance defined as a ratio of acoustic energy at the nostrils to that at the mouth, with some form of acoustic separation present between the mouth and nose. In the nasalance measurement system sold by WEVOSYS, the acoustic separation is provided by a mask-tube system, nasalance measurement system sold by Kay-Pentax, the acoustic separation is provided by a solid flat partition held against the upper lip, while in the system sold by Glottal Enterprises the acoustic separation can be by either a solid flat partition or a two-chamber mask.However, devices for measuring nasalance do not measure nasal emission during pressure consonants. Because of this, a means for measuring the degree of velopharyngeal closure in consonants is also needed. A commercially available device for making such measurements is the Perci-Sar system from Microtronics. The Nasality Visualization System from Glottal Enterprises allows both the measurement of Nasal Emission and Nasalance. In the presence of a cleft palate, either of these systems can be helpful in evaluating the need for an appliance or surgical intervention to close the cleft or the success of an appliance or a surgical attempt to close the cleft. Exercises If a child finds it difficult to blow, pinching the nose can help regulate airflow. The child should then practice speech sounds without pinching the nose. These exercises only work as treatments if hypernasality is small. Severe deviations should be treated surgically. CPAP There is insufficient evidence to support the use of traditional non-speech oral motor exercises can reduce hypernasality. Velopharyngeal closure patterns and their underlying neuromotor control may differ for speech and nonspeech activities. Therefore, the increase in velar movement through blowing, sucking, and swallowing may not transfer to speech tasks. Thus, hypernasality remains while individual speak. Kuehn proposed a new way of treatment by using a CPAP machine during speech tasks. The positive pressure provided by a CPAP machine provides resistance to strengthen velopharyngeal muscles. With nasal mask in place, an individual is asked to produce VNCV syllables and short sentences. It is believed that CPAP therapy can increase both muscle endurance as well as strength because it overloads the levator veli palatini muscle and involves a regimen with a large number of repetitions of velar elevation. Research findings proved that patients with hypernasality due to flaccid dysarthria, TBI or cleft palate do eliminate hypernasality after receiving this training program. Surgery The two main surgical techniques for correcting the aberrations the soft palate present in hypernasality are the posterior pharyngeal flap and the sphincter pharyngoplasty. After surgical interventions, speech therapy is necessary to learn how to control the newly constructed flaps. Posterior pharyngeal flap Posterior pharyngeal flap surgery is mostly used for vertical clefts of the soft palate. The surgeon cuts through the upper layers of the back of the throat, creating a small square of tissue. This flap remains attached on one side (usually at the top). The other side is attached to (parts of) the soft palate. This ensures that the nasal cavity is partially separated from the oral cavity. When the child speaks, the remaining openings close from the side due to the narrowing of the throat caused by the muscle movements necessary for speech. In a relaxed state, the openings allow breathing through the nose. Sphincter pharyngoplasty Sphincter pharyngoplasty is mostly used for horizontal clefts of the soft palate. Two small flaps are made on the left and right side of the entrance to the nasal cavity, attached to the back of the throat. For good results, the patient must have good palatal motion, as the occlusion of the nasal cavity is mainly carried out by muscles already existing and functioning. Complications The most common complications of the posterior pharyngeal wall flap are hyponasality, nasal obstruction, snoring, and sleep apnea. Rarer complications include flap separation, sinusitis, postoperative bleeding, and aspiration pneumonia. Possible complications of the sphincter pharyngoplasty are snoring, nasal obstruction, difficulty blowing the nose. Some researches suggest that sphincter pharyngoplasty introduces less hyponasality and obstructive sleep symptoms than the posterior pharyngeal wall flap. Both surgeries have a favourable effect on the function of the Eustachian tube. See also Rhinolalia clausa Nasalization Nasalance References == External links ==

Hi Aarogya, explain a situation where Sister occurs

Sister

A sister is a woman or a girl who shares one or more parents with another individual; a female sibling. The male counterpart is a brother. Although the term typically refers to a familial relationship, it is sometimes used endearingly to refer to non-familial relationships. A full sister is a first degree relative. Overview The English word sister comes from Old Norse systir which itself derives from Proto-Germanic *swestēr, both of which have the same meaning, i.e. sister. Some studies have found that sisters display more traits indicating jealousy around their siblings than their male counterparts, brothers. In some cultures, sisters are afforded a role of being under the protection by male siblings, especially older brothers from issues ranging from bullies or sexual advances by womanizers. In some quarters the term sister has gradually broadened its colloquial meaning to include individuals stipulating kinship. In response, in order to avoid equivocation, some publishers prefer the usage of female sibling over sister. Males with a twin sister sometimes view her as their female alter ego, or what they would have been like, if they had two X chromosomes. A study in Perth Australia found that girls having only youngers brothers resulted in a chastity effect, losing their virginity on average more than a year later than average. This has been hypothesized as being attributed to the pheromones in their brothers sweat and household-related errands. Sororal relationships Various studies have shown that older sisters are likely to give a varied gender role to their younger siblings as well as being more likely to develop a close bond with their younger siblings. Older sisters are more likely to play with their younger siblings. Younger siblings display a more needy behavior when in close proximity to their older sister and are more likely to be tolerant of an older sisters bad behavior. Boys with only an older sister are more likely to display stereotypically male behavior, and such masculine boys increased their masculine behavior with the more sisters they have. The reverse is true for young boys with several sisters, as they tend to be feminine, however, they outgrow this by the time they approach pubescence. Boys with older sisters were less likely to be delinquent or have emotional and behavioral disorders. A younger sister is less likely to be scolded by older siblings than a younger brother. The most common recreational activity between older brother/younger sister pairs is art drawing. Some studies also found a correlation between having an older sister and constructive discussions about safe sexual practices. Some studies have shown that men without sisters are more likely to be ineffectual at courtship and romantic relationships. Fictional works about sisters Films What Ever Happened to Baby Jane? (1962) Hannah and Her Sisters (1986) Hanging Up (2000) Frozen (2013) Little Women (2019) Literature Little Women Laura Lee Hopes Bobbsey Twins novels, which included two sets of fraternal twins: 12-year-old Nan and Bert, and six-year-old Flossie and Freddie In Her Shoes (2002), novel #Toots (2019), novel Television Hope & Faith, American sitcom Sisters (TV series) What I Like About You, TV series Sister, Sister, TV series Games Jessica & Zofia Blazkowicz , Wolfenstein: Youngblood Mileena & Kitana, Mortal Kombat Kat and Ana, WarioWare See also Brother Sisterhood (disambiguation) Religious sister References External links The dictionary definition of sister at Wiktionary

Aarogya, can you share information about a health condition involving Monocytosis

Monocytosis

Monocytosis is an increase in the number of monocytes circulating in the blood. Monocytes are white blood cells that give rise to macrophages and dendritic cells in the immune system. In humans, monocytosis occurs when there is a sustained rise in monocyte counts greater than 800/mm3 to 1000/mm3.Monocytosis has sometimes been called mononucleosis, but that name is usually reserved specifically for infectious mononucleosis. Causes Monocytosis often occurs during chronic inflammation. Diseases that produce such a chronic inflammatory state: Infections: tuberculosis, brucellosis, listeriosis, subacute bacterial endocarditis, syphilis, and other viral infections and many protozoal and rickettsial infections (e.g. kala azar, malaria, Rocky Mountain spotted fever). Blood and immune causes: chronic neutropenia and myeloproliferative disorders. Autoimmune diseases and vasculitis: systemic lupus erythematosus, rheumatoid arthritis and inflammatory bowel disease. Malignancies: Hodgkins disease and certain leukaemias, such as chronic myelomonocytic leukaemia (CMML) and monocytic leukemia. Recovery phase of neutropenia or an acute infection. Obesity (cf. Nagareddy et al. (2014), Cell Metabolism, Vol. 19, pp 821–835) Miscellaneous causes: sarcoidosis, lipid storage disease and ZNFX1 deficiency.During these stages of extreme inflammation, monocytosis can damage tissues because it increases the activation of the immune response and prevents the inflammation from subsiding which is seen in cases where sepsis occurs. Diagnosis Blood Test (CBC) (Normal range of Monocytes: 1-10%) (Normal range in males: 0.2-0.8 x 103/microliter) Blood test checking for monocytosis (Abnormal ranges: >10%) (Abnormal range in males: >0.8 x 103/microliter) Treatment Ceftriaxone if there is typhoid fever and levofloxacin or moxifloxacin. Gentamicin and doxycyclin if brucellosis. References == External links ==

Aarogya , Do you know what is Plica syndrome,

Plica syndrome

Plica syndrome is a condition that occurs when a plica (a vestigial extension of the protective synovial capsule of usually the knee) becomes irritated, enlarged, or inflamed. Cause This inflammation is typically caused by the plica being caught on the femur, or pinched between the femur and the patella. The most common location of plica tissue is along the medial (inside) side of the knee. The plica can tether the patella to the femur, be located between the femur and patella, or be located along the femoral condyle. If the plica tethers the patella to the femoral condyle, the symptoms may cause it to be mistaken for chondromalacia. The plica themselves are remnants of the fetal stage of development where the knee is divided into three compartments. The plica normally diminish in size during the second trimester of fetal development, as the three compartments develop into the synovial capsule. In adults, they normally exist as sleeves of tissue called synovial folds. The plica are usually harmless and unobtrusive; plica syndrome only occurs when the synovial capsule becomes irritated, which thickens the plica themselves (making them prone to irritation/inflammation, or being caught on the femur). Diagnosis If the plica tethers the patella to the femoral condyle, the symptoms may cause it to be mistaken for chondromalacia patellae. Diagnosis is often complicated by the thin structures of plicae, fenestrated septum or unfenestrated septum all being too fine to resolve well even in MRI. Treatment Plica syndrome treatment focuses on decreasing inflammation of the synovial capsule. A nonsteroidal anti-inflammatory drug (NSAID) is often used in conjunction with therapeutic exercise and modalities. Iontophoresis and phonophoresis have been utilized successfully against inflammation of the plica and synovial capsule. Failing these, surgical removal of the plica of the affected knee may be necessary. See also Knee pain Patellofemoral pain syndrome Iliotibial band syndrome References == External links ==

Hello Aarogya, could you help me understand about Disorder

Disorder

Disorder may refer to randomness, non-order, or no intelligible pattern. Disorder may also refer to: Healthcare Disorder (medicine), a functional abnormality or disturbance Mental disorder or psychological disorder, a psychological pattern associated with distress or disability that occurs in an individual and is not a part of normal development or culture:Anxiety disorder, different forms of abnormal and pathological fear and anxiety Conversion disorder, neurological symptoms such as numbness, blindness, paralysis, or fits, where no neurological explanation is possible Obsessive–compulsive disorder, an anxiety disorder characterized by repetitive behaviors aimed at reducing anxiety Obsessive–compulsive personality disorder, obsession with perfection, rules, and organization Personality disorder, an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the culture of the individual who exhibits it Law enforcement Civil disorder, one or more forms of disturbance caused by a group of people Lawlessness, a lack of laws or law enforcement Science Crystallographic disorder, disordered atom locations in crystals Order and disorder Arts, entertainment, and media Films Disorder (1962 film), a film by Franco Brusati Disorder (2009 film), a Chinese documentary Disorder (2015 film), a French film Music Disorder (band), a Bristol-based hardcore punk band Disorder (album), an album by The Gazette Disorder (EP), an EP by Front Line Assembly "Disorder", a song by Joy Division from the 1979 album Unknown Pleasures Other uses Dis-order, the mail order service of Displeased Records See also Chaos Order

Aarogya, Please give me a short description about Tinea manuum

Tinea manuum

Tinea manuum is a fungal infection of the hand, mostly a type of dermatophytosis, often part of two feet-one hand syndrome. There is diffuse scaling on the palms or back of usually one hand and the palmer creases appear more prominent. When both hands are affected, the rash looks different on each hand, with palmer creases appearing whitish if the infection has been present for a long time. It can be itchy and look slightly raised. Nails may also be affected.The most common cause is Trichophyton rubrum. The infection can result from touching another area of the body with a fungal infection such as athletes foot or fungal infection of groin, contact with an infected person or animal, or from contact with soil or contaminated towels. Risk factors include diabetes, high blood pressure, weak immune system, humid surroundings, excessive sweating, recurrent hand trauma and cracks in feet. Pet owners and farmworkers are also at higher risk. Machine operators, mechanics, gas/electricity workers and people who work with chemicals have also been reported to be at greater risk.Diagnosis is by visualization, direct microscopy and culture. Psoriasis of the palms, pompholyx and contact dermatitis may appear similar. Treatment is usually with long-term topical antifungal medications. If not resolving, terbinafine or itraconazole taken by mouth might be options.It occurs worldwide. One large study revealed around 84% of tinea manuum was associated with athletes foot, of which 80% admitted scratching their feet, and 60% were male, Signs and symptoms There is usually an itch, with generalised dry flaky thick skin of the palm of a hand. Frequently, one hand is affected, but it can be in both. If the back of the hand is affected, it may appear as reddish circles like in ringworm. Sometimes there are no symptoms. The feet may be affected as in two feet-one hand syndrome. Cause and mechanism The most common cause is Trichophyton rubrum. Other causes include Trichophyton verrucosum (from cattle), Microsporum canis (from a cat or dog), Trichophyton erinacei (from a hedgehog), Trichophyton mentagrophytes, Epidermophyton floccosum, Trichophyton interdigitale, and more rarely Microsporum gypseum, Trichophyton eriotrephon, and Arhroderma benhamiae.Tinea manuum can result from touching another area of the body with a fungal infection such as athletes foot or tinea cruris, contact with an infected person or animal, or from contact with soil or contaminated towels. Risk factors Diabetes, high blood pressure, weak immune system, humid surroundings, excessive sweating, recurrent hand trauma and cracks in feet are risk factors for tinea manuum. Pet owners and farmworkers are also at higher risk. Diagnosis Diagnosis is by visualization, direct microscopy and culture. Differential diagnosis Psoriasis of the palms, pompholyx and contact dermatitis may appear similar. Treatment Treatment is usually with long-term topical antifungal medications. If not resolving, terbinafine or itraconazole by mouth might be options. Other options include clotrimazole, fluconazole and ketoconazole. Prevention Prevention is focussed on hygiene such as washing hands, avoiding scratching the feet or touching fungal toe infections. Epidemiology Tinea manuum is most common in young adult males. Dermatophyte infections occur in up to a quarter of the worlds population, of which the hands and feet are most commonly involved. It occurs worldwide. One large study revealed around 84% of tinea manuum was associated with athletes foot, of which 80% admitted scratching their feet, and 60% were male, See also List of cutaneous conditions References == External links ==

Hello Aarogya, explain a situation where Pantothenate kinase-associated neurodegeneration occurs

Pantothenate kinase-associated neurodegeneration

Pantothenate kinase-associated neurodegeneration (PKAN), formerly called Hallervorden–Spatz syndrome, is a genetic degenerative disease of the brain that can lead to parkinsonism, dystonia, dementia, and ultimately death. Neurodegeneration in PKAN is accompanied by an excess of iron that progressively builds up in the brain. PKAN is caused by loss of function of the enzyme PANK2, due to bi-allelic genetic mutations. It follows autosomal recessive inheritance. This enzyme is the first step in the pathway converting vitamin B5 into coenzyme A. There are currently no treatments that modify disease progress, though there are a number of medications and therapies that can help improve symptoms and there is active research into treatments. Signs and symptoms Symptoms typically begin in childhood and are progressive, often resulting in death by early adulthood. Symptoms of PKAN begin before middle childhood, and most often are noticed before ten years of age. Symptoms include: dystonia (repetitive uncontrollable muscle contractions that may cause jerking or twisting of certain muscle groups) dysphagia & dysarthria due to muscle groups involved in speech being involved rigidity/stiffness of limbs tremor writhing movements dementia spasticity weakness seizures (rare) toe walking retinitis pigmentosa, another degenerative disease that affects the individuals retina, often causing alteration of retinal color and progressive deterioration of the retina at first causing night blindness and later resulting in a complete loss of vision.25% of individuals experience an uncharacteristic form of PKAN that develops post-10 years of age and follows a slower, more gradual pace of deterioration than those pre-10 years of age. These individuals face significant speech deficits as well as psychiatric and behavioral disturbances.Being a progressive, degenerative nerve illness, PKAN leads to early immobility and often death by early adulthood. Death occurs prematurely due to infections such as pneumonia, and the disease in itself is technically not life limiting. Genetics PKAN is an autosomal recessive disorder. Both the parents of an affected child must be heterozygous carriers for the disease and therefore must carry one mutant allele. As it is an autosomal disorder, those heterozygous for the disorder may not display any atypical characteristics that are considered suggestive of the disorder, however there have been reported cases of compound heterozygosity in which heterozygous individuals do develop the classic form of the disease.The disorder is caused by a mutant PANK2 gene located at the chromosomal locus: 20p13-p12.3. PANK2 is responsible for coding the protein Pantothenate kinase 2. PANK2 encodes the enzyme pantothenate kinase, and mutations in the gene lead to an inborn error of vitamin B5 (pantothenate) metabolism. Vitamin B5 is required for the production of coenzyme A in cells. Disruption of this enzyme affects energy and lipid metabolism and may lead to accumulation of potentially harmful compounds in the brain, including iron.PANK2 encodes a 1.85Kb transcript which is derived from seven exons covering a total distance of approximately 3.5Mb of genomic DNA. The PANK2 gene also encodes a 50.5-kDaprotein that is a functional pantothenate kinase, an essential regulatory enzyme in coenzyme A (CoA) biosynthesis, and catalyzing the phosphorylation of pantothenate (vitamin B5), N-pantothenoyl-cysteine, and pantetheine (OMIM). Mutant PANK2 gene coded proteins are often caused by null or missense mutations most notably a 7bp deletion in the PANK2 gene coding sequence.This disorder has been reported in specific communities based on intra-community marriages where both parents of the child are carrying the same mutation. One of the communities reported is Agrawal (Agarwal) Community mainly based in Northern Part of India. The known mutation in Agarwal community is pathogenic mutation 1c.215_216insA in PANK2 gene. This is also coded as chr20:3870292-3870293insA by some labs. It results in a frameshift and premature truncation of the protein 47 amino acids downstream to codon 183 (p.Arg183GlufsTer47; ENST00000316562). Diagnosis A neurological examination would show evidence of muscle rigidity; weakness; and abnormal postures, movements, and tremors. If other family members are also affected, this may help determine the diagnosis. Genetic tests can confirm an abnormal gene causing the disease. However, this test is not yet widely available. Other movement disorders and diseases must be ruled out. Individuals exhibiting any of the above listed symptoms are often tested using MRI (Magnetic Resonance Imaging) for a number of neuro-related disorders. An MRI usually shows iron deposits in the basal ganglia. Development of diagnostic criteria continues in the hope of further separating PKAN from other forms of neurodegenerative diseases featuring NBIA. Neuropathology Microscopic features of PKAN include high levels of iron in the globus pallidus and the pars reticulata of substantia nigra, evident as a characteristic rust-brown discoloration in a pattern called the eye-of-the-tiger sign; lipofuscin and neuromelanin concentrated in the iron-accumulating areas; oval, nonnucleated structures representing swollen axons whose cytoplasm swells with vacuoles, referred to as spheroids, axon schollen, or neuroaxonal dystrophy; and Lewy bodies. Treatment Phosphopantothenate has been shown to treat PKAN in a human, and also in a mouse model of the disease. Pantethine (a precursor of pantetheine) has been studied and shown to be effective in a mouse and in a fruit fly model of the disease. Prognosis Survival rates for those diagnosed with typical PKAN, and left untreated is 11.18 years with a standard deviation of 7.8 years. A study reporting good outcomes in a single patient with late onset PKAN has been performed. Epidemiology Prevalence data regarding this disorder remains incomplete, however it is estimated that anywhere between 1 in 1,000,000 to 3 in 1,000,000 individuals will be affected by this disorder (based upon observed cases in a population), but once again this is only an estimate as the disease is so rare it is difficult to statistically and accurately ascertain. History PKAN was first described by Hallervorden and Spatz (1922). Their discovery was brought about by a diagnosis of a family of 12 in which five sisters exhibited progressively increasing dementia and dysarthria. Autopsies revealed brown discolorations in different areas of the brain (particularly of interest were the globus pallidus and substantia nigra regions). Further investigation and description was brought about by Meyer (1958) who diagnosed 30 separate cases of PKAN. Meyer(1958) was followed by Elejalde et al. (1978) who described 5 affected family members and hypothesized that the disorder originated in central Europe, backing up his hypothesis with clinical and genetic analysis. Further investigation and insights were provided by Malmstrom-Groth and Kristensson (1982) and Jankovic et al. (1985).Diagnosis of PKAN hit a milestone with the availability of MRIs, as well as the in-depth descriptions of those MRIs provided by Littrup and Gebarski (1985), Tanfani et al. (1987), Sethi et al. (1988), Angelini et al. (1992), Casteels et al. (1994), and Malandrini et al. (1995). The gene was localized to chromosome 20p by Taylor et al. (1996) who suggested that this disorder should be referred to as neurodegeneration with brain iron accumulation (NBIA1) to avoid the objectionable eponym of Hallervorden-Spatz. The disease was renamed pantothenate kinase-associated neurodegeneration or PKAN by Zhou et al. (2001) who suggested the name to avoid misinterpretation and to better reflect the true nature of the disorder. Most recently Pellecchia et al. (2005) published a report of 16 patients affected by PKAN, confirmed by genetic analysis. References External links 02041 at CHORUSsynd/1082 at Who Named It? nbia at NINDS

Hi Aarogya, could you help me understand about Activity

Activity

Activity may refer to: Action (philosophy), in general Human activity: human behavior, in sociology behavior may refer to all basic human actions, economics may study human economic activities and along with cybernetics and psychology may study their modulation Recreation, or activities of leisure The Aristotelian concept of energeia, Latinized as actus Activity (UML), a major task in Unified Modeling Language Activity, the rate of catalytic activity, such as enzyme activity (enzyme assay), in physical chemistry and enzymology Thermodynamic activity, the effective concentration of a solute for the purposes of mass action Activity (project management) Activity, the number of radioactive decays per second Activity (software engineering) Activity (soil mechanics) HMS Activity (D94), an aircraft carrier of the Royal Navy "Activity", a song by Way Out West from Intensify Cultural activities, activities referred to culture. See also Activity theory, a learning theory in education Social activity (disambiguation), several concepts in the social sciences Activiti (software), an open source Business Process Management platform Active (disambiguation)

Can you describe Thoracic cavity, to me Aarogya

Thoracic cavity

The thoracic cavity (or chest cavity) is the chamber of the body of vertebrates that is protected by the thoracic wall (rib cage and associated skin, muscle, and fascia). The central compartment of the thoracic cavity is the mediastinum. There are two openings of the thoracic cavity, a superior thoracic aperture known as the thoracic inlet and a lower inferior thoracic aperture known as the thoracic outlet. The thoracic cavity includes the tendons as well as the cardiovascular system which could be damaged from injury to the back, spine or the neck. Structure Structures within the thoracic cavity include: structures of the cardiovascular system, including the heart and great vessels, which include the thoracic aorta, the pulmonary artery and all its branches, the superior and inferior vena cava, the pulmonary veins, and the azygos vein structures of the respiratory system, including the diaphragm, trachea, bronchi and lungs structures of the digestive system, including the esophagus, endocrine glands, including the thymus gland, structures of the nervous system including the paired vagus nerves, and the paired sympathetic chains, lymphatics including the thoracic duct.It contains three potential spaces lined with mesothelium: the paired pleural cavities and the pericardial cavity. The mediastinum comprises those organs which lie in the centre of the chest between the lungs. The cavity also contains two openings one at the top, the superior thoracic aperture also called the thoracic inlet, and a lower inferior thoracic aperture which is much larger than the inlet. Clinical significance If the pleural cavity is breached from the outside, as by a bullet wound or knife wound, a pneumothorax, or air in the cavity, may result. If the volume of air is significant, one or both lungs may collapse, which requires immediate medical attention. Additional images See also References External links thoraxlesson3 at The Anatomy Lesson by Wesley Norman (Georgetown University)

Would you describe Trichorrhexis nodosa, to me Aarogya

Trichorrhexis nodosa

Trichorrhexis nodosa is a defect in the hair shaft characterized by thickening or weak points (nodes) that cause the hair to break off easily.: 766 : 636  This group of conditions contributes to the appearance of hair loss, lack of growth, and damaged-looking hair. Symptoms Among the symptoms (and signs) for this condition are the following: lack of apparent hair growth hair appears patchy hair breaks easily close to scalp hair may have thickenings or nodes in the shaft ends of hair thinned or split whitish discoloration of hair tips hair breaks easily at tips Complications This condition is not dangerous but may affect self-esteem. Causes Trichorrhexis may have a genetic basis but appears to be precipitated by environmental factors. Among Caucasians the defect often appears at the ends of the hair shaft with splitting of the ends, thinning and whitish discoloration. These conditions are directly related to environmental causes such as "perming", blow drying, aggressive hair brushing, and excessive chemical exposure. In some cases, trichorrhexis nodosa may be caused by an underlying disorder such as argininosuccinic aciduria, Menkes kinky hair syndrome, Nethertons syndrome, hypothyroidism, or trichothiodystrophy. Diagnosis Examination of the hair shafts with a microscope may reveal changes of trichorrhexis nodosa. Prevention Avoid aggressive brushing and grooming, strong chemicals, permanents, straightening, and similar hair-damaging habits. Treatment Improving environmental factors will reduce damage to the hair. Gentle brushing with a soft brush should replace more aggressive brushing, ratting, or other procedures. Harsh chemicals such as hair straightening compounds and permanents should be avoided. The hair should not be ironed. Excessively harsh shampoo should be avoided. Hair conditioners should be used. Prognosis This condition is self-limiting. Improvements in grooming techniques and in environmental conditions will correct the abnormality. See also Trichomegaly Infrared Heat & Negative Ion Straighteners List of cutaneous conditions Notes References MedlinePlus Encyclopedia: Trichorrhexis nodosa == External links ==

Hi Aarogya, explain a situation where Alcohol dependence occurs

Alcohol dependence

Alcohol dependence is a previous (DSM-IV and ICD-10) psychiatric diagnosis in which an individual is physically or psychologically dependent upon alcohol (also chemically known as ethanol). In 2013, it was reclassified as alcohol use disorder in DSM-5, which combined alcohol dependence and alcohol abuse into this diagnosis. Definition Diagnosis DSM: Alcohol dependence According to the DSM-IV criteria for alcohol dependence, at least three out of seven of the following criteria must be manifest during a 12-month period: Tolerance Withdrawal symptoms or clinically defined alcohol withdrawal syndrome Use in larger amounts or for longer periods than intended Persistent desire or unsuccessful efforts to cut down on alcohol use Time is spent obtaining alcohol or recovering from effects Social, occupational and recreational pursuits are given up or reduced because of alcohol use Use is continued despite knowledge of alcohol-related harm (physical or psychological) Other alcohol-related disorders Because only 3 of the 7 DSM-IV criteria for alcohol dependence are required, not all patients meet the same criteria and therefore not all have the same symptoms and problems related to drinking. Not everyone with alcohol dependence, therefore, experiences physiological dependence. Alcohol dependence is differentiated from alcohol abuse by the presence of symptoms such as tolerance and withdrawal. Both alcohol dependence and alcohol abuse are sometimes referred to by the less specific term alcoholism. However, many definitions of alcoholism exist, and only some are compatible with alcohol abuse. There are two major differences between alcohol dependence and alcoholism as generally accepted by the medical community. Alcohol dependence refers to an entity in which only alcohol is the involved addictive agent. Alcoholism refers to an entity in which alcohol or any cross-tolerant addictive agent is involved. In alcohol dependence, reduction of alcohol, as defined within DSM-IV, can be attained by learning to control the use of alcohol. That is, a client can be offered a social learning approach that helps them to cope with external pressures by re-learning their pattern of drinking alcohol. In alcoholism, patients are generally not presumed to be in remission unless they are abstinent from alcohol.The following elements are the template for which the degree of dependence is judged: Narrowing of the drinking repertoire. Increased salience of the need for alcohol over competing needs and responsibilities. An acquired tolerance to alcohol. Withdrawal symptoms. Relief or avoidance of withdrawal symptoms by further drinking. Subjective awareness of compulsion to drink. Reinstatement after abstinence. Screening AUDIT has replaced older screening tools such as CAGE but there are many shorter alcohol screening tools, mostly derived from the AUDIT. The Severity of Alcohol Dependence Questionnaire (SAD-Q) is a more specific twenty-item inventory for assessing the presence and severity of alcohol dependence. AUDIT The Alcohol Use Disorders Identification Test (AUDIT) is considered the most accurate alcohol screening tool for identifying potential alcohol misuse, including dependence. It was developed by the World Health Organisation, designed initially for use in primary healthcare settings with supporting guidance. CAGE The CAGE questionnaire, the name of which is an acronym of its four questions, is a widely used method of screening for alcoholism. Online version of the CAGE questionnaire SADQ The Severity of Alcohol Dependence Questionnaire (SADQ or SAD-Q) is a 20 item clinical screening tool designed to measure the presence and level of alcohol dependence. Withdrawal Withdrawals from alcohol dependence is a common side effect that occurs when a person with the dependency stops drinking abruptly or even cuts back on their drinking after a prolonged period of indulgence. Withdrawal from alcohol dependence can vary from mild, moderate to severe, depending on several factors such as: how long the person has been drinking, are they a binge drinker, do they relapse chronically, how much do they drink daily. All these factors can vary from one person to the next depending on psychological, environmental, and biological factors. Some common withdrawal side effects are as listed: Mild Nausea Vomiting Rapid heartbeat Elevated blood pressure Fatigue Body aches / tremors Anxiety / Irritability / Depression Fuzzy brain Issues with sleeping Severe Vomiting Hypertensive crisis Seizures / Tremors Delusions / Hallucinations Dehydration Fever Chills / Shakes Extreme mood lability Mental pandemonium Little to no appetiteThe spectrum of alcohol withdrawal symptoms range from such minor symptoms as insomnia and tremulousness to severe complications such as withdrawal seizures and delirium tremens. Alcohol withdrawal syndrome can be very tricky to diagnose, due to other preliminary conditions that may exist from individual to individual. Treatment Treatments for alcohol dependence can be separated into two groups, those directed towards severely alcohol-dependent people, and those focused for those at risk of becoming dependent on alcohol. Treatment for alcohol dependence often involves utilizing relapse prevention, support groups, psychotherapy, and setting short-term goals. The Twelve-Step Program is also a popular faith-based process used by those wishing to recover from alcohol dependence.The ultimate goal when it comes to treating alcohol dependence or as the DSM-5 now calls it alcohol use disorder, is to help with establishing abstinence from drinking. There are several other benefits that come along with treatment. For some, it is reconnecting with themselves and obtaining self-esteem and confidence, a healthier lifestyle (physically and mentally), creating new relationships with other like-minded people as well as rekindling or mending old relationships if possible. The treatment process consists typically of two parts short-term and long-term. First, there is the path to abstinence and/or recovery. There are several reasons why someone with alcohol use disorder or alcohol dependency would seek treatment. This can either be a personal reason or because of law enforcement. There is a series of different levels of treatment processes depending on the severity subtype. Some would or could benefit from medication treatment with psychosocial treatment, while others could just benefit from psychosocial treatment. Listed below are different some different types of treatments that are used with treating alcohol dependency/alcohol use disorder depending on several factors that vary from person to person. Types of treatments: Withdrawals (no medication aid needed) Withdrawals (depending on severity of symptoms, could be accompanied with supervision by medical personal and medication) Psychosocial treatment (counseling, CBT, psychoeducation, assertive community treatment) Alcoholics Anonymous Inpatient or outpatient programs Social services (case management) Al-Anon/Alateen Epidemiology About 12% of American adults have had an alcohol dependence problem at some time in their life. In the UK the NHS estimates that around 9% of men and 4% of UK women show signs of alcohol dependence. History The term alcohol dependence has replaced alcoholism as a term in order that individuals do not internalize the idea of cure and disease, but can approach alcohol as a chemical they may depend upon to cope with outside pressures. The contemporary definition of alcohol dependence is still based upon early research. There has been considerable scientific effort over the past several decades to identify and understand the core features of alcohol dependence. This work began in 1976, when the British psychiatrist Griffith Edwards and his American colleague Milton M. Gross collaborated to produce a formulation of what had previously been understood as alcoholism – the alcohol dependence syndrome. The alcohol dependence syndrome was seen as a cluster of seven elements that concur. It was argued that not all elements may be present in every case, but the picture is sufficiently regular and coherent to permit clinical recognition. The syndrome was also considered to exist in degrees of severity rather than as a categorical absolute. Thus, the proper question is not whether a person is dependent on alcohol, but how far along the path of dependence has a person progressed. See also Alcohol intoxication Alcoholic drink Alcohol-related dementia CRAFFT Screening Test Disulfiram-like drug High-functioning alcoholic Long-term effects of alcohol consumption Paddington alcohol test Notes External links Arnold Little, MD Alcohol Dependence – extensive article SADD – Short Alcohol Dependence Data Questionnaire. A brief, self-administered questionnaire sometimes utilised in individual or group treatments. R.R.Garifullin Using coding therapy to treat alcohol and drug addiction. Manipulations in psychotherapy. Rostov-on-Don, Feniks, 251 p. 2004. 251 p. ISBN 5-222-04382-7

Aarogya, What does Sputum mean

Sputum

Sputum is mucus that is coughed up from the lower airways (the trachea and bronchi). In medicine, sputum samples are usually used for a naked eye examination, microbiological investigation of respiratory infections and cytological investigations of respiratory systems. It is crucial that the specimen does not include any mucoid material from the nose or oral cavity. A naked eye exam of the sputum can be done at home by a patient in order to note the various colors (see below). Any hint of yellow or green color (pus) suggests an airway infection (but does not indicate the type of organism causing it). Such color hints are best detected when the sputum is viewed on a very white background such as white paper, a white pot or a white sink surface. The more intense the yellow color, the more likely it is a caused by an infection (bronchitis, bronchopneumonia or pneumonia). Having green, yellow, or thickened phlegm (sputum) does not always indicate the presence of an infection. Also, if an infection is present, the color of the phlegm (sputum) does not determine whether a virus, a bacterium or another pathogen has caused it. Simple allergies can also cause changes in the color of the mucus. Description The best sputum samples contain very little saliva, as saliva contaminates the sample with oral bacteria. This is especially true for samples for laboratory testing in cytology or microbiology. Specimen adequacy is assessed by the laboratory technologists by examining a Gram stain or cytology stain of the sputum. More than 25 squamous epithelial cells at low power magnification exam under the microscope strongly suggest salivary contamination. Sputum samples have been used to quantify the degree of airway inflammation in human diseases such as asthma. Specifically, this work has demonstrated that a subgroup of severe asthma patients has airway inflammation that is resistant to treatment with corticosteroids.When a sputum specimen is plated out in microbiology, it is best to get the portion of the sample that almost looks like yellow pus onto the swab. If there is any blood in the sputum, this should also be on the swab. Microbiological sputum samples are used to look for infections, such as Moraxella catarrhalis, Mycobacterium tuberculosis, Streptococcus pneumoniae, and Haemophilus influenzae. Other pathogens can also be found. Purulent sputum contains pus, composed of white blood cells, cellular debris, dead tissue, serous fluid, and viscous liquid (mucus). Purulent sputum is typically yellow or green. It is seen in cases of pneumonia, bronchiectasis, lung abscess, or an advanced stage of bronchitis. Interpretation Sputum can be (when examined by the naked eye): Bloody (hemoptysis) Blood-streaked sputum –an indicator of possible inflammation of the throat (larynx and/or trachea) or bronchi; lung cancer; other bleeding erosions, ulcers, or tumors of the lower airway. Pink sputum – it indicates sputum evenly mixed with blood from alveoli and/or small peripheral bronchi as is seen in potential pulmonary edema. Massive blood – an indicator of possible cavitary tuberculosis or tumor such as lung cancer, or lung abscess; bronchiectasis; lung infarction; pulmonary embolism. Red, jelly-like sputum - an indicator of possible pneumonia caused by Klebsiella. Green or greenish colored - indicative of potential longstanding respiratory infection (green from degenerative changes in cell debris) as in pneumonia, ruptured lung abscess, chronic infectious bronchitis, and infected bronchiectasis or cystic fibrosis. Rust colored – usually caused by pneumococcal bacteria (in pneumonia), pulmonary embolism, lung cancer or pulmonary tuberculosis. Brownish –potential indicator of chronic bronchitis (greenish/yellowish/brown); chronic pneumonia (whitish-brown); tuberculosis; lung cancer. Yellow, yellowish purulent – an indicator of the sample containing pus. "The sputum color of patients with acute cough and no underlying chronic lung disease does not imply therapeutic consequences such as prescription of antibiotics." The color can provide hints as to effective treatment in chronic bronchitis patients:A yellow-greenish (mucopurulent) color suggests that treatment with antibiotics can reduce symptoms. The green color is caused by degenerating neutrophil verdoperoxidase. Whitish gray sputum color against a white color background (such as a white sink surface) tends to indicate either a specimen from someone who is dehydrated, and/or from an older person, and/or a specimen with a mixed, modest number of eosinophils and maybe some acute inflammatory neutrophil cells (this last choice tends to suggest chronic allergic bronchitis). A white, milky, or opaque (mucoid) appearance means that antibiotics are less likely to be effective in treatment because the likelihood is greater of a viral infection or allergy (even asthma...thick sputum) than of antibiotic-responsive micro-organisms. Foamy white – may come from earlier-phase pulmonary edema. Frothy pink – may indicate more severe pulmonary edema. Antibiotics may not be necessary at this time. Clear – pulmonary embolism (clear to frothy); COPD chronic obstructive pulmonary disease (clear to gray); viral respiratory infection (clear to whitish and sometimes a hint of yellow); asthma (thick and white to yellowish). See also Phlegm References == External links ==

Aarogya, explain a scenario commonly referred as Congenital heart defect

Congenital heart defect

A congenital heart defect (CHD), also known as a congenital heart anomaly and congenital heart disease, is a defect in the structure of the heart or great vessels that is present at birth. A congenital heart defect is classed as a cardiovascular disease. Signs and symptoms depend on the specific type of defect. Symptoms can vary from none to life-threatening. When present, symptoms may include rapid breathing, bluish skin (cyanosis), poor weight gain, and feeling tired. CHD does not cause chest pain. Most congenital heart defects are not associated with other diseases. A complication of CHD is heart failure.The cause of a congenital heart defect is often unknown. Risk factors include certain infections during pregnancy such as rubella, use of certain medications or drugs such as alcohol or tobacco, parents being closely related, or poor nutritional status or obesity in the mother. Having a parent with a congenital heart defect is also a risk factor. A number of genetic conditions are associated with heart defects, including Down syndrome, Turner syndrome, and Marfan syndrome. Congenital heart defects are divided into two main groups: cyanotic heart defects and non-cyanotic heart defects, depending on whether the child has the potential to turn bluish in color. The defects may involve the interior walls of the heart, the heart valves, or the large blood vessels that lead to and from the heart.Congenital heart defects are partly preventable through rubella vaccination, the adding of iodine to salt, and the adding of folic acid to certain food products. Some defects do not need treatment. Others may be effectively treated with catheter based procedures or heart surgery. Occasionally a number of operations may be needed, or a heart transplant may be required. With appropriate treatment, outcomes are generally good, even with complex problems.Congenital heart defects are the most common birth defect. In 2015, they were present in 48.9 million people globally. They affect between 4 and 75 per 1,000 live births, depending upon how they are diagnosed. In about 6 to 19 per 1,000 they cause a moderate to severe degree of problems. Congenital heart defects are the leading cause of birth defect-related deaths: in 2015, they resulted in 303,300 deaths, down from 366,000 deaths in 1990. Signs and symptoms Signs and symptoms are related to type and severity of the heart defect. Symptoms frequently present early in life, but it is possible for some CHDs to go undetected throughout life. Some children have no signs while others may exhibit shortness of breath, cyanosis, fainting, heart murmur, under-development of limbs and muscles, poor feeding or growth, or respiratory infections. Congenital heart defects cause abnormal heart structure resulting in production of certain sounds called heart murmur. These can sometimes be detected by auscultation; however, not all heart murmurs are caused by congenital heart defects. Associated conditions Congenital heart defects are associated with an increased incidence of seven other specific medical conditions, together being called the VACTERL association: V — Vertebral anomalies A — Anal atresia C — Cardiovascular anomalies T — Tracheoesophageal fistula E — Esophageal atresia R — Renal (Kidney) and/or radial anomalies L — Limb defectsVentricular septal defect (VSD), atrial septal defects, and tetralogy of Fallot are the most common congenital heart defects seen in the VACTERL association. Less common defects in the association are truncus arteriosus and transposition of the great arteries. Causes The cause of congenital heart disease may be genetic, environmental, or a combination of both. Genetic Genetic mutations, often sporadic, represent the largest known cause of congenital heart defects. They are described in the table below. Molecular pathways The genes regulating the complex developmental sequence have only been partly elucidated. Some genes are associated with specific defects. A number of genes have been associated with cardiac manifestations. Mutations of a heart muscle protein, α-myosin heavy chain (MYH6) are associated with atrial septal defects. Several proteins that interact with MYH6 are also associated with cardiac defects. The transcription factor GATA4 forms a complex with the TBX5 which interacts with MYH6. Another factor, the homeobox (developmental) gene, NKX2-5 also interacts with MYH6. Mutations of all these proteins are associated with both atrial and ventricular septal defects; In addition, NKX2-5 is associated with defects in the electrical conduction of the heart and TBX5 is related to the Holt–Oram syndrome which includes electrical conduction defects and abnormalities of the upper limb. The Wnt signaling co-factors BCL9, BCL9L and PYGO might be part of this molecular pathways, as when their genes are mutated, this causes phenotypes similar to the features present in Holt-Oram syndrome. Another T-box gene, TBX1, is involved in velo-cardio-facial syndrome DiGeorge syndrome, the most common deletion which has extensive symptoms including defects of the cardiac outflow tract including tetralogy of Fallot. The notch signaling pathway, a regulatory mechanism for cell growth and differentiation, plays broad roles in several aspects of cardiac development. Notch elements are involved in determination of the right and left sides of the body plan, so the directional folding of the heart tube can be impacted. Notch signaling is involved early in the formation of the endocardial cushions and continues to be active as the develop into the septa and valves. It is also involved in the development of the ventricular wall and the connection of the outflow tract to the great vessels. Mutations in the gene for one of the notch ligands, Jagged1, are identified in the majority of examined cases of arteriohepatic dysplasia (Alagille syndrome), characterized by defects of the great vessels (pulmonary artery stenosis), heart (tetralogy of Fallot in 13% of cases), liver, eyes, face, and bones. Though less than 1% of all cases, where no defects are found in the Jagged1 gene, defects are found in Notch2 gene. In 10% of cases, no mutation is found in either gene. For another member of the gene family, mutations in the Notch1 gene are associated with bicuspid aortic valve, a valve with two leaflets instead of three. Notch1 is also associated with calcification of the aortic valve, the third most common cause of heart disease in adults.Mutations of a cell regulatory mechanism, the Ras/MAPK pathway are responsible for a variety of syndromes, including Noonan syndrome, LEOPARD syndrome, Costello syndrome and cardiofaciocutaneous syndrome in which there is cardiac involvement. While the conditions listed are known genetic causes, there are likely many other genes which are more subtle. It is known that the risk for congenital heart defects is higher when there is a close relative with one. Environmental Known environmental factors include certain infections during pregnancy such as rubella, drugs (alcohol, hydantoin, lithium and thalidomide) and maternal illness (diabetes mellitus, phenylketonuria, and systemic lupus erythematosus). Alcohol exposure in the father also appears to increase the risk of congenital heart defects.Being overweight or obese increases the risk of congenital heart disease. Additionally, as maternal obesity increases, the risk of heart defects also increases. A distinct physiological mechanism has not been identified to explain the link between maternal obesity and CHD, but both pre-pregnancy folate deficiency and diabetes have been implicated in some studies. Mechanism There is a complex sequence of events that result in a well formed heart at birth and disruption of any portion may result in a defect. The orderly timing of cell growth, cell migration, and programmed cell death ("apoptosis") has been studied extensively and the genes that control the process are being elucidated. Around day 15 of development, the cells that will become the heart exist in two horseshoe shaped bands of the middle tissue layer (mesoderm), and some cells migrate from a portion of the outer layer (ectoderm), the neural crest, which is the source of a variety of cells found throughout the body. On day 19 of development, a pair of vascular elements, the "endocardial tubes", form. The tubes fuse when cells between then undergo programmed death and cells from the first heart field migrate to the tube, and form a ring of heart cells (myocytes) around it by day 21. On day 22, the heart begins to beat and by day 24, blood is circulating.At day 22, the circulatory system is bilaterally symmetrical with paired vessels on each side and the heart consisting of a simple tube located in the midline of the body layout. The portions that will become the atria and will be located closest to the head are the most distant from the head. From days 23 through 28, the heart tube folds and twists, with the future ventricles moving left of center (the ultimate location of the heart) and the atria moving towards the head.On day 28, areas of tissue in the heart tube begin to expand inwards; after about two weeks, these expansions, the membranous "septum primum" and the muscular "endocardial cushions", fuse to form the four chambers of the heart. A failure to fuse properly will result in a defect that may allow blood to leak between chambers. After this happens, cells that have migrated from the neural crest begin to divide the bulbus cordis, the main outflow tract is divided in two by the growth a spiraling septum, becoming the great vessels—the ascending segment of the aorta and the pulmonary trunk. If the separation is incomplete, the result is a "persistent truncus arteriosus". The vessels may be reversed ("transposition of the great vessels"). The two halves of the split tract must migrate into the correct positions over the appropriate ventricles. A failure may result in some blood flowing into the wrong vessel (e.g.overriding aorta). The four-chambered heart and the great vessels have features required for fetal growth. The lungs are unexpanded and cannot accommodate the full circulatory volume. Two structures exist to shunt blood flow away from the lungs. Cells in part of the septum primum die creating a hole while muscle cells, the "septum secundum", grow along the right atrial side the septum primum, except for one region, leaving a gap through which blood can pass from the right artium to the left atrium, the foramen ovale. A small vessel, the ductus arteriosus allows blood from the pulmonary artery to pass to the aorta. Changes at birth The ductus arteriosus stays open because of circulating factors including prostaglandins. The foramen ovale stays open because of the flow of blood from the right atrium to the left atrium. As the lungs expand, blood flows easily through the lungs and the membranous portion of the foramen ovale (the septum primum) flops over the muscular portion (the septum secundum). If the closure is incomplete, the result is a patent foramen ovale. The two flaps may fuse, but many adults have a foramen ovale that stays closed only because of the pressure difference between the atria. Theories Rokitansky (1875) explained congenital heart defects as breaks in heart development at various ontogenesis stages. Spitzer (1923) treats them as returns to one of the phylogenesis stages. Krimski (1963), synthesizing two previous points of view, considered congenital heart diseases as a stop of development at the certain stage of ontogenesis, corresponding to this or that stage of the phylogenesis. Hence these theories can explain feminine and neutral types of defects only. Diagnosis Many congenital heart defects can be diagnosed prenatally by fetal echocardiography. This is a test which can be done during the second trimester of pregnancy, when the woman is about 18–24 weeks pregnant. It can be an abdominal ultrasound or transvaginal ultrasound.If a baby is born with cyanotic heart disease, the diagnosis is usually made shortly after birth due to the blue colour of their skin (called cyanosis).If a baby is born with a septal defect or an obstruction defect, often their symptoms are only noticeable after several months or sometimes even after many years. Classification A number of classification systems exist for congenital heart defects. In 2000 the International Congenital Heart Surgery Nomenclature was developed to provide a generic classification system. Hypoplasia Hypoplasia can affect the heart, typically resulting in the underdevelopment of the right ventricle or the left ventricle. This causes only one side of the heart to be capable of pumping blood to the body and lungs effectively. Hypoplasia of the heart is rare but is the most serious form of CHD. It is called hypoplastic left heart syndrome when it affects the left side of the heart and hypoplastic right heart syndrome when it affects the right side of the heart. In both conditions, the presence of a patent ductus arteriosus (and, when hypoplasia affects the right side of the heart, a patent foramen ovale) is vital to the infants ability to survive until emergency heart surgery can be performed, since without these pathways blood cannot circulate to the body (or lungs, depending on which side of the heart is defective). Hypoplasia of the heart is generally a cyanotic heart defect. Obstructive defects Obstructive defects occur when heart valves, arteries, or veins are abnormally narrow or blocked. Common defects include pulmonic stenosis, aortic stenosis, and coarctation of the aorta, with other types such as bicuspid aortic valve stenosis and subaortic stenosis being comparatively rare. Any narrowing or blockage can cause heart enlargement or hypertension. Septal defects The septum is a wall of tissue which separates the left heart from the right heart. Defects in the interatrial septum or the interventricular septum allow blood to flow from the left side of the heart to the right, reducing the hearts efficiency. Ventricular septal defects are collectively the most common type of CHD, although approximately 30% of adults have a type of atrial septal defect called probe patent foramen ovale. Cyanotic defects Cyanotic heart defects are called such because they result in cyanosis, a bluish-grey discoloration of the skin due to a lack of oxygen in the body. Such defects include persistent truncus arteriosus, total anomalous pulmonary venous connection, tetralogy of Fallot, transposition of the great vessels, and tricuspid atresia. Defects Aortic stenosis Arrhythmogenic right ventricular cardiomyopathy Atrial septal defect (ASD) Atrioventricular septal defect (AVSD) Bicuspid aortic valve Cardiomyopathy Complete heart block (CHB) Dextrocardia Double inlet left ventricle (DILV) Double outlet right ventricle (DORV) Ebsteins anomaly Early Repolarization Syndrome Hypoplastic left heart syndrome (HLHS) Hypoplastic right heart syndrome (HRHS) Mitral stenosis Myocardial bridge Persistent truncus arteriosus Pulmonary atresia Pulmonary stenosis Rhabdomyomas (Tumors of the Heart) Transposition of the great vessels dextro-Transposition of the great arteries (d-TGA) levo-Transposition of the great arteries (l-TGA) Tricuspid atresia Ventricular septal defect (VSD) Wolff–Parkinson–White syndrome (WPW)Some conditions affect the great vessels or other vessels in close proximity to the heart, but not the heart itself, but are often classified as congenital heart defects. Coarctation of the aorta (CoA) Double aortic arch, aberrant subclavian artery, and other malformations of the great arteries Interrupted aortic arch (IAA) Patent ductus arteriosus (PDA) Scimitar syndrome (SS) Partial anomalous pulmonary venous connection (PAPVC) Total anomalous pulmonary venous connection (TAPVC)Some constellations of multiple defects are commonly found together. Tetralogy of Fallot (ToF) Pentalogy of Cantrell Shones syndrome/ Shones complex / Shones anomaly Treatment CHD may require surgery and medications. Medications include diuretics, which aid the body in eliminating water, salts, and digoxin for strengthening the contraction of the heart. This slows the heartbeat and removes some fluid from tissues. Some defects require surgical procedures to restore circulation back to normal and in some cases, multiple surgeries are needed.Interventional cardiology now offers minimally invasive alternatives to surgery for some patients. The Melody Transcatheter Pulmonary Valve (TPV), approved in Europe in 2006 and in the U.S. in 2010 under a Humanitarian Device Exemption (HDE), is designed to treat congenital heart disease patients with a dysfunctional conduit in their right ventricular outflow tract (RVOT). The RVOT is the connection between the heart and lungs; once blood reaches the lungs, it is enriched with oxygen before being pumped to the rest of the body. Transcatheter pulmonary valve technology provides a less-invasive means to extend the life of a failed RVOT conduit and is designed to allow physicians to deliver a replacement pulmonary valve via a catheter through the patients blood vessels.Many people require lifelong specialized cardiac care, first with a pediatric cardiologist and later with an adult congenital cardiologist. There are more than 1.8 million adults living with congenital heart defects. Epidemiology Heart defects are among the most common birth defect, occurring in 1% of live births (2–3% including bicuspid aortic valve). In 2013, 34.3 million people had CHD. In 2010, they resulted in 223,000 deaths, down from 278,000 deaths in 1990.For congenital heart defects that arise without a family history (de novo), the recurrence risk in offspring is 3–5%. This risk is higher in left ventricular outflow tract obstructions, heterotaxy, and atrioventricular septal defects. Terminology Congenital heart defects are known by a number of names including congenital heart anomaly, congenital heart disease, heart defects, and congenital cardiovascular malformations. See also Congenital Heart Surgeons Society Congenital heart block References External links Congenital heart defect at Curlie Congenital heart disease information for parents.

Hello Aarogya , Do you know what is Levocardia,

Levocardia

Levocardia is where the heart is on the normal side of the body (the left), as opposed to dextrocardia, in which the heart is in the right side of the thoracic cavity. This can be associated with situs solitus, where the remainder of the organs are on normal side as well; or situs inversus, in which the viscera (stomach, liver, intestines, lungs, etc.) on the opposite side as normal. The latter condition may or may not be associated with clinically relevant abnormalities. See also Isolated levocardia References == External links ==

Hi Aarogya, could you help me understand about Thalassemia

Thalassemia

Thalassemias are inherited blood disorders characterized by decreased hemoglobin production. Symptoms depend on the type and can vary from none to severe. Often there is mild to severe anemia (low red blood cells or hemoglobin). Anemia can result in feeling tired and pale skin. There may also be bone problems, an enlarged spleen, yellowish skin, and dark urine. Slow growth may occur in children.Thalassemias are genetic disorders inherited from a persons parents. There are two main types, alpha thalassemia and beta thalassemia. The severity of alpha and beta thalassemia depends on how many of the four genes for alpha globin or two genes for beta globin are missing. Diagnosis is typically by blood tests including a complete blood count, special hemoglobin tests, and genetic tests. Diagnosis may occur before birth through prenatal testing.Treatment depends on the type and severity. Treatment for those with more severe disease often includes regular blood transfusions, iron chelation, and folic acid. Iron chelation may be done with deferoxamine, deferasirox or deferiprone. Occasionally, a bone marrow transplant may be an option. Complications may include iron overload from the transfusions with resulting heart or liver disease, infections, and osteoporosis. If the spleen becomes overly enlarged, surgical removal may be required. Thalassemia patients who do not respond well to blood transfusions can take hydroxyurea or thalidomide, and sometimes a combination of both. Hydroxyurea is the only FDA approved drug for thalassemia. Patients who took 10 mg/kg of hydroxyurea every day for a year had significantly higher hemoglobin levels, and it was a well-tolerated treatment for patients who did not respond well to blood transfusions. Another hemoglobin-inducer includes thalidomide, although it has not been tested in a clinical setting. The combination of thalidomide and hydroxyurea resulted in hemoglobin levels increasing significantly in transfusion-dependent and non-transfusion dependent patients As of 2015, thalassemia occurs in about 280 million people, with about 439,000 having severe disease. It is most common among people of Greek, Italian, Middle Eastern, South Asian, and African descent. Males and females have similar rates of disease. It resulted in 16,800 deaths in 2015, down from 36,000 deaths in 1990. Those who have minor degrees of thalassemia, similar to those with sickle-cell trait, have some protection against malaria, explaining why they are more common in regions of the world where malaria exists. Signs and symptoms Iron overload: People with thalassemia can get an overload of iron in their bodies, either from the disease itself or from frequent blood transfusions. Too much iron can result in damage to the heart, liver, and endocrine system, which includes glands that produce hormones that regulate processes throughout the body. The damage is characterized by excessive deposits of iron. Without adequate iron chelation therapy, almost all patients with beta-thalassemia accumulate potentially fatal iron levels. Infection: People with thalassemia have an increased risk of infection. This is especially true if the spleen has been removed. Bone deformities: Thalassemia can make the bone marrow expand, which causes bones to widen. This can result in abnormal bone structure, especially in the face and skull. Bone marrow expansion also makes bones thin and brittle, increasing the risk of broken bones. Enlarged spleen: The spleen aids in fighting infection and filters unwanted material, such as old or damaged blood cells. Thalassemia is often accompanied by the destruction of a large number of red blood cells and the task of removing these cells causes the spleen to enlarge. Splenomegaly can make anemia worse, and it can reduce the life of transfused red blood cells. Severe enlargement of the spleen may necessitate its removal. Slowed growth rates: anemia can cause the growth of a child to slow down. Puberty may also be delayed in children with thalassemia. Heart problems: Diseases, such as congestive heart failure and abnormal heart rhythms, may be associated with severe thalassemia. Hemoglobin structural biology Normal human hemoglobins are tetrameric proteins composed of two pairs of globin chains, each of which contains one alpha-like (α-like) chain and one beta-like (β-like) chain. Each globin chain is associated with an iron-containing heme moiety. Throughout life, the synthesis of the alpha-like and the beta-like (also called non-alpha-like) chains is balanced so that their ratio is relatively constant and there is no excess of either type.The specific alpha and beta-like chains that are incorporated into Hb are highly regulated during development: Embryonic Hbs are expressed as early as four to six weeks of embryogenesis and disappear around the eighth week of gestation as they are replaced by fetal Hb. Embryonic Hbs include: Hb Gower-1, composed of two ζ globins (zeta globins) and two ε globins (epsilon globins) (ζ2ε2) Hb Gower-2, composed of two alpha globins and two epsilon globins (α2ε2) Hb Portland, composed of two zeta globins and two gamma globins (ζ2γ2) Fetal Hb (Hb F) is produced from approximately eight weeks of gestation through birth and constitutes approximately 80 percent of Hb in the full-term neonate. It declines during the first few months of life and, in the normal state, constitutes <1 percent of total Hb by early childhood. Hb F is composed of two alpha globins and two gamma globins (α2γ2). Adult Hb (Hb A) is the predominant Hb in children by six months of age and onward; it constitutes 96-97% of total Hb in individuals without a hemoglobinopathy. It is composed of two alpha globins and two beta globins (α2β2). Hb A2 is a minor adult Hb that normally accounts for approximately 2.5-3.5% of total Hb from six months of age onward. It is composed of two alpha globins and two delta globins (α2δ2). Cause Both α- and β-thalassemias are often inherited in an autosomal recessive manner. Cases of dominantly inherited α- and β-thalassemias have been reported, the first of which was in an Irish family with two deletions of 4 and 11 bp in exon 3 interrupted by an insertion of 5 bp in the β-globin gene. For the autosomal recessive forms of the disease, both parents must be carriers for a child to be affected. If both parents carry a hemoglobinopathy trait, the risk is 25% for each pregnancy for an affected child.The genes involved in thalassemia control the production of healthy hemoglobin. Hemoglobin binds oxygen in the lungs and releases it when the red cells reach peripheral tissues, such as the liver. The binding and release of oxygen by hemoglobin are essential for survival. Evolution Having a single genetic variant for thalassemia may protect against malaria and thus can be an advantage.People diagnosed with heterozygous (carrier) β-thalassemia have some protection against coronary heart disease. Pathophysiology Normally, the majority of adult hemoglobin (HbA) is composed of four protein chains, two α and two β-globin chains arranged into a heterotetramer. In thalassemia, patients have defects in either the α or β-globin chain, causing production of abnormal red blood cells.The thalassemias are classified according to which chain of the hemoglobin molecule is affected. In α-thalassemias, production of the α-globin chain is affected, while in β-thalassemia, production of the β-globin chain is affected.The β-globin chains are encoded by a single gene on chromosome 11; α-globin chains are encoded by two closely linked genes on chromosome 16. Thus, in a normal person with two copies of each chromosome, two loci encode the β chain, and four loci encode the α chain. Deletion of one of the α loci has a high prevalence in people of African or Asian descent, making them more likely to develop α-thalassemia. β-Thalassemias are not only common in Africans, but also in Greeks and Turks. Alpha-thalassemias The α-thalassemias involve the genes HBA1 and HBA2, inherited in a Mendelian recessive fashion. Two gene loci and so four alleles exist. Two genetic loci exist for α-globin, thus four alleles are in diploid cells. Two alleles are maternal and two alleles are paternal in origin. The severity of the α-thalassemias is correlated with the number of affected α-globin; alleles: the greater, the more severe will be the manifestations of the disease. Alpha-thalassemias result in decreased alpha-globin production; therefore, fewer alpha-globin chains are produced, resulting in an excess of β chains in adults and excess γ chains in newborns. The excess β chains form unstable tetramers (called hemoglobin H or HbH of 4 beta chains), which have abnormal oxygen dissociation curves. Alpha thalassemias often are found in people from Southeast Asia, the Middle East, China, and in those of African descent. Beta-thalassemia Beta thalassemias are due to mutations in the HBB gene on chromosome 11, also inherited in an autosomal, recessive fashion. The severity of the disease depends on the nature of the mutation and on the presence of mutations in one or both alleles. Mutated alleles are called β+ when partial function is conserved (either the protein has a reduced function, or it functions normally but is produced in reduced quantity) or βo, when no functioning protein is produced. The situation of both alleles determines the clinical picture: β thalassemia major (Mediterranean anemia or Cooley anemia) is caused by a βo/βo genotype. No functional β chains are produced, and thus no hemoglobin A can be assembled. This is the most severe form of β-thalassemia; β thalassemia intermedia is caused by a β+/βo or β+/β+ genotype. In this form, some hemoglobin A is produced; β thalassemia minor is caused by a β/βo or β/β+ genotype. Only one of the two β globin alleles contains a mutation, so β chain production is not terribly compromised and patients may be relatively asymptomatic.Beta thalassemia most often occurs in people of Mediterranean origin. To a lesser extent, Chinese, other Asians, and African Americans can be affected. Delta-thalassemia As well as alpha and beta chains present in hemoglobin, about 3% of adult hemoglobin is made of alpha and delta chains. Just as with beta thalassemia, mutations that affect the ability of this gene to produce delta chains can occur. Combination hemoglobinopathies Thalassemia can coexist with other hemoglobinopathies. The most common of these are: Hemoglobin E/thalassemia: common in Cambodia, Thailand, and parts of India, it is clinically similar to β thalassemia major or thalassemia intermedia. Hemoglobin S/thalassemia: common in African and Mediterranean populations, it is clinically similar to sickle-cell anemia, with the additional feature of splenomegaly. Hemoglobin C/thalassemia: common in Mediterranean and African populations, hemoglobin C/βo thalassemia causes a moderately severe hemolytic anemia with splenomegaly; hemoglobin C/β+ thalassemia produces a milder disease. Hemoglobin D/thalassemia: common in the northwestern parts of India and Pakistan (Punjab region). Diagnosis Thalassemia can be diagnosed via a complete blood count, hemoglobin electrophoresis or high-performance liquid chromatography, and DNA testing. Hemoglobin electrophoresis is not widely available in developing countries, but the Mentzer index can also be used for diagnosis of thalassemia; it is not a definitive test but it can suggest the possibility of thalassemia. The Mentzer index can be calculated from a complete blood count report. Prevention The American College of Obstetricians and Gynecologists recommends all people thinking of becoming pregnant be tested to see if they have thalassemia. Genetic counseling and genetic testing are recommended for families who carry a thalassemia trait.A screening policy exists in Cyprus to reduce the rate of thalassemia, which, since the programs implementation in the 1970s (also including prenatal screening and abortion), has reduced the number of children born with the disease from one of every 158 births to almost zero. Greece also has a screening program to identify people who are carriers.In Iran as a premarital screening, the mans red cell indices are checked first. If he has microcytosis (mean cell hemoglobin < 27 pg or mean red cell volume < 80 fl), the woman is tested. When both are microcytic, their hemoglobin A2 concentrations are measured. If both have a concentration above 3.5% (diagnostic of thalassemia trait) they are referred to the local designated health post for genetic counseling.Large-scale awareness campaigns are being organized in India both by government and non-government organizations to promote voluntary premarital screening, with marriage between carriers strongly discouraged. Management Mild thalassemia: people with thalassemia traits do not require medical or follow-up care after the initial diagnosis is made. People with β-thalassemia trait should be warned that their condition can be misdiagnosed as the more common iron-deficiency anemia. They should avoid routine use of iron supplements, but iron deficiency may develop during pregnancy or from chronic bleeding. Counseling is indicated for all persons with genetic disorders, especially when the family is at risk of a severe form of disease that may be prevented. Anemia People with severe thalassemia require medical treatment. A blood transfusion regimen is the first effective measure in prolonging life. Growth hormone therapy There is some evidence that growth hormone replacement therapy may help to increase the rate at which children with thalassemia grow taller. Iron overload Multiple blood transfusions may result in iron overload. The iron overload related to thalassemia may be treated by chelation therapy with the medications deferoxamine, deferiprone, or deferasirox. These treatments have resulted in longer life expectancy for those with thalassemia major.Deferoxamine is only effective as a daily injection, complicating its long-term use. However, it is inexpensive and safe. Adverse effects include primary skin reactions around the injection site and hearing loss.Deferasirox and deferiprone are both oral medications, whose common side effects include nausea, vomiting and diarrhea. Deferasirox is not effective for all patients and may not be suitable for those with significant cardiac issues related to iron overload, while deferiprone appears to be the most effective agent when the heart is involved. Furthermore, the cost of deferasirox is also significant.There is no evidence from randomized controlled trial to support zinc supplementation for those with thalassemia. Bone-marrow transplantation Bone-marrow transplantation may offer the possibility of a cure in young people who have an HLA-matched donor. Success rates have reached the 80–90% range. Mortality from the procedure is about 3%. There are no randomized controlled trials that have tested the safety and efficacy of non-identical donor bone-marrow transplantation in persons with β- thalassemia who are dependent on blood transfusion.Graft-versus-host diseases (GvHD) are one relevant side effect of bone-marrow transplantation. Further research is necessary to evaluate whether mesenchymal stromal cells can be used as prophylaxis or treatment for GvHD.If the patient does not have an HLA-matched compatible donor, bone-marrow transplantation from haploidentical mother to child (mismatched donor) may be attempted. In a study of 31 people, the thalassemia-free survival rate was 70%, rejection 23% and mortality 7%. The most positive results tend to occur with very young people. Epidemiology The beta form of thalassemia is particularly prevalent among Mediterranean peoples, and this geographical association is responsible for its original name. Thalassemia resulted in 25,000 deaths in 2013 down from 36,000 deaths in 1990.In Europe, the highest concentrations of the disease are found in Greece, coastal regions in Turkey (particularly the Aegean Region such as İzmir, Balıkesir, Aydın, Muğla, and Mediterranean Region such as Antalya, Adana, Mersin), in southern Spain, in parts of Italy, particularly southern Italy. With the exception of the Balearics, the major Mediterranean Islands, such as Sicily, Sardinia, Malta, Corsica, Cyprus, and Crete are heavily affected. Other Mediterranean peoples, as well as those in the vicinity of the Mediterranean, also have high rates of thalassemia, including people from North Africa and West Asia. Far from the Mediterranean, South Asians are also affected, with the worlds highest concentration of carriers (16–18% of the population) in the Maldives.The disease is also found in populations living in Africa, the Americas, and in Tharu people in the Terai region of Nepal and India. It is believed to account for much lower rates of malaria illnesses and deaths, accounting for the historic ability of Tharus to survive in areas with heavy malaria infestation while others could not. Thalassemias are particularly associated with people of Mediterranean origin, Arabs (especially Palestinians and people of Palestinian descent), and Asians. The estimated prevalence is 16% in people from Cyprus, 1% in Thailand, and 3–8% in populations from Bangladesh, China, India, Malaysia and Pakistan. Estimates suggest that approximately 1.5% of the global population (80 – 90 million people) are β-thalassemia carriers. However, exact data on carrier rates in many populations are lacking, particularly in developing areas of the world known or expected to be heavily affected. Because of the prevalence of the disease in countries with little knowledge of thalassemia, access to proper treatment and diagnosis can be difficult. While there are some diagnostic and treatment facilities in developing countries, in most cases these are not provided by government services and are available only to patients who can afford them. In general, poorer populations only have access to limited diagnostic facilities and blood transfusions. In some developing countries, there are virtually no facilities for diagnosis or management of thalassemia. Etymology and synonym The word thalassemia () derives from the Greek thalassa (θάλασσα), "sea", and New Latin -emia (from the Greek compound stem -aimia (-αιμία), from haima (αἷμα), "blood"). It was coined because the condition called "Mediterranean anemia" was first described in people of Mediterranean ethnicities. "Mediterranean anemia" was renamed thalassemia major once the genetics were better understood. The word thalassemia was first used in 1932.: 877 Society and culture In 2008, in Spain, a baby was selectively implanted to be a cure for his brothers thalassemia. The child was born from an embryo screened to be free of the disease before implantation with in vitro fertilization. The babys supply of immunologically compatible cord blood was saved for transplantation to his brother. The transplantation was considered successful. In 2009, a group of doctors and specialists in Chennai and Coimbatore registered the successful treatment of thalassemia in a child using an unaffected siblings umbilical cord blood. Research Gene therapy Gene therapy is being studied for thalassemia. The procedure involves collecting hematopoietic stem cells (HSCs) from the affected persons blood. The HSCs then have a beta-globin gene added using a lentiviral vector. After destroying the affected persons bone marrow with a dose of chemotherapy (a myeloablative conditioning regimen), the altered HSCs are infused back into the affected person where they become engrafted in the bone marrow where they proliferate. This potentially results in a progressive increase in hemoglobin A2 synthesis in all subsequent developing red blood cells, with resultant resolution of the anemia.While one person with beta thalassemia has no longer required blood transfusions following treatment within a research trial, it is not an approved treatment as of 2018. HbF induction HbF induction is an attempt to reactivate fetal globin gene transcription. Efforts involve trying to disrupt the fetal globin gene promoter. References External links Thalassemia at Curlie Learning About Thalassemia published by the National Human Genome Research Institute.

Do you know what is Orthostatic albuminuria, Aarogya

Orthostatic albuminuria

Orthostatic proteinuria (synonyms: orthostatic albuminuria, postural proteinuria) is a benign condition. A change in renal hemodynamics, which in some otherwise normal individuals, causes protein (mostly albumin) to appear in urine when they are in the standing position. Urine formed when these individuals are lying down is protein-free.There is normal urinary protein excretion during the night but increased excretion during the day, associated with activity and upright posture. Total urinary protein excretion may be increased but levels above 1 g per 24 hours are more likely to be associated with underlying renal disease. The exact cause for orthostatic proteinuria is not known. == References ==

Would you describe Mast cell leukemia, to me Aarogya

Mast cell leukemia

Mast cell leukemia is an extremely aggressive subtype of acute myeloid leukemia that usually occurs de novo but can, rarely, evolve from transformation of chronic myeloid leukemia into the more aggressive acute myeloid leukemia. In a small proportion of cases, acute mast cell leukemia may evolve from a more progressive form of systemic mastocytosis. The diagnosis of acute mast cell leukemia by the WHO criteria includes the requirement for a prevalence of 20% neoplastic mast cells in marrow and 10% in blood. If the mast cells represent less than 10% of blood cells, the tumor is called "aleukemic" mast cell leukemia. Signs and symptoms Acute mast cell leukemia is a rapidly progressive disorder with leukemic mast cells in blood and in large numbers in marrow. The common signs and symptoms include fever, headache, flushing of face and trunk. The typical cutaneous mast cell infiltrates of urticaria pigmentosa are usually not present before, during, or after diagnosis in patients who have mast cell leukemia. Symptoms include abdominal pain, bone pain, and peptic ulcer which are more prevalent than in other subtypes of acute myeloid leukemia. These former symptoms are due to release of a substance called histamine from neoplastic mast cells. Enlargement of the liver and spleen, or hepatosplenomegaly is characteristic. The mast cells release also many anticoagulants like heparin which can lead to serious bleeding. Liver and splenic dysfunction also contributes to hemorrhage. Involvement of the bone can lead to osteoporosis. Abdominal ultrasound or computerized tomography (CT) scanning is used to look for hepatosplenomegaly and lymphadenopathy. Plain radiography and bone densitometry can be used to assess bone involvement and the presence of osteoporosis. Endoscopy and biopsy can be useful if gut involvement is suspected. Diagnosis Cytochemistry Cytochemical properties of the leukemic cells must be typical of mast cell derivation (presence of metachromatic granules staining with alpha-naphthyl chloroacetate esterase, but not with peroxidase). Mast cell tryptase is an enzyme contained in mast cell granules. Mast cell numbers are best estimated by tryptase immunostaining because very poorly granulated cells may stain very weakly if at all for alpha-naphthol chloroacetate esterase. Tumor markers The leukemic cells usually are strongly positive for CD13, CD33, CD68, and CD117. Characteristically, basophil (e.g. CD11b, CD123) and monocyte markers (CD14, CD15) are absent. The cells usually express CD2 and CD25. Malignant mast cells overexpress the anti-apoptosis gene, bcl-2. A mutation called KIT mutation is detected in most patients. Biochemistry Total serum tryptase is elevated in mast cell leukemia. Normal total (alpha + beta) serum tryptase is approximately 6 micro g/L (range 0 to 11 micro g/L). Values of several hundred micro g/L are characteristic of mast cell leukemia. Plasma and urinary histamine levels are frequently elevated in mast cell leukemia. Histidine decarboxylase (HDC) is the enzyme that catalyzes the reaction which produces histamine from histidine. Measurement of histidine carboxylase in the marrow cells of patients with mast cell leukemia is a very sensitive marker of mast cells. Treatment Immunoglobulin E (IgE) is important in mast cell function. Immunotherapy with anti-IgE immunoglobulin raised in sheep resulted in a transient decrease in the numbers of circulating mast cells in one patient with mast cell leukemia. Although splenectomy has led to brief responses in patients with mast cell leukemia, no firm conclusions as to the efficacy of this treatment are possible. Chemotherapy with combination of cytosine arabinoside and either idarubicin, daunomycin, or mitoxantrone as for acute myeloid leukemia has been used. Stem cell transplantation is an option, although no experience exists concerning responses and outcome. Prognosis Acute mast cell leukemia is extremely aggressive and has a grave prognosis. In most cases, multi-organ failure including bone marrow failure develops over weeks to months. Median survival after diagnosis is only about 6 months. References == External links ==

Hello Aarogya, what is Anterior compartment syndrome

Anterior compartment syndrome

A compartment syndrome is an increased pressure within a muscular compartment that compromises the circulation to the muscles. Symptoms and signs Diffuse tightness and tenderness over the entire belly of the tibialis anterior muscle that does not respond to elevation or pain medication can be early warning signs and suggestive of Anterior Compartment Syndrome. Other common symptoms include excessive swelling that causes the skin to become hot, stretched and glossy. Pain, paresthesias, and tenderness in both the ischemic muscles and the region supplied by the deep common fibular nerve are exhibited by patients with this condition. Sensitivity to passive stretch and active contraction are common, and tend to increase the symptoms. Pathology A compartment space is anatomically determined by an unyielding fascial (and osseous) enclosure of the muscles. The anterior compartment syndrome of the lower leg (often referred to simply as anterior compartment syndrome), can affect any and all four muscles of that compartment: tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius.This term is often mistakenly used to describe various related/proximal conditions, including Anterior Shin Splints. It is important to distinguish between the two, as shin splints rarely causes serious health problems, while Anterior Compartment Syndrome can lead to irreversible damage.The true compartment syndrome arises due to increased pressure within the unyielding anterior compartment of the leg. The pressure obstructs venous outflow, which causes further swelling and increased pressure. The resultant ischemia leads to necrosis (death of tissue) of the muscles and nerves. The process can begin with swelling of the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and/or the peroneus tertius muscles in response to strong eccentric contractions sufficient to produce postexercise soreness. Diagnosis If these symptoms are observed/experienced it is important to contact a physician specializing in sports medicine (MD/DO), a doctor of podiatric medicine (DPM), or other qualified health care professional immediately so as to get the appropriate advice/treatment before serious damage occurs.The 5 Ps of Anterior Compartment Syndrome: Pain Pallor Paresthesia Pulselessness Paralysis (If not treated) Treatment The only option to treat acute compartment syndrome is surgery. The procedure, called a fasciotomy, involves a surgeon cutting open the skin and the fascia to relieve the pressure. Options to treat chronic compartment syndrome include physiotherapy, shoe inserts, and anti-inflammatory medications. References ADAM Health Illustrated Encyclopedia Article, 8/3/2004 == External links ==

Hi Aarogya, explain a situation where External cause occurs

External cause

In medicine, an external cause is a reason for the existence of a medical condition which can be associated with a specific object or acute process that was caused by something outside the body. Such causes are classified as "E codes" in ICD 9.External Cause of Injury Codes (E codes) are ICD-9-CM codes or ICD-10 codes that are used to define the mechanism of death or injury, along with the place of occurrence of the event. [1] E codes are assigned on death certificates based on the manner of death. ICD-10 codes in the range V01–X59 refer to unintentional injuries. Codes in the range X60–X84 refer to intentional self-harm. Codes in the range Y85–Y09 refer to assault, and codes in the range Y10–Y34 refer to events of undetermined intent.E codes are well-collected on death certificate data, but less so on hospital discharge data. Numerous initiatives have increased the percentage of records coded (CDC, MMWR March 28, 2008 / Vol. 57 / No. RR-1). == References ==

Hello Aarogya, what is Acute myelomonocytic leukemia

Acute myelomonocytic leukemia

Acute myelomonocytic leukemia (AMML) is a form of acute myeloid leukemia that involves a proliferation of CFU-GM myeloblasts and monoblasts. AMML occurs with a rapid increase amount in white blood cell count and is defined by more than 20% of myeloblast in the bone marrow. It is classified under "M4" in the French-American-British classification (FAB). It is classified under "AML, not otherwise classified" in the WHO classification.Translocations have been observed. Progression from myelodysplastic syndrome has been reported. Signs and symptoms Some patients may experience: Fatigue Easy Bruising Abnormal Bleeding Anemia Thrombocytopenia DyspneaIf the blast count gets too high and clog up blood vessels, some patients may experience: Slurred Speech Headache Confusion Weakness on one side of the body Sleepiness Cause The cause has not yet been determined. It has been said that acute myeloid leukemia can occur from a progression of chronic myelomonocytic leukemia type 1 and 2. Normal red blood cells decrease and a rapid proliferation of the abnormal myeloblasts occur. Apoptosis functional ability decreases which causes a back up of myeloblasts in the bone marrow and blood. AML with a translocation or inversion is seen in different chromosomes. Specifically, AML with inversion in chromosome 16 also known as inv(16) is commonly seen in children. Mechanism AMML does not have an exact mechanism. The underlying pathophysiology of acute myeloid leukemia consist of maturational arrest of the bone marrow cell during the early stages of development. A myeloblast is an immature precursor cell that will change into a monocyte, healthy white blood cell. In AML, Myeloblast do not mature but grow and multiply with regulation. The abnormal cells build up in the bone marrow and prevent the development of other healthy cells. This type of arrest is still under study but in most cases, a gene inactivation or activation has occurred due to chromosome translocations or inversion. AML-M4 with an inversion of chromosome 16 is caused by breakage and rearrangement within itself. Diagnosis Criteria for AMML is confirmed if the myeloblasts and promonocytes in the bone marrow are greater than 20 percent. It can also be confirmed if the blood monocytes is 5x109/L or higher. Testing available to diagnosis AML includes a complete blood count which is characterized by blood that is taken from the vein in the arm to test for leukemia, a peripheral blood smear and a bone marrow test. During a peripheral blood smear, a sample of blood is checked for blast cells, white blood cell count and changes in shape of blood cells. During a bone marrow test, bone marrow is taken from the hip bone in a search for leukemia cells. Aspiration and biopsy are two types of testing that can be done in order to obtain bone marrow. Further classification can be done for the type of AML by examining the cells shape and size. Generally youll find immature cells which lack normal features of a cell. Treatment AMML can be treated depending on the degree of disease, age of patient, and current patients health status. Treatment consists of a multi-drug chemotherapy regimen. Chemotherapy drugs often used to treat AML are cytarabine and an anthracycline drug. Chemotherapy is broken down into 2 phases: Induction therapy: first short and invasive phase of treatment with the goal to the blood of blasts and reduce the number of blasts in the bone marrow back to normal. Consolidation therapy: second phase given in cycles that occur after the patient has recovered from induction therapy. Its objective is to kill remaining blasts that cant be seen.In some cases, an allogenic bone marrow transplantation can be performed. If AML with chromosomal abnormalities such as inv(16) are often cured by the standard chemotherapy regimen. Prognosis With AMML being difficult to fully treat, the five-year survival rate is about 38-72% which typically decrease to 35-60% if theres no bone marrow transplantation performed. Generally older patients over 60 have a poor outlook due to prior health status before the diagnosis and the aggressive chemotherapy regimen used. The aggressive chemotherapy regimen can lead to long-term side effects such as prolonged anemia, leukocytopenia, neutropenia, and thrombocytopenia. The use of anthracycline drugs can cause a decrease in cardiac contractility, both short and long term. Those with AML-M4 inv(16) have a favorable prognosis with a five-year overall survival rate of 61%. Epidemiology AML is commonly seen in pediatric patients with higher pediatric incidence in Hispanics and Asians as compared to non-Hispanic Caucasian and African Americans in the USA. Predisposition to AML includes but not limited to:Down syndrome, Klinefelters syndrome, and Fanconis anemia. Acquired predisposing factors include: aplastic anemia, chemotherapy, prenatal exposure to tobacco, marihuana, and alcohol. Research directions Considering the disease is rare, not much research is being done specifically for the AML-M4 subtype. Research regarding the production of granulocyte colony stimulating factor (G-CSF) is being conducted to investigate AMML ability to secrete and synthesize G-CSF. Multiple chemotherapy drugs and its effects are being research in comparison to its treatment success in AML not specifically AML-M4. See also Juvenile myelomonocytic leukemia References == External links ==

Hi Aarogya, could you help me understand about Acute bronchitis

Acute bronchitis

Acute bronchitis, also known as a chest cold, is short-term bronchitis – inflammation of the bronchi (large and medium-sized airways) of the lungs. The most common symptom is a cough. Other symptoms include coughing up mucus, wheezing, shortness of breath, fever, and chest discomfort. The infection may last from a few to ten days. The cough may persist for several weeks afterward with the total duration of symptoms usually around three weeks. Some have symptoms for up to six weeks.In more than 90% of cases, the cause is a viral infection. These viruses may be spread through the air when people cough or by direct contact. Risk factors include exposure to tobacco smoke, dust, and other air pollution. A small number of cases are due to high levels of air pollution or bacteria such as Mycoplasma pneumoniae or Bordetella pertussis. Diagnosis is typically based on a persons signs and symptom. The color of the sputum does not indicate if the infection is viral or bacterial. Determining the underlying organism is typically not needed. Other causes of similar symptoms include asthma, pneumonia, bronchiolitis, bronchiectasis, and COPD. A chest X-ray may be useful to detect pneumonia.Prevention is by not smoking and avoiding other lung irritants. Frequent hand washing and flu vaccination may also be protective. Treatment of acute bronchitis typically involves rest, paracetamol (acetaminophen), and NSAIDs to help with the fever. Cough medicine has little support for its use and is not recommended in children less than six years of age. Antibiotics should generally not be used. An exception is when acute bronchitis is due to pertussis. Tentative evidence supports honey and pelargonium to help with symptoms.Acute bronchitis is one of the most common diseases. About 5% of adults are affected and about 6% of children have at least one episode a year. It occurs more often in the winter. More than 10 million people in the United States visit a doctor each year for this condition with approximately 70% receiving antibiotics, most of which are not needed. There are efforts to decrease the use of antibiotics in acute bronchitis. Signs and symptoms The primary symptom is cough with sputum that may be purulent. The illness may also cause shortness of breath or wheezing. Upper respiratory tract infections often precede acute bronchitis, with overlapping symptoms including headache, nasal congestion, sore throat. Fever and other systemic symptoms are rare in acute bronchitis; their presence raises suspicion for influenza or pneumonia. Cause Acute bronchitis can be caused by contagious pathogens, most commonly viruses. Typical viruses include respiratory syncytial virus, rhinovirus, influenza, and others. Bacteria are uncommon pathogens but may include Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bordetella pertussis, Streptococcus pneumoniae, and Haemophilus influenzae. Damage caused by irritation of the airways leads to inflammation and leads to neutrophils infiltrating the lung tissue. Mucosal hypersecretion is promoted by a substance released by neutrophils. Further obstruction to the airways is caused by more goblet cells in the small airways. This is typical of chronic bronchitis. Although infection is not the reason or cause of chronic bronchitis, it is seen to aid in sustaining the bronchitis. Diagnosis A physical examination will often reveal decreased intensity of breath sounds, wheezing, rhonchi, and prolonged expiration. During examination for physicians rely on history and the presence of persistent or acute onset of cough, followed by a URTI with no traces of pneumonia. Acute bronchitis is typically a clinical diagnosis that relies on patients history and exam, and should be suspected in patients with an acute onset of cough, which often follows a URTI without traces of pneumonia.Although there is no universally-accepted clinical definition for acute bronchitis, there is a proposed set of practical criteria (Macfarlane, 2001) that include: An acute illness of less than three weeks. Cough as the predominant symptom. At least one other lower respiratory tract symptom, such as sputum production, wheezing, chest pain. No alternative explanation for the symptoms.A variety of tests may be performed in people presenting with cough and shortness of breath: A chest X-ray is useful to exclude pneumonia which is more common in those with a fever, fast heart rate, fast respiratory rate, or who are old. A sputum sample showing neutrophil granulocytes (inflammatory white blood cells) and culture showing that has pathogenic microorganisms such as Streptococcus species. A blood test would indicate inflammation (as indicated by a raised white blood cell count and elevated C-reactive protein).Decreased breath sounds, crackles, wheezing, and rhonchi that clears with coughs may be heard in the chest. Dullness to percussion and pleural rub suggest disease extension beyond the bronchi such as seen with pneumonia. Paroxysms of cough followed by inspiratory whoop and vomiting suggests pertussis. Prevention Prevention is by not smoking and avoiding other lung irritants. Frequent hand washing may also be protective. Furthermore, an oral whole cell nontypeable Haemophilus influenzae vaccine given in the fall has demonstrated short term effectiveness in reducing the frequency and severity of the disease during the winter. Treatment Most cases are self-limited and resolve themselves in a few weeks. Pain medications may help with symptoms. Other recommendations may include rest and keeping well hydrated. Antibiotics Evidence does not support the general use of antibiotics in acute bronchitis. A systematic review found antibiotics reduced cough by an average of 12 hours (out of a total average of about 14–28 days). Antibiotics caused more side effects such as nausea and diarrhoea, and also may promote antibiotic-resistant bacteria. It is possible they are useful in susceptible groups such as the frail and elderly but there was not enough research information to determine this.Calling acute bronchitis with benign-sounding labels such as chest cold or viral infections may reduce antibiotic usage by improving patients satisfaction when antibiotics are not prescribed. Smoking cessation To help the bronchial tree heal faster and not make bronchitis worse, smokers should quit smoking completely. Alternative therapeutic approaches Salbutamol is not effective in children with an acute cough who do not have restricted airways. There is weak evidence that salbutamol may be useful in adults with wheezing due to a restricted airway; however, it may result in nervousness, shakiness or a tremor. Prognosis Acute bronchitis usually lasts a few days or weeks. It may accompany or closely follow a cold or the flu, or may occur on its own. Bronchitis usually begins with a dry cough, including waking the patient at night. After a few days, it progresses to a wetter or productive cough, which may be accompanied by fever, fatigue, and headache. The fever, fatigue, and malaise may last only a few days, but the wet cough may last up to several weeks. Epidemiology Acute bronchitis is one of the most common diseases. About 5% of adults are affected and about 6% of children have at least one episode a year. It occurs more often in the winter.In infants under one year of age, acute bronchitis was the most common reason for admission to the hospital after an emergency department visit in the US in 2011. References External links Acute Bronchitis FamilyDoctor.org (American Academy of Family Physicians) "Acute Bronchitis". MedlinePlus. U.S. National Library of Medicine.

Hello Aarogya, explain a situation where Tract occurs

Tract

Tract may refer to: Geography and real estate Housing tract, an area of land that is subdivided into smaller individual lots Land lot or tract, a section of land Census tract, a geographic region defined for the purpose of taking a census Writings Tract (literature), a short written work, usually of a political or religious nature Tract (liturgy), a component of Roman Catholic liturgy Treatise Biology Nerve tract, a bundle of fibers that connects different parts of the central nervous system - analogous to a nerve in the peripheral nervous system A genetic tract, a sequence of repeating nucleotides or amino acids, such as a polyglutamine tract A collection of related anatomic structures, such as: Gastrointestinal tract Genitourinary tract Reproductive tract A grouping of feathers, e.g. primaries, auricular, scapular Businesses Tract (imprint), an imprint of the German group VDM Publishing devoted to the reproduction of Wikipedia content See also Track (disambiguation) All pages with titles beginning with Tract All pages with titles containing Tract

Hi Aarogya, explain a situation where Osteolysis occurs

Osteolysis

Osteolysis is an active resorption of bone matrix by osteoclasts and can be interpreted as the reverse of ossification. Although osteoclasts are active during the natural formation of healthy bone the term "osteolysis" specifically refers to a pathological process. Osteolysis often occurs in the proximity of a prosthesis that causes either an immunological response or changes in the bones structural load. Osteolysis may also be caused by pathologies like bone tumors, cysts, or chronic inflammation. Joint replacement While bone resorption is commonly associated with many diseases or joint problems, the term osteolysis generally refers to a problem common to artificial joint replacements such as total hip replacements, total knee replacements and total shoulder replacements. Osteolysis can also be associated with the radiographic changes seen in those with bisphosphonate-related osteonecrosis of the jaw.There are several biological mechanisms which may lead to osteolysis. In total hip replacement, the generally accepted explanation for osteolysis involves wear particles (worn off the contact surface of the artificial ball and socket joint). As the body attempts to clean up these wear particles (typically consisting of plastic or metal), it triggers an autoimmune reaction which causes resorption of living bone tissue. Osteolysis has been reported to occur as early as 12 months after implantation and is usually progressive. This may require a revision surgery (replacement of the prosthesis).Although osteolysis itself is clinically asymptomatic, it can lead to implant loosening or bone breakage, which in turn causes serious medical problems. Distal clavicular osteolysis Distal clavicular osteolysis (DCO) is often associated with problems weightlifters have with their acromioclavicular joints due to high mechanical stresses put on the clavicle as it meets with the acromion. This condition is often referred to as "weight lifters shoulder". Medical ultrasonography readily depicts resorption of the distal clavicle as irregular cortical erosions, whereas the acromion remains intact. Associated findings may include distended joint capsule, soft tissue swelling, and joint instability. A common surgery to treat recalcitrant DCO is resection of distal clavicle by removing a few millimetres of bone from the very end of the bone. See also Osteolytic lesion Biomineralization References == External links ==

Aarogya, What does Caught mean

Caught

Caught is a method of dismissing a batsman in cricket. A batsman is out caught if the batsman hits the ball, from a legitimate delivery, with the bat, and the ball is caught by the bowler or a fielder before it hits the ground. If the ball hits the stumps after hitting the wicket-keeper, If the wicket-keeper fails to do this, the delivery is a "no ball", and the batsman cannot be stumped (nor run out, unless he attempts to run to the other wicket.) If the catch taken by the wicket-keeper,then informally it is known as caught behind or caught at the wicket. A catch by the bowler is known as caught and bowled. This has nothing to do with the dismissal bowled but is rather a shorthand for saying the catcher and bowler are the same player. (The scorecard annotation is usually c. and b. or c&b followed by the bowlers name.) Caught is the most common method of dismissal at higher levels of competition, accounting for 36,190 Test match dismissals between 1877 and 2012, which is 56.9% of all Test match dismissals in this period.South African wicket-keeper Mark Boucher holds the record for the most Test match catches, with 532, while Rahul Dravid holds the record for the most Test match catches by non-wicket-keepers, with 210. Laws This method of dismissal is covered by Law 33 of the Laws of cricket which reads: The striker is out Caught if a ball delivered by the bowler, not being a No ball, touches his/her bat without having previously been in contact with any fielder, and is subsequently held by a fielder as a fair catch,..., before it touches the wicket and ground.This means that the batsman cannot be out caught if: The ball is called a no-ball or dead ball. The batsman does not hit the ball with his bat or a gloved hand holding the bat. The ball, having been hit, makes contact with the field before a fielder catches the ball. The ball does not remain under the control of the fielder. The ball is hit and lands beyond or on the boundary; (six runs). A fielder taking the catch makes contact with the boundary rope or the area outside the boundary, with any part of his body, equipment, when touching the ball. An airborne fielder taking the catch, having not previously legally touched the ball, had his last contact with the ground not entirely within the boundary.Note that if a batsman could be given out both caught and by another method, caught takes precedence, unless the other method is bowled.If a batsman is out caught, any runs scored off that delivery are voided. If a batsman is caught, the bowler is credited with the batsmans wicket and the catching fielder is credited for the dismissal, there is no catch assists for a saving boundaries before catch, or deflecting the ball to a different fielder in the slips cordon. If the two batsmen cross each other, in attempting to take a run, before the catch was taken, the non-striking batsman at the time remains at the opposite end of the pitch as the new incoming batsman comes to the crease at his former end. This means, unless it is now a new over, he is now on strike and the incoming batsman is not. Adjudication If the catch taken is pronounced or obvious, the players need not appeal to the umpire; the batsman normally chooses to acknowledge the dismissal himself. However, if the ball brushes the edge of the bat, or the catch is taken very close to the ground, or the ball appears to have bounced off the batsmans foot (so it has not touched the ground), or the ball appearing to come off the bat very close to the pitch surface (bump ball), or if the batsman is reluctant to accept that he has been dismissed, then the fielding team has to appeal to the umpire for this decision. In international competition, if neither field umpire can clearly decide if a catch has been made or not, they may refer to the third (television) umpire for a review. The third umpire may also be used if the Umpire Decision Review System is available and a team wishes to dispute a call concerning a possible catch. Celebration Before 2000, the Laws of Cricket defined a catch as being completed when the player had "complete control over the further disposal of the ball". In the very strictest sense, this meant that the player did not finish catching the ball until he threw it away, though the player doesnt have to throw the ball to anyone in particular in so doing. For this reason, even today many cricketers celebrate a catch by lobbing the ball into the air. In a Super Sixes match in the 1999 Cricket World Cup, South African Herschelle Gibbs caught Australian captain Steve Waugh but Waugh was given not out when Gibbs was ruled to not have control of the ball when attempting to throw the ball in celebration. Waugh went on to score a match-winning 120 not out to qualify his team for the semi-finals; Australia went on to win the tournament. Records Test matches The wicket-keepers with the highest number of catches taken in Test matches are as follows. Note this excludes catches made while not fielding as a wicket-keeper. Source: Cricinfo Statsguru. Last updated: 19 April 2019. The non-wicket-keepers with the highest number of catches taken in Test matches are as follows. Note this excludes any catches made while fielding as a wicket-keeper. Source: Cricinfo Statsguru. Last updated: 19 April 2019. One Day Internationals T20 Internationals First Class cricket See also Other sports Catch (baseball) == References ==

What does Coma scale mean Aarogya

Coma scale

A coma scale is a system to assess the severity of coma. There are several such systems: Glasgow Coma Scale The Glasgow Coma Scale is neurological scale which aims to give a reliable, objective way of recording the conscious state of a person, for initial as well as continuing assessment. A patient is assessed against the criteria of the scale, and the resulting points give a patient score between 3 (indicating deep unconsciousness) and either 14 (original scale) or 15 (the more widely used modified or revised scale). GCS was initially used to assess level of consciousness after head injury and the scale is now used by first aid, EMS and doctors as being applicable to all acute medical and trauma patients. In hospital it is also used in chronic patient monitoring, in for instance, intensive care. Pediatric Glasgow Coma Scale The Pediatric Glasgow Coma Scale (also known as Pediatric Glasgow Coma Score or simply PGCS) is the equivalent of the Glasgow Coma Scale (GCS) used to assess the mental state of adult patients. As many of the assessments for an adult patient would not be appropriate for infants, the scale was modified slightly. As with the GCS, the PGCS comprises three tests: eye, verbal and motor responses. The three values separately as well as their sum are considered. The lowest possible PGCS (the sum) is 3 (deep coma or death) whilst the highest is 15 (fully awake and aware person). Blantyre Coma Scale The Blantyre Coma Scale is a modification of the Pediatric Glasgow Coma Scale, designed to assess malarial coma in children. It was designed by doctors Terrie Taylor and Malcolm Molyneux in 1987, and named for the Malawian city of Blantyre, site of the Blantyre Malaria Project. Rancho Los Amigos Scale The Rancho Los Amigos Scale is used to assess individuals after a closed head injury based on cognitive and behavioural presentations as they emerge from coma. It is named after the Rancho Los Amigos National Rehabilitation Center, located in Downey, California, United States. FOUR score See also Level of consciousness == References ==

Hello Aarogya , Do you know what is Tuberous sclerosis,

Tuberous sclerosis

Tuberous sclerosis complex (TSC) is a rare multisystem autosomal dominant genetic disease that causes non-cancerous tumours to grow in the brain and on other vital organs such as the kidneys, heart, liver, eyes, lungs and skin. A combination of symptoms may include seizures, intellectual disability, developmental delay, behavioral problems, skin abnormalities, lung disease, and kidney disease.TSC is caused by a mutation of either of two genes, TSC1 and TSC2, which code for the proteins hamartin and tuberin, respectively, with TSC2 mutations accounting for the majority and tending to cause more severe symptoms. These proteins act as tumor growth suppressors, agents that regulate cell proliferation and differentiation.Prognosis is highly variable and depends on the symptoms, but life expectancy is normal for many.The prevalence of the disease is estimated to be 7 to 12 in 100,000. The disease is often abbreviated to tuberous sclerosis, which refers to the hard swellings in the brains of patients, first described by French neurologist Désiré-Magloire Bourneville in 1880. Signs and symptoms The physical manifestations of TSC are due to the formation of hamartia (malformed tissue such as the cortical tubers), hamartomas (benign growths such as facial angiofibroma and subependymal nodules), and very rarely, cancerous hamartoblastomas. The effect of these on the brain leads to neurological symptoms such as seizures, intellectual disability, developmental delay, and behavioral problems. Neurological Three types of brain tumours are associated with TSC: Giant cell astrocytoma: (grows and blocks the cerebrospinal fluid flow, leading to dilatation of ventricles causing headache and vomiting) Cortical tubers: after which the disease is named Subependymal nodules: form in the walls of ventriclesClassic intracranial manifestations of TSC include subependymal nodules and cortical/subcortical tubers.The tubers are typically triangular in configuration, with the apex pointed towards the ventricles, and are thought to represent foci of abnormal neuronal migration. The T2 signal abnormalities may subside in adulthood, but will still be visible on histopathological analysis. On magnetic resonance imaging (MRI), TSC patients can exhibit other signs consistent with abnormal neuron migration such as radial white matter tracts hyperintense on T2WI and heterotopic grey matter.Subependymal nodules are composed of abnormal, swollen glial cells and bizarre multinucleated cells which are indeterminate for glial or neuronal origin. Interposed neural tissue is not present. These nodules have a tendency to calcify as the patient ages. A nodule that markedly enhances and enlarges over time should be considered suspicious for transformation into a subependymal giant cell astrocytoma, which typically develops in the region of the foramen of Monro, in which case it is at risk of developing an obstructive hydrocephalus.A variable degree of ventricular enlargement is seen, either obstructive (e.g. by a subependymal nodule in the region of the foramen of Monro) or idiopathic in nature. Neuropsychiatric About 90% of people with TSC develop a range of neurodevelopmental, behavioural, psychiatric, and psychosocial difficulties. The "TSC‐associated neuropsychiatric disorders" are abbreviated TAND. These difficulties are less frequently identified and thus undertreated when compared with the neurological symptoms. Most problems are associated with more severe intellectual delay or associated with childhood and adolescence, and some (for example depressed mood) may be unreported if the person is unable to communicate. TAND can be investigated and considered at six levels: behavioural, psychiatric, intellectual, academic, neuropsychological, and psychosocial.Behavioural problems most commonly seen include overactivity, impulsivity and sleeping difficulties. Also common are anxiety, mood swings, and severe aggression. Less common are depressed mood, self-injury, and compulsive behaviours.People with TSC are frequently also diagnosed with psychiatric disorders: autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), anxiety disorder and depressive disorder. TSC is one of the most common genetic causes of autism spectrum disorder, which affects nearly half of people with TSC. ASD is more common in TSC2 than TSC1 and more common with earlier and more severe epilepsy, and with lower intellectual ability. ADHD is nearly as frequently seen in TSC as ASD (up to half of all people with TSC). Anxiety and depressive disorders, when they occur, are typically diagnosed in early adulthood and among those intellectually able to express their moods. Schizophrenia (and symptoms like hallucinations or psychosis) is no more common in TSC than the general population.The intellectual ability of people with TSC varies enormously. About 40–50% have a normal IQ. A normal IQ is much more commonly seen in TSC1 than TSC2, and profound intellectual disability seen in 34% of TSC2 compared with 10% of TSC1 in one study. Many studies have examined whether early onset, type and severity of epilepsy associates with intellectual ability. Academic issues occur even in people with TSC who have normal intellectual ability. These are often specific learning disorders such as dyscalculia (understanding mathematics), but also include other aspects affecting school life such as anxiety, lack of social skills or low self-esteem.About half of people with TSC, when assessed for neuropsychological skills, are in the bottom 5th percentile in some areas, which indicates a severe impairment. These include problems with attention (for example, being able to concentrate on two separate things like looking and listening), memory (particularly recall, verbal and spatial working memory) and executive function (for example, planning, self-monitoring, cognitive flexibility).The psychosocial impacts of TSC include low self-esteem and self-efficacy in the individual, and a burden on the family coping with a complex and unpredictable disorder. Kidneys Between 60 and 80% of TSC patients have benign tumors (once thought hamartomatous, but now considered true neoplasms) of the kidneys called angiomyolipomas frequently causing hematuria. These tumors are composed of vascular (angio–), smooth muscle (–myo–), and fat (–lip-) tissue. Although benign, an angiomyolipoma larger than 4 cm is at risk for a potentially catastrophic hemorrhage either spontaneously or with minimal trauma. Angiomyolipomas are found in about one in 300 people without TSC. However, those are usually solitary, whereas in TSC they are commonly multiple and bilateral.About 20-30% of people with TSC have renal cysts, causing few problems. However, 2% may also have autosomal dominant polycystic kidney disease.Very rare (< 1%) problems include renal cell carcinoma and oncocytomas (benign adenomatous hamartoma). Lungs Patients with TSC can develop progressive replacement of the lung parenchyma with multiple cysts, known as lymphangioleiomyomatosis (LAM). Recent genetic analysis has shown that the proliferative bronchiolar smooth muscle in TSC-related lymphangioleiomyomatosis is monoclonal metastasis from a coexisting renal angiomyolipoma. Cases of TSC-related lymphangioleiomyomatosis recurring following lung transplant have been reported. Heart Small tumours of the heart muscle, called cardiac rhabdomyomas, are rare in the general population (perhaps 0.2% of children) but very common in people with TSC. Around 80% of children under two-years-old with TSC have at least one rhabdomyoma, and about 90% of those will have several. The vast majority of children with at least one rhabdomyoma, and nearly all children with multiple rhabdomyomas will be found to have TSC. Prenatal ultrasound, performed by an obstetric sonographer specializing in cardiology, can detect a rhabdomyoma after 20 weeks. Rhabdomyoma vary in size from a few millimetres to several centimetres, and are usually found in the lower chambers (ventricles) and less often in the upper chambers (atria). They grow in size during the second half of pregnancy, but regress after birth, and are seen in only around 20% of children over two years old.Most rhabdomyomas cause no problems but some may cause heart failure in the foetus or first year of life. Rhabdomyomas are believed to be responsible for the development of heart arrhythmia later in life, which is relatively common in TSC. Arrhythmia can be hard to spot in people with TSC, other than by performing routine ECG. For example, arrhythmia may cause fainting that is confused with drop seizures, and symptoms of arrhythmia such as palpitations may not be reported in an individual with developmental delay. Skin Some form of dermatological sign is present in 96% of individuals with TSC. Most cause no problems, but are helpful in diagnosis. Some cases may cause disfigurement, necessitating treatment. The most common skin abnormalities include: Hypomelanic macules ("ash leaf spots") are present in about 90% of people with TSC. These small white or lighter patches of skin may appear anywhere on the body, and are caused by a lack of melanin. They are usually the only visible sign of TSC at birth. In fair-skinned individuals, a Woods lamp (ultraviolet light) may be required to see them. On the scalp, the effect may be a white patch of hair (poliosis). Patches smaller than 3mm are known as "confetti" skin lesions. Facial angiofibromas are present in about 75% of people with TSC. These are a rash of reddish spots or bumps on the nose and cheeks in a butterfly distribution, which consist of blood vessels and fibrous tissue. This potentially socially embarrassing rash starts to appear during childhood. Ungual fibromas: Also known as Koenens tumors, these are small fleshy tumors that grow around and under the toenails or fingernails. These are rare in childhood, but common by middle age. They are generally more common on toes than on fingers, develop at 15–29 years, and are more common in women than in men. Fibrous cephalic plaques are present in about 25% of people with TSC. These are raised, discoloured areas usually found on the forehead, but sometimes on the face or elsewhere on the scalp. Shagreen patches are present in about half of people with TSC, appearing in childhood. They are areas of thick leathery skin that are dimpled like an orange peel, and pigmented, they are usually found on the lower back or nape of the neck, or scattered across the trunk or thighs. The frequency of these lesions rises with age. Dental enamel pits are found in almost all adults with TSC. Intraoral fibromas are small surface-tumours found in the gums, inside the cheeks or tongue. Gum (gingival) fibromas are found in about 20-50% of people with TSC, more commonly in adults. Eyes Retinal lesions, called astrocytic hamartomas (or "phakomas"), which appear as a greyish or yellowish-white lesion in the back of the globe on the ophthalmic examination. Astrocytic hamartomas can calcify, and they are in the differential diagnosis of a calcified globe mass on a CT scan.Nonretinal lesions associated with TSC include: Coloboma Angiofibromas of the eyelids Papilledema (related to hydrocephalus) Pancreas Pancreatic neuroendocrine tumours have been described in rare cases of TSC. Variability Individuals with TSC may experience none or all of the clinical signs discussed above. The following table shows the prevalence of some of the clinical signs in individuals diagnosed with TSC. Genetics TSC is a genetic disorder with an autosomal dominant pattern of inheritance, variable expressivity, and incomplete penetrance. Two-thirds of TSC cases result from sporadic genetic mutations, not inheritance, but their offspring may inherit it from them. Current genetic tests have difficulty locating the mutation in roughly 20% of individuals diagnosed with the disease. So far, it has been mapped to two genetic loci, TSC1 and TSC2.TSC1 encodes for the protein hamartin, is located on chromosome 9 q34, and was discovered in 1997. TSC2 encodes for the protein tuberin, is located on chromosome 16 p13.3, and was discovered in 1993. TSC2 is contiguous with PKD1, the gene involved in one form of polycystic kidney disease (PKD). Gross deletions affecting both genes may account for the 2% of individuals with TSC who also develop polycystic kidney disease in childhood. TSC2 has been associated with a more severe form of TSC. However, the difference is subtle and cannot be used to identify the mutation clinically. Estimates of the proportion of TSC caused by TSC2 range from 55% to 90%.TSC1 and TSC2 are both tumor suppressor genes that function according to Knudsons "two hit" hypothesis. That is, a second random mutation must occur before a tumor can develop. This explains why, despite its high penetrance, TSC has wide expressivity. Pathophysiology Hamartin and tuberin function as a complex which is involved in the control of cell growth and cell division. The complex appears to interact with RHEB GTPase, thus sequestering it from activating mTOR signalling, part of the growth factor (insulin) signalling pathway. Thus, mutations at the TSC1 and TSC2 loci result in a loss of control of cell growth and cell division, and therefore a predisposition to forming tumors. TSC affects tissues from different germ layers. Cutaneous and visceral lesions may occur, including angiofibroma, cardiac rhabdomyomas, and renal angiomyolipomas. The central nervous system lesions seen in this disorder include hamartomas of the cortex, hamartomas of the ventricular walls, and subependymal giant cell tumors, which typically develop in the vicinity of the foramina of Monro.Molecular genetic studies have defined at least two loci for TSC. In TSC1, the abnormality is localized on chromosome 9q34, but the nature of the gene protein, called hamartin, remains unclear. No missense mutations occur in TSC1. In TSC2, the gene abnormalities are on chromosome 16p13. This gene encodes tuberin, a guanosine triphosphatase–activating protein. The specific function of this protein is unknown. In TSC2, all types of mutations have been reported; new mutations occur frequently. Few differences have yet been observed in the clinical phenotypes of patients with mutation of one gene or the other.Cells from individuals with pathogenic mutations in the TSC2 gene display abnormal accumulation of glycogen that is associated with depletion of lysosomes and autophagic impairment. The defective degradation of glycogen by the autophagy-lysosome pathway is, at least in part, independent of impaired regulation of mTORC1 and is restored, in cultured cells, by the combined use of PKB/Akt and mTORC1 pharmacological inhibitors. Diagnosis Tuberous sclerosis complex is diagnosed with clinical and genetic tests. There are many different mutations in the TSC1 and TSC2 genes that have been identified in individuals with TSC. A pathogenic mutation in the gene prevents the proteins from being made or inactivates the proteins. If such a pathogenic mutation is found then this alone is sufficient to diagnose TSC. However, some mutations are less clear in their effect, and so not sufficient alone for diagnosis. Between 1 in 10 and 1 in 4 of individuals with TSC have no mutation that can be identified. Once a particular mutation is identified in someone with TSC, this mutation can be used to make confident diagnoses in other family members.For clinical diagnosis, there isnt one sign that is unique (pathognomonic) to TSC, nor are all signs seen in all individuals. Therefore, several signs are considered together, classed as either major or minor features. An individual with two major features, or one major feature and at least two minor features can be given a definite diagnosis of TSC. If only one major feature or at least two minor features are present, the diagnosis is only regarded as possibly TSC. TSC can be first diagnosed at any stage of life. Prenatal diagnosis is possible by chance if heart tumours are discovered during routine ultrasound. In infancy, epilepsy, particularly infantile spasms, or developmental delay may lead to neurological tests. The white patches on the skin may also first become noticed. In childhood, behavioural problems and autism spectrum disorder may provoke a diagnosis. During adolescence, the skin problems appear. In adulthood, kidney and lung problems may develop. An individual may also be diagnosed at any time as a result of genetic testing of family members of another affected person. Management Tuberous sclerosis complex affects multiple organ systems so a multidisciplinary team of medical professionals is required.In suspected or newly diagnosed TSC, the following tests and procedures are recommended by 2012 International Tuberous Sclerosis Complex Consensus Conference. Take a personal and family history covering three generations. Genetic counselling and tests determine if other individuals are at risk. A magnetic resonance imaging (MRI) of the brain to identify tubers, subependymal nodules (SEN) and sub-ependymal giant cell astrocytomas (SEGA). Children undergo a baseline electroencephalograph (EEG) and family educated to identify seizures if/when they occur. Assess children for behavioural issues, autism spectrum disorder, psychiatric disorders, developmental delay, and neuropsychological problems. Scan the abdomen for tumours in various organs, but most importantly angiomyolipomata in the kidneys. MRI is superior to CT or ultrasound. Take blood pressure and test renal function. In adult women, test pulmonary function and perform a high-resolution computed tomography (HRCT) of the chest. Examine the skin under a Woods lamp (hypomelanotic macules), the fingers and toes (ungual fibroma), the face (angiofibromas), and the mouth (dental pits and gingival fibromas). In infants under three, perform an echocardiogram to spot rhabdomyomas, and electrocardiogram (ECG) for any arrhythmia. Use a fundoscope to spot retinal hamartomas or achromic patches.The various symptoms and complications from TSC may appear throughout life, requiring continued surveillance and adjustment to treatments. The following ongoing tests and procedures are recommended by 2012 International Tuberous Sclerosis Complex Consensus Conference. In children and adults younger than 25 years, a magnetic resonance imaging (MRI) of the brain is performed every one to three years to monitor for subependymal giant cell astrocytoma (SEGA). If a SEGA is large, growing or interfering with ventricles, the MRI is performed more frequently. After 25 years, if there are no SEGAs then periodic scans may no longer be required. A SEGA causing acute symptoms are removed with surgery, otherwise either surgery or drug treatment with an mTOR inhibitor may be indicated. Repeat screening for TSC-associated neuropsychiatric disorders (TAND) at least annually. Sudden behavioural changes may indicate a new physical problem (for example with the kidneys, epilepsy or a SEGA). Routine EEG determined by clinical need. Infantile spasms are best treated with vigabatrin and adrenocorticotropic hormone used as a second-line therapy. Other seizure types have no TSC-specific recommendation, though epilepsy in TSC is typically difficult to treat (medically refractory). Repeat MRI of abdomen every one to three years throughout life. Check renal (kidney) function annually. Should angiomyolipoma bleed, this is best treated with embolisation and then corticosteroids. Removal of the kidney (nephrectomy) is strongly to be avoided. An asymptomatic angiomyolipoma that is growing larger than 3 cm is best treated with an mTOR inhibitor drug. Other renal complications spotted by imaging include polycystic kidney disease and renal cell carcinoma. Repeat chest HRCT in adult women every five to 10 years. Evidence of lymphangioleiomyomatosis (LAM) indicates more frequent testing. An mTOR inhibitor drug can help, though a lung transplant may be required. A 12-lead ECG should be performed every three to five years.The mTOR inhibitor everolimus was approved in the US for treatment of TSC-related tumors in the brain (subependymal giant cell astrocytoma) in 2010 and in the kidneys (renal angiomyolipoma) in 2012. Oral everolimus (rapalog) reduces tumour size, is effective in terms of response to skin lesions and does not increase the risk of adverse events. Everolimus also showed evidence of effectiveness at treating epilepsy in some people with TSC. In 2017, the European Commission approved everolimus for treatment of refractory partial-onset seizures associated with TSC.Neurosurgical intervention may reduce the severity and frequency of seizures in TSC patients. Embolization and other surgical interventions can be used to treat renal angiomyolipoma with acute hemorrhage. Surgical treatments for symptoms of lymphangioleiomyomatosis (LAM) in adult TSC patients include pleurodesis to prevent pneumothorax and lung transplantation in the case of irreversible lung failure.Other treatments that have been used to treat TSC manifestations and symptoms include a ketogenic diet for intractable epilepsy and pulmonary rehabilitation for LAM. Facial angiofibromas can be reduced with laser treatment and the effectiveness of mTOR inhibitor topical treatment is being investigated. Laser therapy is painful, requires anaesthesia, and has risks of scarring and dyspigmentation. Prognosis The prognosis for individuals with TSC depends on the severity of symptoms, which range from mild skin abnormalities to varying degrees of learning disabilities and epilepsy to severe intellectual disability, uncontrollable seizures, and kidney failure. Those individuals with mild symptoms generally do well and live long, productive lives, while individuals with the more severe form may have serious disabilities. However, with appropriate medical care, most individuals with the disorder can look forward to normal life expectancy.A study of 30 TSC patients in Egypt found, "...earlier age of seizures commencement (<6 months) is associated with poor seizure outcome and poor intellectual capabilities. Infantile spasms and severely epileptogenic EEG patterns are related to the poor seizure outcome, poor intellectual capabilities and autistic behavior. Higher tubers numbers is associated with poor seizure outcome and autistic behavior. Left-sided tuber burden is associated with poor intellect, while frontal location is more encountered in ASD [autism spectrum disorders]. So, close follow up for the mental development and early control of seizures are recommended in a trial to reduce the risk factors of poor outcome. Also early diagnosis of autism will allow for earlier treatment and the potential for better outcome for children with TSC."Leading causes of death include renal disease, brain tumour, lymphangioleiomyomatosis of the lung, and status epilepticus or bronchopneumonia in those with severe intellectual disability. Cardiac failure due to rhabdomyomas is a risk in the fetus or neonate but is rarely a problem subsequently. Kidney complications such as angiomyolipoma and cysts are common and more frequent in females than males and in TSC2 than TSC1. Renal cell carcinoma is uncommon. Lymphangioleiomyomatosis is only a risk for females with angiomyolipomas. In the brain, the subependymal nodules occasionally degenerate to subependymal giant cell astrocytomas. These may block the circulation of cerebrospinal fluid around the brain, leading to hydrocephalus.Detection of the disease should be followed by genetic counselling. It is also important to realise that though the disease does not have a cure, symptoms can be treated symptomatically. Hence, awareness regarding different organ manifestations of TSC is important. Epidemiology TSC occurs in all races and ethnic groups, and in both genders. The live-birth prevalence is estimated to be between 10 and 16 cases per 100,000. A 1998 study estimated total population prevalence between about 7 and 12 cases per 100,000, with more than half of these cases undetected. Prior to the invention of CT scanning to identify the nodules and tubers in the brain, the prevalence was thought to be much lower, and the disease associated with those people diagnosed clinically with learning disability, seizures and facial angiofibroma. Whilst still regarded as a rare disease, TSC is common when compared to many other genetic diseases, with at least 1 million individuals affected worldwide. History TSC first came to medical attention when dermatologists described the distinctive facial rash (1835 and 1850). A more complete case was presented by von Recklinghausen (1862), who identified heart and brain tumours in a newborn who had only briefly lived. However, Bourneville (1880) is credited with having first characterized the disease, coining the name "tuberous sclerosis", thus earning the eponym Bournevilles disease. The neurologist Vogt (1908) established a diagnostic triad of epilepsy, idiocy, and adenoma sebaceum (an obsolete term for facial angiofibroma).Symptoms were periodically added to the clinical picture. The disease as presently understood was first fully described by Gomez (1979). The invention of medical ultrasound, CT and MRI has allowed physicians to examine the internal organs of live patients and greatly improved diagnostic ability.In 2002, treatment with rapamycin was found to be effective at shrinking tumours in animals. This has led to human trials of rapamycin as a drug to treat several of the tumors associated with TSC. References External links tuberous-sclerosis at NIH/UW GeneTests GeneReview/NCBI/NIH/UW entry on Tuberous Sclerosis Complex

What does Agnosia mean Aarogya

Agnosia

Agnosia is the inability to process sensory information. Often there is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss. It is usually associated with brain injury or neurological illness, particularly after damage to the occipitotemporal border, which is part of the ventral stream. Agnosia only affects a single modality, such as vision or hearing. More recently, a top-down interruption is considered to cause the disturbance of handling perceptual information. Types Visual agnosia Visual agnosia is a broad category that refers to a deficiency in the ability to recognize visual objects. Visual agnosia can be further subdivided into two different subtypes: apperceptive visual agnosia and associative visual agnosia.Individuals with apperceptive visual agnosia display the ability to see contours and outlines when shown an object, but they experience difficulty if asked to categorize objects. Apperceptive visual agnosia is associated with damage to one hemisphere, specifically damage to the posterior sections of the right hemisphere.In contrast, individuals with associative visual agnosia experience difficulty when asked to name objects. Associative agnosia is associated with damage to both the right and left hemispheres at the occipitotemporal border. A specific form of associative visual agnosia is known as prosopagnosia. Prosopagnosia is the inability to recognize faces. For example, these individuals have difficulty recognizing friends, family and coworkers. However, individuals with prosopagnosia can recognize all other types of visual stimuli. Speech agnosia Speech agnosia, or auditory verbal agnosia, refers to "an inability to comprehend spoken words despite intact hearing, speech production and reading ability". Patients report that they hear sounds being produced, but that the sounds are fundamentally unrecognizable or untranslatable. EXAMINER: What did you eat for breakfast? PATIENT: Breakfast, breakfast, it sounds familiar but it doesnt speak to me. (Obler & Gjerlow 1999:45)Despite an inability to process what the speaker is saying, some patients have been reported to recognize certain characteristic information about the speakers voice (such as being a man or woman). Causes Agnosia can result from strokes, dementia, or other neurological disorders. It may also be trauma-induced by a head injury, brain infection, or hereditary. Additionally, some forms of agnosia may be the result of developmental disorders. Damage causing agnosia usually occurs in either the occipital or parietal lobes of the brain. Although one modality may be affected, cognitive abilities in other areas are preserved.Patients who experience dramatic recovery from blindness experience significant to total agnosia.The effect of damage to the superior temporal sulcus is consistent with several types of neurolinguistic deficiencies, and some contend that agnosia is one of them. The superior temporal sulcus is vital for speech comprehension because the region is highly involved with the lexical interface. According to the 1985 TRACE II Model, the lexical interface associates sound waves (phonemes) with morphological features to produce meaningful words. This association process is accomplished by lateral inhibition/excitement of certain words within an individuals lexicon (vocabulary). For instance, if an experimenter were to say DOG aloud, the utterance would activate and inhibit various words within the subjects lexical interface: DOG activates 3, and inhibits 0 letters in DOG. – +3 DOG activates 2, and inhibits 1 letters in FOG. – +2 DOG activates 1, and inhibits 2 letters in DAN. – +1The consistency of this model to agnosia is shown by evidence that bilateral lesions to the superior temporal sulcus produces pure word deafness (Kussmaul, 1877), or as it is understood today, speech agnosia. Patients with pure word deafness demonstrate the inability to recognize and process speech sounds with normal auditory processing for non-speech sounds below the level of the cortex. Diagnosis In order to assess an individual for agnosia, it must be verified that the individual does not have a loss of sensation, and that both their language abilities and intelligence are intact. In order for an individual to be diagnosed with agnosia, they must only be experiencing a sensory deficit in a single modality. To make a diagnosis, the distinction between apperceptive and associative agnosia must be made. This distinction can be made by having the individual complete copying and matching tasks. If the individual has a form of apperceptive agnosia they will not be able to match two stimuli that are identical in appearance. In contrast, if an individual has a form of associative agnosia, they will not be able to match different examples of a stimulus. For example, an individual who has been diagnosed with associative agnosia in the visual modality would not be able to match pictures of a laptop that is open with a laptop that is closed. Pure alexia Individuals with pure alexia usually have difficulty reading words as well as difficulty with identifying letters. In order to assess whether an individual has pure alexia, tests of copying and recognition must be performed. An individual with pure alexia should be able to copy a set of words, and should be able to recognize letters. Prosopagnosia Individuals are usually shown pictures of human faces that may be familiar to them such as famous actors, singers, politicians or family members. The pictures shown to the patient are selected to be age and culture appropriate. The task involves the examiner asking the individual to name each face. If the individual cannot name whose face appears in the picture, the examiner may ask a question that would help to recognize the face in the picture. Treatment For all practical purposes, there is no direct cure. Patients may improve if information is presented in other modalities than the damaged one. Different types of therapies can help to reverse the effects of agnosia. In some cases, occupational therapy or speech therapy can improve agnosia, depending on its cause.Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This may be caused by anosognosia which is the lack of awareness of a deficit. This lack of awareness usually leads to a form of denial and resistance to any form of help or treatment. There are various methods that can be used which can help the individual recognize the impairment in perception or recognition that they may have. A patient can be presented with a stimulus to the impaired modality only to help increase their awareness of their deficit. Alternatively, a task can be broken down into its component parts so that the individual can see each part of the problem caused by the deficit. Once the individual acknowledges their perceptual or recognition deficit, a form of treatment may be recommended. There are various forms of treatment such as compensatory strategies with alternate modalities, verbal strategies, alternate cues and organizational strategies. Verbal strategies Using verbal descriptions may be helpful for individuals with certain types of agnosia. Individuals such as prosopagnosics may find it useful to listen to a description of their friend or family member and recognize them based on this description more easily than through visual cues. Alternate cues Alternate cues may be particularly useful to an individual with environmental agnosia or prosopagnosia. Alternate cues for an individual with environmental agnosia may include color cues or tactile markers to symbolize a new room or to remember an area by. Prosopagnosics may use alternate cues such as a scar on an individuals face or crooked teeth in order to recognize the individual. Hair color and length can be helpful cues as well. Organizational strategies Organizational strategies may be extremely helpful for an individual with visual agnosia. For example, organizing clothes according to different hangers provides tactile cues for the individual, making it easier to identify certain forms of clothing as opposed to relying solely on visual cues. Alternative medicine These strategies elicit the use of an unaffected modality. For example, visual agnosics can use tactile information in replacement of visual information. Alternatively, an individual with prosopagnosia can use auditory information in order to replace visual information. For example, an individual with prosopagnosia can wait for someone to speak, and will usually recognize the individual from their speech. Current research There are clinical trials being done to further research for treatments. At the National Institute of Neurological Disorders and Stroke (NINDS) they support research for rare diseases like agnosia. Some organizations that are recruiting for trials are using clincaltrials.gov and give status updates on the trials. History The term agnosia comes from the Ancient Greek ἀγνωσία (agnosia), "ignorance", "absence of knowledge". It was introduced by Sigmund Freud in 1891: "For disturbances in the recognition of objects, which Finkelnburg classes as asymbolia, I should like to propose the term agnosia." Prior to Freuds introduction of the term, some of the first ideas about agnosia came from Carl Wernicke, who created theories about receptive aphasia in 1874. He noted that individuals with receptive aphasia did not possess the ability to understand speech or repeat words. He believed that receptive aphasia was due to lesions of the posterior third of the left superior temporal gyrus. Due to these lesions, Wernicke believed that individuals with receptive aphasia had a limited deafness for certain sounds and frequencies in speech.After Wernicke, came Kussmaul in 1877 who attempted to explain why auditory verbal agnosia, also known as word deafness, occurs. Contrary to Wernickes explanations, Kussmaul believed auditory verbal agnosia was the result of major destruction to the first left temporal gyrus. Kussmaul also posited about the origins of alexia (acquired dyslexia) also known as word blindness. He believed that word blindness was the result of lesions to the left angular and supramarginal gyri.Heinrich Lissauer shared his ideas about agnosia after Wernicke and Kussmaul. In 1890, he theorized that there were two ways in which object recognition impairment could occur. One way in which impairment could occur was if there was damage to early perceptual processing or if there was damage to the actual object representation. If the actual object representation was damaged, this would not allow the object to be stored in visual memory, and therefore the individual would not be able to recognize the object. During the time of Wernicke, Kussmaul and Lissauer there was little known about the cerebral cortex. Today, with new neuroimaging techniques, we have been able to expand our knowledge on agnosia greatly. References External links Types and brain areas Total Recall: Memory Requires More than the Sum of Its Parts Scientific American (accessdate 2007-06-05)

Hi Aarogya, could you help me understand about Death

Death

Death is the irreversible cessation of all biological functions that sustain an organism. For organisms with a brain, death can also be defined as the irreversible cessation of functioning of the whole brain, including brainstem, and brain death is sometimes used as a legal definition of death. The remains of a former organism normally begin to decompose shortly after death. Death is an inevitable process that eventually occurs in almost all organisms. Death is generally applied to whole organisms; the similar process seen in individual components of an organism, such as cells or tissues, is necrosis. Something that is not considered an organism, such as a virus, can be physically destroyed but is not said to die. As of the early 21st century, over 150,000 humans die each day, with ageing being by far the most common cause of death.Many cultures and religions have the idea of an afterlife, and also may hold the idea of judgement of good and bad deeds in ones life (heaven, hell, karma). Diagnosis Problems of definition The concept of death is a key to human understanding of the phenomenon. There are many scientific approaches and various interpretations of the concept. Additionally, the advent of life-sustaining therapy and the numerous criteria for defining death from both a medical and legal standpoint, have made it difficult to create a single unifying definition. One of the challenges in defining death is in distinguishing it from life. As a point in time, death would seem to refer to the moment at which life ends. Determining when death has occurred is difficult, as cessation of life functions is often not simultaneous across organ systems. Such determination, therefore, requires drawing precise conceptual boundaries between life and death. This is difficult, due to there being little consensus on how to define life. It is possible to define life in terms of consciousness. When consciousness ceases, an organism can be said to have died. One of the flaws in this approach is that there are many organisms that are alive but probably not conscious (for example, single-celled organisms). Another problem is in defining consciousness, which has many different definitions given by modern scientists, psychologists and philosophers. Additionally, many religious traditions, including Abrahamic and Dharmic traditions, hold that death does not (or may not) entail the end of consciousness. In certain cultures, death is more of a process than a single event. It implies a slow shift from one spiritual state to another. Other definitions for death focus on the character of cessation of organismic functioning and a human death which refers to irreversible loss of personhood. More specifically, death occurs when a living entity experiences irreversible cessation of all functioning. As it pertains to human life, death is an irreversible process where someone loses their existence as a person.Historically, attempts to define the exact moment of a humans death have been subjective, or imprecise. Death was once defined as the cessation of heartbeat (cardiac arrest) and of breathing, but the development of CPR and prompt defibrillation have rendered that definition inadequate because breathing and heartbeat can sometimes be restarted. This type of death where circulatory and respiratory arrest happens is known as the circulatory definition of death (DCDD). Proponents of the DCDD believe that this definition is reasonable because a person with permanent loss of circulatory and respiratory function should be considered dead. Critics of this definition state that while cessation of these functions may be permanent, it does not mean the situation is irreversible, because if CPR was applied, the person could be revived. Thus, the arguments for and against the DCDD boil down to a matter of defining the actual words "permanent" and "irreversible," which further complicates the challenge of defining death. Furthermore, events which were causally linked to death in the past no longer kill in all circumstances; without a functioning heart or lungs, life can sometimes be sustained with a combination of life support devices, organ transplants and artificial pacemakers. Today, where a definition of the moment of death is required, doctors and coroners usually turn to "brain death" or "biological death" to define a person as being dead; people are considered dead when the electrical activity in their brain ceases. It is presumed that an end of electrical activity indicates the end of consciousness. Suspension of consciousness must be permanent, and not transient, as occurs during certain sleep stages, and especially a coma. In the case of sleep, EEGs can easily tell the difference. The category of "brain death" is seen as problematic by some scholars. For instance, Dr. Franklin Miller, senior faculty member at the Department of Bioethics, National Institutes of Health, notes: "By the late 1990s... the equation of brain death with death of the human being was increasingly challenged by scholars, based on evidence regarding the array of biological functioning displayed by patients correctly diagnosed as having this condition who were maintained on mechanical ventilation for substantial periods of time. These patients maintained the ability to sustain circulation and respiration, control temperature, excrete wastes, heal wounds, fight infections and, most dramatically, to gestate fetuses (in the case of pregnant "brain-dead" women)."While "brain death" is viewed as problematic by some scholars, there are certainly proponents of it that believe this definition of death is the most reasonable for distinguishing life from death. The reasoning behind the support for this definition is that brain death has a set of criteria that is reliable and reproducible. Also, the brain is crucial in determining our identity or who we are as human beings. The distinction should be made that "brain death" cannot be equated with one who is in a vegetative state or coma, in that the former situation describes a state that is beyond recovery.Those people maintaining that only the neo-cortex of the brain is necessary for consciousness sometimes argue that only electrical activity should be considered when defining death. Eventually it is possible that the criterion for death will be the permanent and irreversible loss of cognitive function, as evidenced by the death of the cerebral cortex. All hope of recovering human thought and personality is then gone given current and foreseeable medical technology. At present, in most places the more conservative definition of death – irreversible cessation of electrical activity in the whole brain, as opposed to just in the neo-cortex – has been adopted (for example the Uniform Determination Of Death Act in the United States). In 2005, the Terri Schiavo case brought the question of brain death and artificial sustenance to the front of American politics. Even by whole-brain criteria, the determination of brain death can be complicated. EEGs can detect spurious electrical impulses, while certain drugs, hypoglycemia, hypoxia, or hypothermia can suppress or even stop brain activity on a temporary basis. Because of this, hospitals have protocols for determining brain death involving EEGs at widely separated intervals under defined conditions. In the past, adoption of this whole-brain definition was a conclusion of the Presidents Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioral Research in 1980. They concluded that this approach to defining death sufficed in reaching a uniform definition nationwide. A multitude of reasons were presented to support this definition including: uniformity of standards in law for establishing death; consumption of a familys fiscal resources for artificial life support; and legal establishment for equating brain death with death in order to proceed with organ donation.Aside from the issue of support of or dispute against brain death, there is another inherent problem in this categorical definition: the variability of its application in medical practice. In 1995, the American Academy of Neurology (AAN), established a set of criteria that became the medical standard for diagnosing neurologic death. At that time, three clinical features had to be satisfied in order to determine "irreversible cessation" of the total brain including: coma with clear etiology, cessation of breathing, and lack of brainstem reflexes. This set of criteria was then updated again most recently in 2010, but substantial discrepancies still remain across hospitals and medical specialties.The problem of defining death is especially imperative as it pertains to the dead donor rule, which could be understood as one of the following interpretations of the rule: there must be an official declaration of death in a person before starting organ procurement or that organ procurement cannot result in death of the donor. A great deal of controversy has surrounded the definition of death and the dead donor rule. Advocates of the rule believe the rule is legitimate in protecting organ donors while also countering against any moral or legal objection to organ procurement. Critics, on the other hand, believe that the rule does not uphold the best interests of the donors and that the rule does not effectively promote organ donation. Signs Signs of death or strong indications that a warm-blooded animal is no longer alive are: Respiratory arrest (no breathing) Cardiac arrest (no pulse) Brain death (no neuronal activity)The stages that follow after death are: Pallor mortis, paleness which happens in 15–120 minutes after death Algor mortis, the reduction in body temperature following death. This is generally a steady decline until matching ambient temperature Rigor mortis, the limbs of the corpse become stiff (Latin rigor) and difficult to move or manipulate Livor mortis, a settling of the blood in the lower (dependent) portion of the body Putrefaction, the beginning signs of decomposition Decomposition, the reduction into simpler forms of matter, accompanied by a strong, unpleasant odor. Skeletonization, the end of decomposition, where all soft tissues have decomposed, leaving only the skeleton. Fossilization, the natural preservation of the skeletal remains formed over a very long period Legal The death of a person has legal consequences that may vary between different jurisdictions. A death certificate is issued in most jurisdictions, either by a doctor, or by an administrative office upon presentation of a doctors declaration of death. Misdiagnosed There are many anecdotal references to people being declared dead by physicians and then "coming back to life", sometimes days later in their own coffin, or when embalming procedures are about to begin. From the mid-18th century onwards, there was an upsurge in the publics fear of being mistakenly buried alive, and much debate about the uncertainty of the signs of death. Various suggestions were made to test for signs of life before burial, ranging from pouring vinegar and pepper into the corpses mouth to applying red hot pokers to the feet or into the rectum. Writing in 1895, the physician J.C. Ouseley claimed that as many as 2,700 people were buried prematurely each year in England and Wales, although others estimated the figure to be closer to 800.In cases of electric shock, cardiopulmonary resuscitation (CPR) for an hour or longer can allow stunned nerves to recover, allowing an apparently dead person to survive. People found unconscious under icy water may survive if their faces are kept continuously cold until they arrive at an emergency room. This "diving response", in which metabolic activity and oxygen requirements are minimal, is something humans share with cetaceans called the mammalian diving reflex.As medical technologies advance, ideas about when death occurs may have to be re-evaluated in light of the ability to restore a person to vitality after longer periods of apparent death (as happened when CPR and defibrillation showed that cessation of heartbeat is inadequate as a decisive indicator of death). The lack of electrical brain activity may not be enough to consider someone scientifically dead. Therefore, the concept of information-theoretic death has been suggested as a better means of defining when true death occurs, though the concept has few practical applications outside the field of cryonics. There have been some scientific attempts to bring dead organisms back to life, but with limited success. Causes The leading cause of human death in developing countries is infectious disease. The leading causes in developed countries are atherosclerosis (heart disease and stroke), cancer, and other diseases related to obesity and aging. By an extremely wide margin, the largest unifying cause of death in the developed world is biological aging, leading to various complications known as aging-associated diseases. These conditions cause loss of homeostasis, leading to cardiac arrest, causing loss of oxygen and nutrient supply, causing irreversible deterioration of the brain and other tissues. Of the roughly 150,000 people who die each day across the globe, about two thirds die of age-related causes. In industrialized nations, the proportion is much higher, approaching 90%. With improved medical capability, dying has become a condition to be managed. Home deaths, once commonplace, are now rare in the developed world. In developing nations, inferior sanitary conditions and lack of access to modern medical technology makes death from infectious diseases more common than in developed countries. One such disease is tuberculosis, a bacterial disease which killed 1.8M people in 2015. Malaria causes about 400–900M cases of fever and 1–3M deaths annually. AIDS death toll in Africa may reach 90–100M by 2025.According to Jean Ziegler (United Nations Special Reporter on the Right to Food, 2000 – Mar 2008), mortality due to malnutrition accounted for 58% of the total mortality rate in 2006. Ziegler says worldwide approximately 62M people died from all causes and of those deaths more than 36M died of hunger or diseases due to deficiencies in micronutrients.Tobacco smoking killed 100 million people worldwide in the 20th century and could kill 1 billion people around the world in the 21st century, a World Health Organization report warned.Many leading developed world causes of death can be postponed by diet and physical activity, but the accelerating incidence of disease with age still imposes limits on human longevity. The evolutionary cause of aging is, at best, only just beginning to be understood. It has been suggested that direct intervention in the aging process may now be the most effective intervention against major causes of death. Selye proposed a unified non-specific approach to many causes of death. He demonstrated that stress decreases adaptability of an organism and proposed to describe the adaptability as a special resource, adaptation energy. The animal dies when this resource is exhausted. Selye assumed that the adaptability is a finite supply, presented at birth. Later on, Goldstone proposed the concept of a production or income of adaptation energy which may be stored (up to a limit), as a capital reserve of adaptation. In recent works, adaptation energy is considered as an internal coordinate on the "dominant path" in the model of adaptation. It is demonstrated that oscillations of well-being appear when the reserve of adaptability is almost exhausted.In 2012, suicide overtook car crashes for leading causes of human injury deaths in the U.S., followed by poisoning, falls, and murder. Causes of death are different in different parts of the world. In high-income and middle income countries nearly half up to more than two thirds of all people live beyond the age of 70 and predominantly die of chronic diseases. In low-income countries, where less than one in five of all people reach the age of 70, and more than a third of all deaths are among children under 15, people predominantly die of infectious diseases. Autopsy An autopsy, also known as a postmortem examination or an obduction, is a medical procedure that consists of a thorough examination of a human corpse to determine the cause and manner of a persons death and to evaluate any disease or injury that may be present. It is usually performed by a specialized medical doctor called a pathologist. Autopsies are either performed for legal or medical purposes. A forensic autopsy is carried out when the cause of death may be a criminal matter, while a clinical or academic autopsy is performed to find the medical cause of death and is used in cases of unknown or uncertain death, or for research purposes. Autopsies can be further classified into cases where external examination suffices, and those where the body is dissected and an internal examination is conducted. Permission from next of kin may be required for internal autopsy in some cases. Once an internal autopsy is complete the body is generally reconstituted by sewing it back together. Autopsy is important in a medical environment and may shed light on mistakes and help improve practices. A necropsy, which is not always a medical procedure, was a term previously used to describe an unregulated postmortem examination. In modern times, this term is more commonly associated with the corpses of animals. Senescence Senescence refers to a scenario when a living being is able to survive all calamities, but eventually dies due to causes relating to old age. Animal and plant cells normally reproduce and function during the whole period of natural existence, but the aging process derives from deterioration of cellular activity and ruination of regular functioning. Aptitude of cells for gradual deterioration and mortality means that cells are naturally sentenced to stable and long-term loss of living capacities, even despite continuing metabolic reactions and viability. In the United Kingdom, for example, nine out of ten of all the deaths that occur on a daily basis relates to senescence, while around the world it accounts for two-thirds of 150,000 deaths that take place daily.Almost all animals who survive external hazards to their biological functioning eventually die from biological aging, known in life sciences as "senescence". Some organisms experience negligible senescence, even exhibiting biological immortality. These include the jellyfish Turritopsis dohrnii, the hydra, and the planarian. Unnatural causes of death include suicide and predation. From all causes, roughly 150,000 people die around the world each day. Of these, two thirds die directly or indirectly due to senescence, but in industrialized countries – such as the United States, the United Kingdom, and Germany – the rate approaches 90% (i.e., nearly nine out of ten of all deaths are related to senescence).Physiological death is now seen as a process, more than an event: conditions once considered indicative of death are now reversible. Where in the process a dividing line is drawn between life and death depends on factors beyond the presence or absence of vital signs. In general, clinical death is neither necessary nor sufficient for a determination of legal death. A patient with working heart and lungs determined to be brain dead can be pronounced legally dead without clinical death occurring. Cryonics Cryonics (from Greek κρύος kryos- meaning icy cold) is the low-temperature preservation of animals and humans who cannot be sustained by contemporary medicine, with the hope that healing and resuscitation may be possible in the future.Cryopreservation of people or large animals is not reversible with current technology. The stated rationale for cryonics is that people who are considered dead by current legal or medical definitions may not necessarily be dead according to the more stringent information-theoretic definition of death.Some scientific literature is claimed to support the feasibility of cryonics. Medical science and cryobiologists generally regards cryonics with skepticism. Life extension Life extension refers to an increase in maximum or average lifespan, especially in humans, by slowing down or reversing the processes of aging through anti-aging measures. Despite the fact that aging is by far the most common cause of death worldwide, it is socially mostly ignored as such and seen as "necessary" and "inevitable" anyway, which is why little money is spent on research into anti-aging therapies, a phenomenon known as the pro-aging trance.Average lifespan is determined by vulnerability to accidents and age or lifestyle-related afflictions such as cancer, or cardiovascular disease. Extension of average lifespan can be achieved by good diet, exercise and avoidance of hazards such as smoking. Maximum lifespan is also determined by the rate of aging for a species inherent in its genes. Currently, the only widely recognized method of extending maximum lifespan is calorie restriction. Theoretically, extension of maximum lifespan can be achieved by reducing the rate of aging damage, by periodic replacement of damaged tissues, or by molecular repair or rejuvenation of deteriorated cells and tissues. A United States poll found that religious people and irreligious people, as well as men and women and people of different economic classes have similar rates of support for life extension, while Africans and Hispanics have higher rates of support than white people. 38 percent of the polled said they would desire to have their aging process cured. Researchers of life extension are a subclass of biogerontologists known as "biomedical gerontologists". They try to understand the nature of aging and they develop treatments to reverse aging processes or to at least slow them down, for the improvement of health and the maintenance of youthful vigor at every stage of life. Those who take advantage of life extension findings and seek to apply them upon themselves are called "life extensionists" or "longevists". The primary life extension strategy currently is to apply available anti-aging methods in the hope of living long enough to benefit from a complete cure to aging once it is developed. Location Before about 1930, most people in Western countries died in their own homes, surrounded by family, and comforted by clergy, neighbors, and doctors making house calls. By the mid-20th century, half of all Americans died in a hospital. By the start of the 21st century, only about 20–25% of people in developed countries died outside of a medical institution. The shift away from dying at home towards dying in a professional medical environment has been termed the "Invisible Death". This shift occurred gradually over the years, until most deaths now occur outside the home. Psychology Death studies is a field within psychology. Many people are afraid of dying. Discussing, thinking about, or planning for their own deaths causes them discomfort. This fear may cause them to put off financial planning, preparing a will and testament, or requesting help from a hospice organization. Different people have different responses to the idea of their own deaths. Philosopher Galen Strawson writes that the death that many people wish for is an instant, painless, unexperienced annihilation. In this unlikely scenario, the person dies without realizing it and without being able to fear it. One moment the person is walking, eating, or sleeping, and the next moment, the person is dead. Strawson reasons that this type of death would not take anything away from the person, as he believes that a person cannot have a legitimate claim to ownership in the future. Society and culture In society, the nature of death and humanitys awareness of its own mortality has for millennia been a concern of the worlds religious traditions and of philosophical inquiry. This includes belief in resurrection or an afterlife (associated with Abrahamic religions), reincarnation or rebirth (associated with Dharmic religions), or that consciousness permanently ceases to exist, known as eternal oblivion (associated with Secular humanism).Commemoration ceremonies after death may include various mourning, funeral practices and ceremonies of honouring the deceased. The physical remains of a person, commonly known as a corpse or body, are usually interred whole or cremated, though among the worlds cultures there are a variety of other methods of mortuary disposal. In the English language, blessings directed towards a dead person include rest in peace (originally the Latin requiescat in pace), or its initialism RIP. Death is the center of many traditions and organizations; customs relating to death are a feature of every culture around the world. Much of this revolves around the care of the dead, as well as the afterlife and the disposal of bodies upon the onset of death. The disposal of human corpses does, in general, begin with the last offices before significant time has passed, and ritualistic ceremonies often occur, most commonly interment or cremation. This is not a unified practice; in Tibet, for instance, the body is given a sky burial and left on a mountain top. Proper preparation for death and techniques and ceremonies for producing the ability to transfer ones spiritual attainments into another body (reincarnation) are subjects of detailed study in Tibet. Mummification or embalming is also prevalent in some cultures, to retard the rate of decay. Legal aspects of death are also part of many cultures, particularly the settlement of the deceased estate and the issues of inheritance and in some countries, inheritance taxation. Capital punishment is also a culturally divisive aspect of death. In most jurisdictions where capital punishment is carried out today, the death penalty is reserved for premeditated murder, espionage, treason, or as part of military justice. In some countries, sexual crimes, such as adultery and sodomy, carry the death penalty, as do religious crimes such as apostasy, the formal renunciation of ones religion. In many retentionist countries, drug trafficking is also a capital offense. In China, human trafficking and serious cases of corruption are also punished by the death penalty. In militaries around the world courts-martial have imposed death sentences for offenses such as cowardice, desertion, insubordination, and mutiny.Death in warfare and in suicide attack also have cultural links, and the ideas of dulce et decorum est pro patria mori, mutiny punishable by death, grieving relatives of dead soldiers and death notification are embedded in many cultures. Recently in the western world, with the increase in terrorism following the September 11 attacks, but also further back in time with suicide bombings, kamikaze missions in World War II and suicide missions in a host of other conflicts in history, death for a cause by way of suicide attack, and martyrdom have had significant cultural impacts. Suicide in general, and particularly euthanasia, are also points of cultural debate. Both acts are understood very differently in different cultures. In Japan, for example, ending a life with honor by seppuku was considered a desirable death, whereas according to traditional Christian and Islamic cultures, suicide is viewed as a sin. Death is personified in many cultures, with such symbolic representations as the Grim Reaper, Azrael, the Hindu god Yama and Father Time. In Brazil, a human death is counted officially when it is registered by existing family members at a cartório, a government-authorized registry. Before being able to file for an official death, the deceased must have been registered for an official birth at the cartório. Though a Public Registry Law guarantees all Brazilian citizens the right to register deaths, regardless of their financial means, of their family members (often children), the Brazilian government has not taken away the burden, the hidden costs and fees, of filing for a death. For many impoverished families, the indirect costs and burden of filing for a death lead to a more appealing, unofficial, local, cultural burial, which in turn raises the debate about inaccurate mortality rates.Talking about death and witnessing it is a difficult issue with most cultures. Western societies may like to treat the dead with the utmost material respect, with an official embalmer and associated rites. Eastern societies (like India) may be more open to accepting it as a fait accompli, with a funeral procession of the dead body ending in an open-air burning-to-ashes of the same. Consciousness Much interest and debate surround the question of what happens to ones consciousness as ones body dies. The belief in the permanent loss of consciousness after death is often called eternal oblivion. Belief that the stream of consciousness is preserved after physical death is described by the term afterlife. Neither are likely to ever be confirmed without the ponderer having to actually die. In biology After death, the remains of a former organism become part of the biogeochemical cycle, during which animals may be consumed by a predator or a scavenger. Organic material may then be further decomposed by detritivores, organisms which recycle detritus, returning it to the environment for reuse in the food chain, where these chemicals may eventually end up being consumed and assimilated into the cells of an organism. Examples of detritivores include earthworms, woodlice and dung beetles. Microorganisms also play a vital role, raising the temperature of the decomposing matter as they break it down into yet simpler molecules. Not all materials need to be fully decomposed. Coal, a fossil fuel formed over vast tracts of time in swamp ecosystems, is one example. Natural selection Contemporary evolutionary theory sees death as an important part of the process of natural selection. It is considered that organisms less adapted to their environment are more likely to die having produced fewer offspring, thereby reducing their contribution to the gene pool. Their genes are thus eventually bred out of a population, leading at worst to extinction and, more positively, making the process possible, referred to as speciation. Frequency of reproduction plays an equally important role in determining species survival: an organism that dies young but leaves numerous offspring displays, according to Darwinian criteria, much greater fitness than a long-lived organism leaving only one. Extinction Extinction is the cessation of existence of a species or group of taxa, reducing biodiversity. The moment of extinction is generally considered to be the death of the last individual of that species (although the capacity to breed and recover may have been lost before this point). Because a species potential range may be very large, determining this moment is difficult, and is usually done retrospectively. This difficulty leads to phenomena such as Lazarus taxa, where species presumed extinct abruptly "reappear" (typically in the fossil record) after a period of apparent absence. New species arise through the process of speciation, an aspect of evolution. New varieties of organisms arise and thrive when they are able to find and exploit an ecological niche – and species become extinct when they are no longer able to survive in changing conditions or against superior competition. Evolution of aging and mortality Inquiry into the evolution of aging aims to explain why so many living things and the vast majority of animals weaken and die with age (exceptions include Hydra and the jellyfish Turritopsis dohrnii, which research shows to be biologically immortal). The evolutionary origin of senescence remains one of the fundamental puzzles of biology. Gerontology specializes in the science of human aging processes. Organisms showing only asexual reproduction (e.g. bacteria, some protists, like the euglenoids and many amoebozoans) and unicellular organisms with sexual reproduction (colonial or not, like the volvocine algae Pandorina and Chlamydomonas) are "immortal" at some extent, dying only due to external hazards, like being eaten or meeting with a fatal accident. In multicellular organisms (and also in multinucleate ciliates), with a Weismannist development, that is, with a division of labor between mortal somatic (body) cells and "immortal" germ (reproductive) cells, death becomes an essential part of life, at least for the somatic line.The Volvox algae are among the simplest organisms to exhibit that division of labor between two completely different cell types, and as a consequence include death of somatic line as a regular, genetically regulated part of its life history. Religious views Buddhism In Buddhist doctrine and practice, death plays an important role. Awareness of death was what motivated Prince Siddhartha to strive to find the "deathless" and finally to attain enlightenment. In Buddhist doctrine, death functions as a reminder of the value of having been born as a human being. Being reborn as a human being is considered the only state in which one can attain enlightenment. Therefore, death helps remind oneself that one should not take life for granted. The belief in rebirth among Buddhists does not necessarily remove death anxiety, since all existence in the cycle of rebirth is considered filled with suffering, and being reborn many times does not necessarily mean that one progresses.Death is part of several key Buddhist tenets, such as the Four Noble Truths and dependent origination. Christianity While there are different sects of Christianity with different branches of belief; the overarching ideology on death grows from the knowledge of afterlife. Meaning after death the individual will undergo a separation from mortality to immortality; their soul leaves the body entering a realm of spirits. Following this separation of body and spirit (i.e. death) resurrection will occur. Representing the same transformation Jesus Christ embodied after his body was placed in the tomb for three days. Like Him, each persons body will be resurrected reuniting the spirit and body in a perfect form. This process allows the individuals soul to withstand death and transform into life after death. Hinduism In Hindu texts, death is described as the individual eternal spiritual jiva-atma (soul or conscious self) exiting the current temporary material body. The soul exits this body when the body can no longer sustain the conscious self (life), which may be due to mental or physical reasons, or more accurately, the inability to act on ones kama (material desires). During conception, the soul enters a compatible new body based on the remaining merits and demerits of ones karma (good/bad material activities based on dharma) and the state of ones mind (impressions or last thoughts) at the time of death. Usually the process of reincarnation (souls transmigration) makes one forget all memories of ones previous life. Because nothing really dies and the temporary material body is always changing, both in this life and the next, death means forgetfulness of ones previous experiences (previous material identity). Material existence is described as being full of miseries arising from birth, disease, old age, death, mind, weather, etc. To conquer samsara (the cycle of death and rebirth) and become eligible for one of the different types of moksha (liberation), one has to first conquer kama (material desires) and become self-realized. The human form of life is most suitable for this spiritual journey, especially with the help of sadhu (self-realized saintly persons), sastra (revealed spiritual scriptures), and guru (self-realized spiritual masters), given all three are in agreement. Islam The Islamic view is that death is the separation of the soul from the body as well as the beginning of the afterlife. The afterlife or akhirah is one of the six main beliefs in Islam. Rather than seeing death as the end of life, Muslims consider death as a continuation of life in another form. In Islam, the life on earth right now is a short, temporary life and a testing period for every soul. The true life begins with the Day of Judgement, when all people will be divided into two groups. The righteous believers will be welcomed to janna (heaven) and the disbelievers and evildoers will be punished in jahannam (hellfire).Muslims believe death to be wholly natural and predetermined by God. Only God knows the exact time of a person’s death. The Quran emphasizes that death is inevitable, no matter how much people try to escape death, it will reach everyone. Life on earth is the one and only chance for people to prepare themselves for the life to come and choose to either believe or not believe in God, and death is the end of that learning opportunity. Judaism There are a variety of beliefs about the afterlife within Judaism, but none of them contradict the preference of life over death. This is partially because death puts a cessation to the possibility of fulfilling any commandments. Language The word "death" comes from Old English dēaþ, which in turn comes from Proto-Germanic *dauþuz (reconstructed by etymological analysis). This comes from the Proto-Indo-European stem *dheu- meaning the "process, act, condition of dying".The concept and symptoms of death, and varying degrees of delicacy used in discussion in public forums, have generated numerous scientific, legal, and socially acceptable terms or euphemisms. When a person has died, it is also said they have "passed away", "passed on", "expired", or "gone", among other socially accepted, religiously specific, slang, and irreverent terms. As a formal reference to a dead person, it has become common practice to use the participle form of "decease", as in "the deceased"; another noun form is "decedent". Bereft of life, the dead person is a "corpse", "cadaver", "body", "set of remains" or, when all flesh is gone, a "skeleton". The terms "carrion" and "carcass" are also used, usually for dead non-human animals. The ashes left after a cremation are lately called "cremains". See also References Bibliography Further reading Cochem, Martin of (1899). "On Death" . The four last things: death, judgment, hell, heaven. Benziger Brothers. Daughters of Charity of St. Vincent de Paul. (1856). "Considerations on Death" . St. Vincents Manual. John Murphy & Co. Liguori, Alphonsus (1868). Preparation for Death . Rivingtons. Marques, Susana Moreira (13 October 2015). Now and At the Hour of Our Death. Translated by Sanches, Julia. And Other Stories. ISBN 978-1-908276-62-9. Massillon, Jean-Baptiste (1879). "On Death" . Sermons by John-Baptist Massillon. Thomas Tegg & Sons. Rosenberg, David (17 August 2014). "How One Photographer Overcame His Fear of Death by Photographing It (Walter Schels Life Before Death)". Slate. Sachs, Jessica Snyder (2001). Corpse: Nature, Forensics, and the Struggle to Pinpoint Time of Death (270 pages). Perseus Publishing. ISBN 978-0-7382-0336-2. Warraich, Haider (2017). Modern Death: How Medicine Changed the End of Life. St. Martins Press. ISBN 978-1250104588. External links Death at Curlie "Death". Stanford Encyclopedia of Philosophy. Metaphysics Research Lab, Stanford University. 2016. "Death" . Encyclopædia Britannica. Vol. 7 (11th ed.). 1911. pp. 898–900. Best, Ben. "Causes of Death". BenBest.com. Retrieved 10 June 2016. Schels, Walter; Lakotta, Beate. "Before and After Death". LensCulture.com. Archived from the original on 11 October 2014. Retrieved 19 September 2016. Interviews with people dying in hospices, and portraits of them before, and shortly after, death. U.S. Census. "Causes of Death 1916". AntiqueBooks.net (scanns). Archived from the original on 18 September 2004. Retrieved 19 September 2016. How the medical profession categorized causes of death. Wald, George. "The Origin of Death". ElijahWald.com. A biologist explains life and death in different kinds of organisms, in relation to evolution. "Death" (video; 10:18) by Timothy Ferris, producer of the Voyager Golden Record for NASA. 2021

Give me a short description about Melena , Aarogya

Melena

Melena or melaena refers to the dark black, tarry feces that are associated with upper gastrointestinal bleeding. The black color and characteristic strong odor are caused by hemoglobin in the blood being altered by digestive enzymes and intestinal bacteria.Iron supplements may cause a grayish-black stool that should be distinguished from melena, as should black coloration caused by a number of medications, such as bismuth subsalicylate (the active ingredient in Pepto-Bismol), or by foods such as beetroot, black liquorice, or blueberries. Causes The most common cause of melena is peptic ulcer disease. However, any bleeding within the upper gastrointestinal tract or the ascending colon can lead to melena. Melena may also be a complication of anticoagulant medications, such as warfarin.Causes of upper gastrointestinal bleeding that may result in melena include malignant tumors affecting the esophagus, stomach or small intestine, hemorrhagic blood diseases, such as thrombocytopenia and hemophilia, gastritis, Stomach cancer, esophageal varices, Meckels diverticulum and Mallory-Weiss syndrome.Causes of "false" melena include iron supplements, Pepto-Bismol, Maalox, and lead, blood swallowed as a result of a nose bleed (epistaxis), and blood ingested as part of the diet, as with consumption of black pudding (blood sausage), or with the traditional African Maasai diet, which includes much blood drained from cattle.Melena is considered a medical emergency as it arises from a significant amount of bleeding. Urgent care is required to rule out serious causes and prevent potentially life-threatening emergencies.A less serious, self-limiting case of melena can occur in newborns two to three days after delivery, due to swallowed maternal blood. Diagnosis In acute cases, with a large amount of blood loss, patients may present with anemia or low blood pressure. However, aside from the melena itself, many patients may present with few symptoms. Often, the first approach is to use endoscopy to look for obvious signs of a bleed. In cases where the source of the bleed is unclear, but melena is present, an upper endoscopy is recommended, to try to ascertain the source of the bleed.Lower gastrointestinal bleeding sources usually present with hematochezia or frank blood. A test with poor sensitivity/specificity that may detect the source of bleeding is the tagged red blood cell scan. This is especially used for slow bleeding (<0.5 ml/min). However, for rapid bleeding (>0.5 ml/min), mesenteric angiogram ± embolization is the gold standard. Colonoscopy is often first line, however. Melena versus hematochezia Bleeds that originate from the lower gastrointestinal tract (such as the sigmoid colon and rectum) are generally associated with the passage of bright red blood, or hematochezia, particularly when brisk. Only blood that originates from a more proximal source (such as the small intestine), or bleeding from a lower source that occurs slowly enough to allow for enzymatic breakdown, is associated with melena. For this reason, melena is often associated with blood in the stomach or duodenum (upper gastrointestinal bleeding), for example by a peptic ulcer. A rough estimate is that it takes about 14 hours for blood to be broken down within the intestinal lumen; therefore if transit time is less than 14 hours the patient will have hematochezia, and if greater than 14 hours the patient will exhibit melena.: 322  One often-stated rule of thumb is that melena only occurs if the source of bleeding is above the ligament of Treitz although, as noted below, exceptions occur with enough frequency to render it unreliable. Etymology The origin of melena is dated to the early 19th century via modern Latin, via Greek melaina (feminine of melas, black). See also Blood in stool Dieulafoys lesion Hematemesis References == External links ==

Aarogya, give me a short description about Myxedema coma

Myxedema coma

Myxedema coma is an extreme or decompensated form of hypothyroidism and while uncommon, is potentially lethal. A person may have laboratory values identical to a "normal" hypothyroid state, but a stressful event (such as an infection, myocardial infarction, or stroke) precipitates the myxedema coma state, usually in the elderly. Primary symptoms of myxedema coma are altered mental status and low body temperature. Low blood sugar, low blood pressure, hyponatremia, hypercapnia, hypoxia, slowed heart rate, and hypoventilation may also occur. Myxedema, although included in the name, is not necessarily seen in myxedema coma. Coma is also not necessarily seen in myxedema coma.According to newer theories, myxedema coma could result from allostatic overload in a situation where the effects of hypothyroidism are amplified by nonthyroidal illness syndrome. Causes Myxedema coma represents an extreme or decompensated form of hypothyroidism. Most cases occur in patients who have been previously diagnosed with hypothyroidism, yet in some cases, hypothyroidism may not have been previously identified. Common precipitating factors of myxedema coma include: Hypothermia, especially during winter months Metabolic disruption including hypoglycemia, hyponatremia, acidosis, and hypercalcemia Respiratory compromise including hypoxemia and hypercapnia Infections including pneumonia, cellulitis, and urosepsis Congestive heart failure Cerebrovascular accidents Gastrointestinal bleeding Trauma, motor vehicle accidents, and fractures Medications including anesthetics, sedatives, tranquilizers, narcotics, amiodarone, and lithium Withdrawal of thyroid supplements, especially in relation to a hospitalizationOther precipitating factors include: Other medications including beta-blockers, diuretics, phenothiazines, phenytoin, rifampin, anti-TNF therapy Burns Influenza Surgery Consumption of raw bok choy Diabetic ketoacidosis after total thyroidectomy Pathophysiology The thyroid gland is responsible for regulating whole-body metabolism through the production of two major hormones: thyroxine (T4) and triiodothyronine (T3). Of the metabolically active thyroid hormones, 93% is T4 and 7% is T3. T3 is four times more potent than T4 and most T4 is converted to T3 in the tissues. Iodine is necessary for adequate hormone production. Thyroid-stimulating hormone (TSH) is a circulating or serum hormone from the pituitary gland that stimulates the thyroid gland to produce T3 and T4. Hypothyroidism occurs when the thyroid gland does not produce enough T3 and T4.The most common cause of hypothyroidism worldwide is too little dietary iodine. Hashimotos thyroiditis is the most common cause of hypothyroidism in countries with sufficient dietary iodine. With the cessation of the production of thyroid hormone, the thyroid gland contains enough reserve T3 and T4 to last 2 to 3 months.The thyroid hormones T3 and T4 influence the production by virtually all cells in the body of hundreds of new intracellular proteins and enzymes. This influence includes the expression of the calcium ATPase, regulation of ion channels, oxidative phosphorylation, increased Na-K-ATPase activity, increased carbohydrate metabolism, increased free fatty acids, increased vitamin requirements, and increased overall metabolism. The absence of the thyroid hormones T3 and T4 are responsible for many bodily functions at the genetic and cellular level and an absence of these thyroid hormones as seen in myxedema coma has very serious consequences including a broad spectrum of symptoms and a high mortality rate. Diagnosis Clinical features of myxedema coma: Cardiovascular Bradycardia Bundle branch blocks Complete heart block and arrhythmias Cardiomegaly Elevated diastolic blood pressure—early Hypotension—late Low cardiac output Non-specific ECG findings Pericardial effusion Polymorphic ventricular tachycardia (torsades de pointes) Prolonged QT interval Respiratory Hypoxia Hypercapnia Hyperventilation Myxedema of the larynx Pleural effusion Gastrointestinal Abdominal distention Abdominal pain Anasarca Anorexia and nausea Decreased motility Fecal impaction and constipation Gastrointestinal atony or ileus Myxedema or toxic megacolon—late Neurogenic oropharyngeal dysphagia ileus Neurological Altered mentation Coma Confusion and obtundation Delayed tendon reflexes Depression Poor cognitive function Psychosis Seizures Renal and urinary function Bladder dystonia and distension Fluid retention Appearance and dermatological Alopecia Coarse, sparse hair Dry, cool, doughy skin Myxedematous face Generalized swelling Goiter Macroglossia Non-pitting edema Ptosis Periorbital edema Surgical scar from prior thyroidectomy HypothermiaLaboratory features in myxedema coma: Anemia Elevated creatine kinase (CPK) Elevated creatinine Elevated transaminases Hypercapnia Hypercholesterolemia (elevated LDL) Hyperlipidemia Hypoglycemia Hyponatremia Hypoxia Leukopenia Respiratory acidosis Epidemiology Hypothyroidism is four times more common in women than men. The incidence of myxedema coma has been reported to be 0.22 per 1000000 per year but the data is limited and especially lacking in countries outside the western world and countries along the equator. Myxedema coma is most common in people 60 years old and older and is most common in the winter months when hypothermia is more common. See also Thyroid storm Euthyroid sick syndrome References == External links ==

Hey Aarogya, could you help me understand about Site

Site

Site most often refers to: Archaeological site Campsite, a place used for overnight stay in an outdoor area Construction site Location, a point or an area on the Earths surface or elsewhere Website, a set of related web pages, typically with a common domain nameIt may also refer to: Site, a National Register of Historic Places property type SITE (originally known as Sculpture in the Environment), an American architecture and design firm Site (mathematics), a category C together with a Grothendieck topology on C The Site, a 1990s TV series that aired on MSNBC SITE Intelligence Group, a for-profit organization tracking jihadist and white supremacist organizations SITE Institute, a terrorism-tracking organization, precursor to the SITE Intelligence Group Sindh Industrial and Trading Estate, a company in Sindh, Pakistan SITE Centers, American commercial real estate company SITE Town, a densely populated town in Karachi, Pakistan S.I.T.E Industrial Area, an area in Karachi, Pakistan Satellite Instructional Television Experiment, an experimental satellite communications project launched in India in 1975 Google Sites, web based website editor See also Sites, California All pages with titles beginning with Site All pages with titles containing Site

Hello Aarogya , Do you know what is Hyperesthesia,

Hyperesthesia

Hyperesthesia is a condition that involves an abnormal increase in sensitivity to stimuli of the sense. Stimuli of the senses can include sound that one hears, foods that one tastes, textures that one feels, and so forth. Increased touch sensitivity is referred to as "tactile hyperesthesia", and increased sound sensitivity is called "auditory hyperesthesia". In the context of pain hyperaesthesia can refer to an increase in sensitivity where there is both allodynia and hyperalgesia.In psychology, Jeanne Siaud-Facchin uses the term by defining it as an "exacerbation des sens": 37  that characterizes gifted individuals: for them, the sensory information reaches the brain much faster than the average, and the information is processed in a significantly shorter time. Other animals Feline hyperesthesia syndrome is an uncommon but recognized condition in cats, particularly Siamese, Burmese, Himalayan, and Abyssinian cats. It can affect cats of all ages, though it is most prevalent during maturity. Detection can be somewhat difficult as it is characterized by brief bursts of abnormal behavior, lasting around a minute or two. One of its symptoms is also found in dogs that have canine distemper disease (CD) caused by canine distemper virus (CDV). See also Auditory processing disorder Hyperacusis Multisensory integration Sensory overload Sensory processing Sensory processing disorder Sensory processing sensitivity References == External links ==

Hello Aarogya, explain a situation where Acute myeloid leukemia occurs

Acute myeloid leukemia

Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterized by the rapid growth of abnormal cells that build up in the bone marrow and blood and interfere with normal blood cell production. Symptoms may include feeling tired, shortness of breath, easy bruising and bleeding, and increased risk of infection. Occasionally, spread may occur to the brain, skin, or gums. As an acute leukemia, AML progresses rapidly, and is typically fatal within weeks or months if left untreated.Risk factors include smoking, previous chemotherapy or radiation therapy, myelodysplastic syndrome, and exposure to the chemical benzene. The underlying mechanism involves replacement of normal bone marrow with leukemia cells, which results in a drop in red blood cells, platelets, and normal white blood cells. Diagnosis is generally based on bone marrow aspiration and specific blood tests. AML has several subtypes for which treatments and outcomes may vary.The first-line treatment of AML is usually chemotherapy, with the aim of inducing remission. People may then go on to receive additional chemotherapy, radiation therapy, or a stem cell transplant. The specific genetic mutations present within the cancer cells may guide therapy, as well as determine how long that person is likely to survive.In 2015, AML affected about one million people, and resulted in 147,000 deaths globally. It most commonly occurs in older adults. Males are affected more often than females. The five-year survival rate is about 35% in people under 60 years old and 10% in people over 60 years old. Older people whose health is too poor for intensive chemotherapy have a typical survival of five to ten months. It accounts for roughly 1.1% of all cancer cases, and 1.9% of cancer deaths in the United States. Signs and symptoms Most signs and symptoms of AML are caused by the crowding out in bone marrow of space for normal blood cells to develop. A lack of normal white blood cell production makes people more susceptible to infections. A low red blood cell count (anemia) can cause fatigue, paleness, shortness of breath and palpitations. A lack of platelets can lead to easy bruising, bleeding from the nose (epistaxis), small blood vessels on the skin (petechiae) or gums, or bleeding with minor trauma. Other symptoms may include fever, fatigue worse than what can be attributed to anaemia alone, weight loss and loss of appetite.Enlargement of the spleen may occur in AML, but it is typically mild and asymptomatic. Lymph node swelling is rare in most types of AML, except for acute myelomonocytic leukemia (AMML). The skin can be involved in the form of leukemia cutis; Sweets syndrome; or non-specific findings: flat lesions (macules), raised lesion papules), pyoderma gangrenosum and vasculitis.Some people with AML may experience swelling of the gums because of infiltration of leukemic cells into the gum tissue. Involvement of other parts of the body such as the gastrointestinal tract, respiratory tract and other parts is possible but less common. One area which has particular importance for treatment is whether there is involvement of the meninges around the central nervous system. Risk factors Most cases of AML do not have exposure to any identified risk factors. However, a number of risk factors for developing AML have been identified. These include other blood disorders, chemical exposures, ionizing radiation, and genetic risk factors. Where a defined exposure to past chemotherapy, radiotherapy, toxin or hematologic malignancy is known, this is termed secondary AML. Other blood disorders Other blood disorders, particularly myelodysplastic syndrome (MDS) and less commonly myeloproliferative neoplasms (MPN), can evolve into AML; the exact risk depends on the type of MDS/MPN. The presence of asymptomatic clonal hematopoiesis also raises the risk of transformation into AML. Chemical exposure Exposure to anticancer chemotherapy, in particular alkylating agents, can increase the risk of subsequently developing AML. Other chemotherapy agents, including fludarabine, and topoisomerase II inhibitors are also associated with the development of AML; most commonly after 4–6 years and 1–3 years respectively. These are often associated with specific chromosomal abnormalities in the leukemic cells.Other chemical exposures associated with the development of AML include benzene, chloramphenicol and phenylbutazone. Radiation High amounts of ionizing radiation exposure, such as that used for radiotherapy used to treat some forms of cancer, can increase the risk of AML. People treated with ionizing radiation after treatment for prostate cancer, non-Hodgkin lymphoma, lung cancer, and breast cancer have the highest chance of acquiring AML, but this increased risk returns to the background risk observed in the general population after 12 years. Historically, survivors of the atomic bombings of Hiroshima and Nagasaki had an increased rate of AML, as did radiologists exposed to high levels of X-rays prior to the adoption of modern radiation safety practices. Genetics Most cases of AML arise spontaneously, however there are some genetic mutations associated with an increased risk. Several congenital conditions increase the risk of leukemia; the most common is Down syndrome, with other more rare conditions including Fanconi anemia, Bloom syndrome and ataxia-telangiectasia (all characterised by problems with DNA repair), and Kostmann syndrome. Other factors Being overweight and obese increase the risk of developing AML, as does any amount of active smoking. For reasons that may relate to substance or radiation exposure, certain occupations have a higher rate of AML; particularly work in the nuclear power industry, electronics or computer manufacturing, fishing and animal slaughtering and processing. Pathophysiology The malignant cell in AML is the myeloblast. In normal development of blood cells (hematopoiesis), the myeloblast is an immature precursor of myeloid white blood cells; a normal myeloblast will mature into a white blood cell such as an eosinophil, basophil, neutrophil or monocyte. In AML, though, a single myeloblast accumulates genetic changes which stop maturation, increase its proliferation, and protect it from programmed cell death (apoptosis). Much of the diversity and heterogeneity of AML is because leukemic transformation can occur at a number of different steps along the differentiation pathway. Genetic abnormalities or the stage at which differentiation was halted form part of modern classification systems.Specific cytogenetic abnormalities can be found in many people with AML; the types of chromosomal abnormalities often have prognostic significance. The chromosomal translocations encode abnormal fusion proteins, usually transcription factors whose altered properties may cause the "differentiation arrest". For example, in APL, the t(15;17) translocation produces a PML-RARA fusion protein which binds to the retinoic acid receptor element in the promoters of several myeloid-specific genes and inhibits myeloid differentiation.The clinical signs and symptoms of AML result from the growth of leukemic clone cells, which tends to interfere with the development of normal blood cells in the bone marrow. This leads to neutropenia, anemia, and thrombocytopenia. Other symptoms can arise from the infiltration of malignant cells into parts of the body, such as the gingiva and skin.Many cells develop mutations in genes that affect epigenetics, such as DNA methylation. When these mutations occur, it is likely in the early stages of AML. Such mutations include in the DNA demethylase TET2 and the metabolic enzymes IDH1 and IDH2, which lead to the generation of a novel oncometabolite, D-2-hydroxyglutarate, which inhibits the activity of epigenetic enzymes such as TET2. Epigenetic mutations may lead to the silencing of tumor suppressor genes and/or the activation of proto-oncogenes. Diagnosis A complete blood count, which is a blood test, is one of the initial steps in the diagnosis of AML. It may reveal both an excess of white blood cells (leukocytosis) or a decrease (leukopenia), and a low red blood cell count (anemia) and low platelets (thrombocytopenia) can also be commonly seen. A blood film may show leukemic blast cells. Inclusions within the cells called Auer rods, when seen, make the diagnosis highly likely. A definitive diagnosis requires a bone marrow aspiration and biopsy.Bone marrow is examined under light microscopy, as well as flow cytometry, to diagnose the presence of leukemia, to differentiate AML from other types of leukemia (e.g. acute lymphoblastic leukemia), and to provide information about how mature or immature the affected cells are that can assist in classifying the subtype of disease. A sample of marrow or blood is typically also tested for chromosomal abnormalities by routine cytogenetics or fluorescent in situ hybridization. Genetic studies may also be performed to look for specific mutations in genes such as FLT3, nucleophosmin, and KIT, which may influence the outcome of the disease.Cytochemical stains on blood and bone marrow smears are helpful in the distinction of AML from ALL, and in subclassification of AML. The combination of a myeloperoxidase or Sudan black stain and a nonspecific esterase stain will provide the desired information in most cases. The myeloperoxidase or Sudan black reactions are most useful in establishing the identity of AML and distinguishing it from ALL. The nonspecific esterase stain is used to identify a monocytic component in AMLs and to distinguish a poorly differentiated monoblastic leukemia from ALL.The standard classification scheme for AML is the World Health Organization (WHO) system. According to the WHO criteria, the diagnosis of AML is established by demonstrating involvement of more than 20% of the blood and/or bone marrow by leukemic myeloblasts, except in three forms of acute myeloid leukemia with recurrent genetic abnormalities: t(8;21), inv(16) or t(16;16), and acute promyelocytic leukemia with PML-RARA, in which the presence of the genetic abnormality is diagnostic irrespective of blast percent. Myeloid sarcoma is also considered a subtype of AML independently of the blast count. The older French-American-British (FAB) classification, which is no longer widely used, is a bit more stringent, requiring a blast percentage of at least 30% in bone marrow or peripheral blood for the diagnosis of AML.Because acute promyelocytic leukemia has the highest curability and requires a unique form of treatment, it is important to quickly establish or exclude the diagnosis of this subtype of leukemia. Fluorescent in situ hybridization performed on blood or bone marrow is often used for this purpose, as it readily identifies the chromosomal translocation [t(15;17)(q22;q12);] that characterizes APL. There is also a need to molecularly detect the presence of PML/RARA fusion protein, which is an oncogenic product of that translocation. World Health Organization The WHO classification of AML attempts to be more clinically useful and to produce more meaningful prognostic information than the FAB criteria. Each of the WHO categories contains numerous descriptive subcategories of interest to the hematopathologist and oncologist; however, most of the clinically significant information in the WHO schema is communicated via categorization into one of the subtypes listed below. The revised fourth edition of the WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues was released in 2016. This classification, which is based on a combination of genetic and immunophenotypic markers and morphology, defines the subtypes of AML and related neoplasms as: In 2022 a new classification has been published. Acute leukemias of ambiguous lineage (also known as mixed phenotype or biphenotypic acute leukemia) occur when the leukemic cells can not be classified as either myeloid or lymphoid cells, or where both types of cells are present. French-American-British The French-American-British (FAB) classification system provides terminology that is still sometimes used, and it remains a valuable diagnostic tool in areas without access to genetic testing, this system has largely become obsolete in favor of the WHO classification, which correlates more strongly with treatment outcomes.The FAB system divides AML into eight subtypes, M0 through to M7, based on the type of cell from which the leukemia developed and its degree of maturity. AML of types M0 to M2 may be called acute myeloblastic leukemia. Classification is done by examining the appearance of the malignant cells with light microscopy and/or by using cytogenetics to characterize any underlying chromosomal abnormalities. The subtypes have varying prognoses and responses to therapy. Six FAB subtypes (M1 through to M6) were initially proposed in 1976, although later revisions added M7 in 1985 and M0 in 1987. The morphologic subtypes of AML also include rare types not included in the FAB system, such as acute basophilic leukemia, which was proposed as a ninth subtype, M8, in 1999. Treatment First-line treatment of AML consists primarily of chemotherapy, and is divided into two phases: induction and consolidation. The goal of induction therapy is to achieve a complete remission by reducing the number of leukemic cells to an undetectable level; the goal of consolidation therapy is to eliminate any residual undetectable disease and achieve a cure. Hematopoietic stem cell transplantation is usually considered if induction chemotherapy fails or after a person relapses, although transplantation is also sometimes used as front-line therapy for people with high-risk disease. Efforts to use tyrosine kinase inhibitors in AML continue. Induction The goal of the induction phase is to reach a complete remission. Complete remission does not mean the disease has been cured; rather, it signifies no disease can be detected with available diagnostic methods. All subtypes except acute promyelocytic leukemia are usually given induction chemotherapy with cytarabine and an anthracycline such as daunorubicin or idarubicin. This induction chemotherapy regimen is known as "7+3" (or "3+7"), because the cytarabine is given as a continuous IV infusion for seven consecutive days while the anthracycline is given for three consecutive days as an IV push. Response to this treatment varies with age, with people aged less than 60 years having better remission rates between 60% and 80%, while older people having lower remission rates between 33% and 60%. Because of the toxic effects of therapy and a greater chance of AML resistance to this induction therapy, different treatment, such as that in clinical trials might be offered to people 60–65 years or older.Acute promyelocytic leukemia is treated with all-trans-retinoic acid (ATRA) and either arsenic trioxide (ATO) monotherapy or an anthracycline. A syndrome similar to disseminated intravascular coagulation can develop during the initial few days of treatment or at the time the leukemia is diagnosed, and treatment can be complicated by a differentiation syndrome characterised by fever, fluid overload and low oxygen levels. Acute promyelocytic leukemia is considered curable. There is insufficient evidence to determine if prescribing ATRA in addition to chemotherapy to adults who have other subtypes of acute myeloid leukaemia is helpful. Consolidation Even after complete remission is achieved, leukemic cells likely remain in numbers too small to be detected with current diagnostic techniques. If no consolidation therapy or further postremission is given, almost all people with AML will eventually relapse.The specific type of postremission therapy is individualized based on a persons prognostic factors (see above) and general health. For good-prognosis leukemias (i.e. inv(16), t(8;21), and t(15;17)), people will typically undergo an additional three to five courses of intensive chemotherapy, known as consolidation chemotherapy. This generally involves cytarabine, with the doses administered being higher in younger patients, who are less likely to develop toxicity related to this treatment. Stem cell transplantation Stem cell transplantation from a donor, called allogenic stem cell transplantation, is usually pursued if the prognosis is not considered favourable, a person can tolerate a transplant and has a suitable donor. The basis of allogenic stem cell transplantation is on a graft versus leukemia effect whereby graft cells stimulate an immune response against leukemia cells. Unfortunately this is accompanied by immune responses against other host organs, called a graft versus host disease. Supportive treatment Support is necessary throughout treatment because of problems associated with AML and also arising from treatment. Blood transfusions, including of red blood cells and platelets, are necessary to maintain health levels, preventing complications of anemia (from low red blood cells) and bleeding (from low platelets). AML leads to an increased risk of infections, particularly drug-resistant strains of bacteria and fungi. Antibiotics and antifungals can be used both to treat and to prevent these infections, particularly quinolones.Adding aerobic physical exercises to the standard of care may result in little to no difference in the mortality, in the quality of life and in the physical functioning. These exercises may result in a slight reduction in depression. Furthermore, aerobic physical exercises probably reduce fatigue.Recent research into the role that epigenetic regulators play in hematopoietic malignancies has yielded new insights in the development of targeted epigenetic therapies as a supportive treatment for AML. The FDA has approved certain epigenetic modifying drugs like ivosidenib and enasidenib, which are used in patients that can no longer receive intensive induction chemotherapy; specifically, they are involved in the therapy of IDH1 and IDH2 mutations. Further research must be done to prove the efficacy of epigenetic treatments, but the development of new epigenetic therapies along with immunotherapies holds potential in the future treatment of AML. In pregnancy AML is rare in pregnancy, affecting about 1 in 75,000 to 100,000 pregnant women. It is diagnosed and treated similarly to AML in non pregnancy, with a recommendation that it is treated urgently. However, treatment has significant implications for the pregnancy. First trimester pregnancy is considered unlikely to be viable; pregnancy during weeks 24 – 36 requires consideration of the benefits of chemotherapy to the mother against the risks to the foetus; and there is a recommendation to consider delaying chemotherapy in very late pregnancy (> 36 weeks). Some elements of supportive care, such as which antibiotics to prevent or treat infections, also change in pregnancy. Medication Olutasidenib (Rezlidhia) was approved for medical use in the United States in December 2022. Prognosis Multiple factors influence prognosis in AML, including the presence of specific mutations, and a person with AMLs age. In the United States between 2011 and 2016, the median survival of a person with AML was 8.5 months, with the 5 year survival being 24%. This declines with age, with the poorer prognosis being associated with an age greater than 65 years, and the poorest prognosis seen in those aged 75–84.As of 2001, cure rates in clinical trials have ranged from 20 to 45%; although clinical trials often include only younger people and those able to tolerate aggressive therapies. The overall cure rate for all people with AML (including the elderly and those unable to tolerate aggressive therapy) is likely lower. Cure rates for APL can be as high as 98%. Subtypes Secondary AML has a worse prognosis, as does treatment-related AML arising after chemotherapy for another previous malignancy. Both of these entities are associated with a high rate of unfavorable genetic mutations. Cytogenetics Different genetic mutations are associated with a difference in outcomes. Certain cytogenetic abnormalities are associated with very good outcomes (for example, the (15;17) translocation in APL). About half of people with AML have "normal" cytogenetics; they fall into an intermediate risk group. A number of other cytogenetic abnormalities are known to associate with a poor prognosis and a high risk of relapse after treatment.A large number of molecular alterations are under study for their prognostic impact in AML. However, only FLT3-ITD, NPM1, CEBPA and c-KIT are currently included in validated international risk stratification schema. These are expected to increase rapidly in the near future. FLT3 internal tandem duplications (ITDs) have been shown to confer a poorer prognosis in AML with normal cytogenetics. Several FLT3 inhibitors have undergone clinical trials, with mixed results. Two other mutations – NPM1 and biallelic CEBPA are associated with improved outcomes, especially in people with normal cytogenetics and are used in current risk stratification algorithms.Researchers are investigating the clinical significance of c-KIT mutations in AML. These are prevalent, and potentially clinically relevant because of the availability of tyrosine kinase inhibitors, such as imatinib and sunitinib that can block the activity of c-KIT pharmacologically. It is expected that additional markers (e.g., RUNX1, ASXL1, and TP53) that have consistently been associated with an inferior outcome will soon be included in these recommendations. The prognostic importance of other mutated genes (e.g., DNMT3A, IDH1, IDH2) is less clear. Other prognostic factors Elevated lactate dehydrogenase level were also associated with poorer outcomes. Use of tobacco is associated with a person having a poorer prognosis, and people who are married and live together have a better prognosis. People who are treated at place with a higher volume of AML have a better prognosis than those who are treated at those in the lowest quartile. As with most forms of cancer, performance status (i.e. the general physical condition and activity level of the person) plays a major role in prognosis as well. Epidemiology AML is a relatively rare cancer. There were 19,950 new cases in the United States in 2016. In 2018, AML accounted for 1.2% of all cancer deaths in the United States.The incidence of AML increases with age and varies between countries. The median age when AML is diagnosed ranges between 63 and 71 years in the UK, Canada, Australia and Sweden, compared with 40 to 45 years in India, Brazil and Algeria.AML accounts for about 90% of all acute leukemias in adults, but is rare in children. The rate of therapy-related AML (AML caused by previous chemotherapy) is expected to rise with an increase in the use of chemotherapy, an ageing population and more patients surviving their initial chemotherapy treatment; therapy-related disease accounts for just under 10% of all cases of AML. AML is slightly more common in men, with a male-to-female ratio of 1.3:1 to 1.4:1. Incidence is also seen to differ by ethnicity, with caucasians having higher recorded incidences and the lowest recorded incidences being in Pacific Islanders and native Alaksans.In the UK, AML accounts for 31% of all leukemia cases, and around 3,100 people were diagnosed with the disease each year in 2016–2018. History The first published description of a case of leukemia in medical literature dates to 1827 when French physician Alfred-Armand-Louis-Marie Velpeau described a 63-year-old florist who developed an illness characterized by fever, weakness, urinary stones, and substantial enlargement of the liver and spleen. Velpeau noted the blood of this person had a consistency "like gruel", and speculated the appearance of the blood was due to white corpuscles. In 1845, a series of people who died with enlarged spleens and changes in the "colors and consistencies of their blood" was reported by the Edinburgh-based pathologist J.H. Bennett; he used the term "leucocythemia" to describe this pathological condition.The term "leukemia" was coined by Rudolf Virchow, the renowned German pathologist, in 1856. As a pioneer in the use of the light microscope in pathology, Virchow was the first to describe the abnormal excess of white blood cells in people with the clinical syndrome described by Velpeau and Bennett. As Virchow was uncertain of the etiology of the white blood cell excess, he used the purely descriptive term "leukemia" (Greek: "white blood") to refer to the condition.Further advances in the understanding of AML occurred rapidly with the development of new technology. In 1877, Paul Ehrlich developed a technique of staining blood films which allowed him to describe in detail normal and abnormal white blood cells. Wilhelm Ebstein introduced the term "acute leukemia" in 1889 to differentiate rapidly progressive and fatal leukemias from the more indolent chronic leukemias. The term "myeloid" was coined by Franz Ernst Christian Neumann in 1869, as he was the first to recognize white blood cells were made in the bone marrow (Greek: μυєλός, myelos, lit. (bone) marrow) as opposed to the spleen. The technique of bone marrow examination to diagnose leukemia was first described in 1879 by Mosler. Finally, in 1900, the myeloblast, which is the malignant cell in AML, was characterized by Otto Naegeli, who divided the leukemias into myeloid and lymphocytic.In 2008, AML became the first cancer genome to be fully sequenced. DNA extracted from leukemic cells were compared to unaffected skin. The leukemic cells contained acquired mutations in several genes that had not previously been associated with the disease. References External links PDQ statement on AML for health professionals at National Cancer Institute