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Kidney malformations in Turner syndrome may be more common in mosaicism than in the full 45,X0 karyotype. Serious complications of the kidney anomalies associated with Turner syndrome are rare, although there is some risk of issues such as obstructive uropathy, where the flow of urine from the kidneys is blocked.Women with Turner syndrome are more likely than average to have high blood pressure; as many as 60% of women with the condition are hypertensive. Isolated diastolic hypertension often precedes systolic hypertension in the condition and may develop at a young age. Treatments for hypertension in Turner syndrome are as in the general population.Approximately 25%–80% of women with Turner syndrome have some level of insulin resistance, and a minority develop type 2 diabetes. The risk of diabetes in Turner syndrome varies by karyotype and appears to be raised by specific deletions of the short arm of the X chromosome (Xp). One study found that while a relatively low 9% of women with Xq (long arm) deletions had type 2 diabetes, 18% of those with full 45,X0 karyotypes did, as well as 23% with Xp deletions. 43% of women with isochromosome Xq, who both lacked the short arm and had an additional copy of the long arm, developed type 2 diabetes. Though part of the diabetes risk in Turner syndrome is a function of weight control, some is independent; age- and weight-matched women with non-Turners ovarian failure have a lower diabetes risk than in Turner syndrome. | This may also manifest itself as a difficulty with motor control or with mathematics. While it is not correctable, in most cases it does not cause difficulty in daily living. Most Turner syndrome patients are employed as adults and lead productive lives. Also, a rare variety of Turner syndrome, known as "Ring-X Turner syndrome", has about a 60% association with intellectual disability. This variety accounts for around 2–4% of all Turner syndrome cases. Psychological
Social difficulties appear to be an area of vulnerability for young women. Counseling affected individuals and their families about the need to carefully develop social skills and relationships may prove useful in advancing social adaptation. Women with Turner syndrome may experience adverse psychosocial outcomes which can be improved through early intervention and the provision of appropriate psychological and psychiatric care. Genetic, hormonal, and medical problems associated with Turner syndrome are likely to affect psychosexual development of female adolescent patients, and thus influence their psychological functioning, behavior patterns, social interactions, and learning ability. Although Turner syndrome constitutes a chronic medical condition, with possible physical, social, and psychological complications in a womans life, hormonal and estrogen replacement therapy, and assisted reproduction, are treatments that can be helpful for Turner syndrome patients and improve their quality of life. Research shows a possible association between age at diagnosis and increased substance use and depressive symptoms. Prenatal
Despite the excellent postnatal prognosis, 99% of Turner syndrome conceptions are thought to end in miscarriage or stillbirth, and as many as 15% of all spontaneous abortions have the 45,X karyotype. | 11
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In September 2012, the FDA approved omacetaxine for the treatment of CML in the case of resistance to other chemotherapeutic agents.Independently, ARIAD pharmaceuticals, adapting the chemical structures from first and second-generation TK inhibitors, arrived at a new pan-BCR-ABL1 inhibitor which showed (for the first time) efficacy against T315I, as well as all other known mutations of the oncoprotein. The drug, ponatinib, gained FDA approval in December 2012 for treatment of patients with resistant or intolerant CML. Just as with second-generation TK inhibitors, early approval is being sought to extend the use of ponatinib to newly diagnosed CML also. Vaccination
In 2005, encouraging but mixed results of vaccination were reported with the BCR/ABL1 p210 fusion protein in patients with stable disease, with GM-CSF as an adjuvant. Prognosis
Before the advent of tyrosine kinase inhibitors, the median survival time for CML patients had been about 3–5 years from time of diagnosis.With the use of tyrosine kinase inhibitors, survival rates have improved dramatically. A 2006 follow-up of 553 patients using imatinib (Gleevec) found an overall survival rate of 89% after five years.A 2011 followup of 832 patients using imatinib who achieved a stable cytogenetic response found an overall survival rate of 95.2% after 8 years, which is similar to the rate in the general population. Fewer than 1% of patients died because of leukemia progression. Epidemiology
United Kingdom
CML accounts for 8% of all leukaemias in the UK, and around 680 people were diagnosed with the disease in 2011. | Callosities arise naturally and are present even in late-term whale fetuses, although the work of lice digging into the surface of the skin may make them more jagged and hard over time.Callosities are found on the upper surface of the whales head, above the eyes, on the jawline and chin and surrounding the blowholes. Callosities form a unique pattern on every right whale and though callosities which are overgrown break off, the patterns do not change over a lifetime. This makes them a very useful tool for the purposes of photo-identification and conservation.The evolutionary significance of callosities is unknown. Male right whales have a higher density of callosities than females. Males have been observed scratching one another with their callosities and it has been suggested by Payne & Dorsey (1983) that they are a sexually dimorphic feature, used for intra-specific sexual aggression. That explanation is not entirely satisfactory, because it does not account for the appearance of callosities in females. It has been proposed that the barnacles attached to callosities are important in helping fend off attacks by orcas. See also
Callus
Notes
References
Steudel, K (1981). "Functional Aspects of Primate Pelvic Structure: A Multivariate Approach" (PDF). American Journal of Physical Anthropology. 55 (3): 399–410. doi:10.1002/ajpa.1330550314. PMID 6791507. Archived from the original (PDF) on 2010-06-10. Retrieved 2009-07-19. Callosities by Mason T. Weinrich in the Encyclopedia of Marine Mammals. ISBN 0-12-551340-2. A Dictionary of Zoology 1999, Oxford University Press 1999
"On Butts and Baboons". Artsibasheva, A. http://monkeybuiznezz.wordpress.com/2012/09/27/on-butts-and-baboons/ | 0-1
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Bowman also attempted to restore vision by pulling on the iris with a fine hook inserted through the cornea and stretching the pupil into a vertical slit, like that of a cat. He reported that he had had a measure of success with the technique, restoring vision to an 18-year-old woman who had previously been unable to count fingers at a distance of 8 inches (20 cm). By 1869, when the pioneering Swiss ophthalmologist Johann Horner wrote a thesis entitled On the treatment of keratoconus, the disorder had acquired its current name. The treatment at that time, endorsed by the leading German ophthalmologist Albrecht von Graefe, was an attempt to physically reshape the cornea by chemical cauterization with a silver nitrate solution and application of a miosis-causing agent with a pressure dressing. In 1888, the treatment of keratoconus became one of the first practical applications of the then newly invented contact lens, when the French physician Eugène Kalt manufactured a glass scleral shell that improved vision by compressing the cornea into a more regular shape. Since the start of the 20th century, research on keratoconus has both improved understanding of the disease and greatly expanded the range of treatment options. The first successful corneal transplantation to treat keratoconus was done in 1936 by Ramón Castroviejo. Society and culture
According to the findings of the Collaborative Longitudinal Evaluation of Keratoconus (CLEK), people who have keratoconus could be expected to pay more than $25,000 over their lifetime post-diagnosis, with a standard deviation of $19,396. | There is very low quality evidence indicating that doxycycline use may be associated with an increased risk of indigestion, photosensitivity, vomiting, and yeast infections, when compared with mefloquine and atovaquone-proguanil. Causal prophylaxis
Causal prophylactics target not only the blood stages of malaria, but the initial liver stage as well. This means that the user can stop taking the drug seven days after leaving the area of risk. Malarone and primaquine are the only causal prophylactics in current use. Regimens
Specific regimens are recommended by the WHO, UK HPA and CDC for prevention of P. falciparum infection. HPA and WHO advice are broadly in line with each other (although there are some differences). CDC guidance frequently contradicts HPA and WHO guidance. These regimens include:
doxycycline 100 mg once daily (started one day before travel, and continued for four weeks after returning);
mefloquine 250 mg once weekly (started two-and-a-half weeks before travel, and continued for four weeks after returning);
atovaquone/proguanil (Malarone) 1 tablet daily (started one day before travel, and continued for 1 week after returning). Can also be used for therapy in some cases.In areas where chloroquine remains effective:
chloroquine 300 mg once weekly, and proguanil 200 mg once daily (started one week before travel, and continued for four weeks after returning);
hydroxychloroquine 400 mg once weekly (started one to two weeks before travel and continued for four weeks after returning)What regimen is appropriate depends on the person who is to take the medication as well as the country or region travelled to. | 0-1
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Drowning in saltwater can leave significantly different concentrations of sodium and chloride ions in the left and right chambers of the heart, but they will dissipate if the person survived for some time after the aspiration, or if CPR was attempted, and have been described in other causes of death.Most autopsy findings relate to asphyxia and are not specific to drowning. The signs of drowning are degraded by decomposition. Large amounts of froth will be present around the mouth and nostrils and in the upper and lower airways in freshly drowned bodies. The volume of froth is generally much greater in drowning than from other origins. Lung density may be higher than normal, but normal weights are possible after cardiac arrest or vasovagal reflex. The lungs may be overinflated and waterlogged, filling the thoracic cavity. The surface may have a marbled appearance, with darker areas associated with collapsed alveoli interspersed with paler aerated areas. Fluid trapped in the lower airways may block the passive collapse that is normal after death. Hemorrhagic bullae of emphysema may be found. These are related to the rupture of alveolar walls. These signs, while suggestive of drowning, are not conclusive. Prevention
It is estimated that more than 85% of drownings could be prevented by supervision, training in water skills, technology, and public education. Surveillance: Watching the swimmers is a basic task, because drownings can be silent and unnoticed: a person drowning may not always be able to attract attention, often because they have become unconscious. Surveillance of children is especially important. | Furthermore, splints and braces can be used to support limbs and joints to prevent or treat complications such as contractures and spasticity. The rehabilitation healthcare team should also educate the patient and their family on common stroke symptoms and how to manage an onset of stroke. Continuing follow-up with a physician is essential so that the physician may monitor medication dosage and risk factors. Epidemiology
It is estimated that lacunar infarcts account for 25% of all ischemic strokes, with an annual incidence of approximately 15 per 100,000 people. They may be more frequent in men and in people of African, Mexican, and Hong Kong Chinese descent. References
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As their TIC progresses, these animals will have worsening heart function (e.g. : reduced cardiac output and reduced ejection fraction) for 3–5 weeks. The worsened heart function then persists at a stable state until the heart rate is returned to normal. With normal heart rates, these animals begin to demonstrate improving heart function at 1–2 days, and even complete recovery of ejection fraction at 1 month.Human studies of the timecourse of TIC are not as robust as animal studies, though current studies suggest that the majority of people with TIC will recover a significant degree of heart function over months to years. Causes
TIC has been associated with supraventricular tachycardia (SVT), ventricular tachycardia (VT), frequent premature ventricular contractions (PVCs), rapid atrial and ventricular pacing, and left bundle branch block. The types of SVT associated with TIC include atrial fibrillation, atrial flutter, incessant atrial tachycardia, permanent junctional reciprocating tachycardia, atrioventricular reciprocating tachycardia, and atrioventricular nodal reentry tachycardia. Atrial fibrillation is the most common and well-studied etiology of TIC. Diagnosis
There are no specific diagnostic criteria for TIC, and it can be difficult to diagnose for a number of reasons. First, in patients presenting with both tachycardia and cardiomyopathy, it can be difficult to distinguish which is the causative agent. Additionally, it can occur in patients with or without underlying structural heart disease. Previously normal left ventricular ejection fraction or left ventricular systolic dysfunction out of proportion to a patient’s underlying cardiac disease can be important clues to possible TIC. | Studies indicate that women are more likely to be affected than men, and that the risk decreases with advancing age. There is some evidence that people with Asian ancestry may develop motion sickness more frequently than people of European ancestry, and there are situational and behavioral factors, such as whether a passenger has a view of the road ahead, and diet and eating behaviors. See also
Mal de debarquement - disembarkment syndrome, usually follows a cruise or other motion experience
References
External links
Davis, Christopher J.; Lake-Bakaar, Gerry V.; Grahame-Smith, David G. (2012). Nausea and Vomiting: Mechanisms and Treatment. Springer Science & Business Media. p. 123. ISBN 978-3-642-70479-6. Motion Sickness from MedlinePlus | 0-1
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Environmental conditions
Cold exposure and stay at high altitude may lead to type 1 or type 2 phenotype, depending on duration and other boundary conditions (which determine whether or not stress is associated with energy deprivation). Diagnosis
Affected patients may have normal, low, or slightly elevated TSH depending on the spectrum and phase of illness. Total T4 and T3 levels may be altered by binding protein abnormalities, and medications. Reverse T3 levels are generally increased, while FT3 is decreased. FT4 levels may have a transient increase, before becoming subnormal during severe illness. Correspondingly, in the majority of cases calculated sum activity of peripheral deiodinases (SPINA-GD) is reduced. Generally the levels of free T3 will be lowered, followed by the lowering of free T4 in more severe disease. Several studies described elevated concentrations of 3,5-T2, an active thyroid hormone, in NTIS. 3,5-T2 levels were also observed to correlate with concentrations of rT3 (reverse T3) in patients with euthyroid sick syndrome. NTIS is a component of a complex endocrine adaptation process, so affected patients might also have hyperprolactinemia and elevated levels of corticosteroids (especially cortisol) and growth hormone. NTIS can be difficult to distinguish from other forms of thyroid dysfunction in the hospital setting. Both NTIS and primary hypothyroidism may have reduced fT3 and fT4, and elevated TSH (which is common in the hospital, during the recovery phase of NTIS). Prescribing thyroxine to treat this may lead to lifelong thyroid overtreatment.Hyperthyroidism may be assumed due to decreased TSH and a transient fT4 increase. | In some cases, this can be distinguished from NTIS by a thyroid ultrasound, which is commonly available in the hospital intensive care unit.NTIS looks similar to central hypopituitarism; both frequently have reduced TSH and thyroid hormone levels. Treatment
Debate is ongoing as to whether NTIS is an adaptive or maladaptive mechanism in response to physiological stress. Some sources indicate that NTIS is beneficial as an acute-phase response, but detrimental during the chronic phase of illness. Several trials have investigated a possible therapy for NTIS, but they yielded inconsistent and partly contradictory results. This may be due to the heterogeneity of investigated populations, and to the lack of a consistent definition of NTIS.Administering exogenous T3 and T4 has variable results, but overall seems to confer no improvements to health outcome. Administering TRH to patients with chronic illness, however, seems to normalize thyroid levels and improve catabolic function.When NTIS is caused by the normal fasting response to illness, early parenteral nutrition has been shown to attenuate alterations in thyroid hormone (TSH, T3, T4, rT3) levels, whereas late parenteral nutrition exacerbates it. Late parenteral nutrition, though, also reduced complications and accelerated recovery in one study. History
In 1968, a reduced T4 half-life in athletes was discovered. This was the first awareness of thyroid hormone concentration alterations that were not a result of thyroid gland or pituitary dysfunction. In 1971, they also found a transient increase in T4 during bicycle training.In 1973, Rothenbuchner et al. discovered that starvation is correlated with reduced T3 concentration. | 11
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Surveys show a particular distribution pattern with large clusters and frequencies of gene mutations along the western European coastline. This led the development of the "Viking Hypothesis". Cluster locations and mapped patterns of this mutation correlate closely to the locations of Viking settlements in Europe established c.700 AD to c.1100 AD. The Vikings originally came from Norway, Sweden and Denmark. Viking ships made their way along the coastline of Europe in search of trade, riches, and land. Genetic studies suggest that the extremely high frequency patterns in some European countries are the result of migrations of Vikings and later Normans, indicating a genetic link between hereditary haemochromatosis and Viking ancestry. Modern times
In 1865, Armand Trousseau (a French internist) was one of the first to describe many of the symptoms of a diabetic patient with cirrhosis of the liver and bronzed skin color. The term haemochromatosis was first used by German pathologist Friedrich Daniel von Recklinghausen in 1889 when he described an accumulation of iron in body tissues. Identification of genetic factors
Although it was known most of the 20th century that most cases of haemochromatosis were inherited, they were incorrectly assumed to depend on a single gene.In 1935 J.H. Sheldon, a British physician, described the link to iron metabolism for the first time as well as demonstrating its hereditary nature.In 1996 Felder and colleagues identified the haemochromatosis gene, HFE gene. Felder found that the HFE gene has two main mutations, C282Y and H63D, which were the main cause of hereditary haemochromatosis. | In 2003 Teva partnered with Eisai, giving Eisai the right to jointly market the drug for Parkinsons in the US, and to co-develop and co-market the drug for Alzheimers and other neurological diseases.It was approved by the European Medicines Agency for Parkinsons in 2005 and in the US in 2006.: 255
Research
Rasagiline was tested for efficacy in people with multiple system atrophy in a large randomized, placebo-controlled, double-blind disease-modification trial; the drug failed.Teva conducted clinical trials attempting to prove that rasagiline did not just treat symptoms, but was a disease-modifying drug - that it actually prevented the death of the dopaminergic neurons that characterize Parkinsons disease and slowed disease progression. They conducted two clinical trials, called TEMPO and ADAGIO, to try to prove this. The FDA advisory committee rejected their claim in 2011, saying that the clinical trial results did not prove that rasagiline was neuroprotective. The main reason was that in one of the trials, the lower dose was effective at slowing progression, but the higher dose was not, and this made no sense in light of standard dose-response pharmacology. See also
Selegiline
Ladostigil
References
External links
"Rasagiline". Drug Information Portal. U.S. National Library of Medicine. "Rasagiline mesylate". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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It can cause paranoid and grandiose delusions, agitation, hallucinations (visual and auditory), bizarre behavior, fear, short-term memory loss, and confusion.HIV encephalopathy can lead to dementia. Types
There are many types of encephalopathy. Some examples include:
Mitochondrial encephalopathy: Metabolic disorder caused by dysfunction of mitochondrial DNA. Can affect many body systems, particularly the brain and nervous system. Glycine encephalopathy: A genetic metabolic disorder involving excess production of glycine. Hepatic encephalopathy: Arising from advanced cirrhosis of the liver. Hypoxic ischemic encephalopathy: Permanent or transitory encephalopathy arising from severely reduced oxygen delivery to the brain. Static encephalopathy: Unchanging, or permanent, brain damage, usually caused by prenatal exposure to ethanol. Uremic encephalopathy: Arising from high levels of toxins normally cleared by the kidneys—rare where dialysis is readily available. Wernickes encephalopathy: Arising from thiamine (B1) deficiency, usually in the setting of alcoholism. Hashimotos encephalopathy: Arising from an auto-immune disorder. Anti-NMDA receptor encephalitis: An auto-immune encephalitis. Hyperammonemia: a condition caused by high levels of ammonia, which is due to inborn errors of metabolism (including urea cycle disorder or multiple carboxylase deficiency), a diet with excessive levels of protein, deficiencies of specific nutrients such as arginine or biotin, or organ failure. Hypertensive encephalopathy: Arising from acutely increased blood pressure. Chronic traumatic encephalopathy: a progressive degenerative disease associated with multiple concussions and other forms of brain injury
Lyme encephalopathy: Arising from Lyme disease bacteria, including Borrelia burgdorferi. Toxic encephalopathy: A form of encephalopathy caused by chemicals and prescription drugs, often resulting in permanent brain damage. | Toxic-metabolic encephalopathy: A catch-all for brain dysfunction caused by infection, organ failure, or intoxication. Transmissible spongiform encephalopathy: A collection of diseases all caused by prions, and characterized by "spongy" brain tissue (riddled with holes), impaired locomotion or coordination, and a 100% mortality rate. Includes bovine spongiform encephalopathy (mad cow disease), scrapie, and kuru among others. Neonatal encephalopathy (hypoxic-ischemic encephalopathy): An obstetric form, often occurring due to lack of oxygen in bloodflow to brain-tissue of the fetus during labour or delivery. Salmonella encephalopathy: A form of encephalopathy caused by food poisoning (especially out of peanuts and rotten meat) often resulting in permanent brain damage and nervous system disorders. Encephalomyopathy: A combination of encephalopathy and myopathy. Causes may include mitochondrial disease (particularly MELAS) or chronic hypophosphatemia, as may occur in cystinosis. Creutzfeldt–Jakob disease (CJD; transmissible spongiform encephalopathy). HIV encephalopathy (encephalopathy associated with HIV infection and AIDS, characterized by atrophy and ill-defined white matter hyperintensity). Sepsis-associated encephalopathy (this type can occur in the setting of apparent sepsis, trauma, severe burns, or trauma, even without clear identification of an infection). Epileptic encephalopathies:
Early infantile epileptic encephalopathy (acquired or congenital abnormal cortical development). Early myoclonic epileptic encephalopathy (possibly due to metabolic disorders). Gluten encephalopathy: Focal abnormalities of the white matter (generally area of low perfusion) are appreciated through magnetic resonance. Migraine is the most common symptom reported. Toxicity from chemotherapy
Chemotherapy medication, for example, fludarabine can cause a
permanent severe global encephalopathy. | 11
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Recent findings have also identified blunted activity in anterior cingulate cortex, striatum, orbitofrontal cortex, and insula in mothers with PPD when viewing images of their own infants.More robust studies on neural activation regarding PPD have been conducted with rodents than humans. These studies have allowed for greater isolation of specific brain regions, neurotransmitters, hormones, and steroids. Onset and duration
Postpartum depression onset usually begins between two weeks to a month after delivery. A study done at an inner-city mental health clinic has shown that 50% of postpartum depressive episodes there began prior to delivery. Therefore, in the DSM-5 postpartum depression is diagnosed under "depressive disorder with peripartum onset", in which "peripartum onset" is defined as anytime either during pregnancy or within the four weeks following delivery. PPD may last several months or even a year. Postpartum depression can also occur in women who have suffered a miscarriage. For fathers, several studies show that men experience the highest levels of postpartum depression between 3–6 months postpartum. Parent-infant relationship
Postpartum depression can interfere with normal maternal-infant bonding and adversely affect acute and longterm child development. Postpartum depression may lead mothers to be inconsistent with childcare. These childcare inconsistencies may include feeding routines, sleep routines, and health maintenance.In rare cases, or about 1 to 2 per 1,000, the postpartum depression appears as postpartum psychosis. In these, or among women with a history of previous psychiatric hospital admissions, infanticide may occur. | The NICHD has worked alongside organizations like the World Health Organization to conduct research on the psychosocial development of children with part of their efforts going towards the support of mothers health and safety. Training and education services are offered through the NICHD to equip women and their health care providers with evidence-based knowledge on PPD.Other initiatives include the Substance Abuse and Mental Health Services Administration (SAMHSA) whose disaster relief program provides medical assistance at both the national and local level. The disaster relief fund not only helps to raise awareness of the benefits of having healthcare professionals screen for PPD, but also helps childhood professionals (home visitors and early care providers) develop the skills to diagnose and prevent PPD. The Infant and Early Childhood Mental Health Consultation (IECMH) center is a related technical assistance program that utilizes evidence-based treatments services in order to address issues of PPD. The IECMH facilitates parenting and home visit programs, early care site interventions with parents and children and a variety of other consultation-based services. The IECMHs initiatives seek to educate home visitors on screening protocols for PPD as well as ways to refer depressed mothers to professional help. Links to government-funded programs
National Child and Maternal Health Education Program
National Institute of Child Health and Human Development
Substance Abuse and Mental Health Services Administration
Infant and Early Childhood Mental Health Consultation Center
Psychotherapy
Therapeutic methods of intervention can begin as early as a few days post-birth when most mothers are discharged from hospitals. | 11
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Unfortunately, due to the progressive nature of the disease, recurrence is common (60% recurrence rate), with the creation of new arrhythmogenic foci. Indications for catheter ablation include drug-refractory VT and frequent recurrence of VT after ICD placement, causing frequent discharges of the ICD. Implantable cardioverter-defibrillator
An ICD is the most effective prevention against sudden cardiac death. Due to the prohibitive cost of ICDs, they are not routinely placed in all individuals with ACM. Indications for ICD placement in the setting of ACM include:
Cardiac arrest due to VT or VF
Symptomatic VT that is not inducible during programmed stimulation
Failed programmed stimulation-guided drug therapy
Severe RV involvement with poor tolerance of VT
Sudden death of immediate family memberSince ICDs are typically placed via a transvenous approach into the right ventricle, there are complications associated with ICD placement and follow-up. Due to the extreme thinning of the RV free wall, it is possible to perforate the RV during implantation, potentially causing pericardial tamponade. Because of this, every attempt is made at placing the defibrillator lead on the ventricular septum. After a successful implantation, the progressive nature of the disease may lead to fibro-fatty replacement of the myocardium at the site of lead placement. This may lead to undersensing of the individuals electrical activity (potentially causing inability to sense VT or VF), and inability to pace the ventricle. Heart transplant
Heart transplant may be performed in ACM. It may be indicated if the arrhythmias associated with the disease are uncontrollable or if there is severe bi-ventricular heart failure that is not manageable with pharmacological therapy. | Late gadolinium enhancement shows increased signal of the midwall at the inferolateral wall of the base of the left ventricle, usually in the non-hypertrophic ventricle. T1-weighted imaging can show low T1 signal due to sphingolipid storage in the heart even without ventricular hypertrophy in 40% of the those affected by the disease. Thus, MRI is a useful way of diagnosing the disease early. T2 signal is increased in inflammation and oedema. Treatment
The treatments available for Fabry disease can be divided into therapies that aim to correct the underlying problem of decreased activity of the alpha galactosidase A enzyme and thereby reduce the risk of organ damage, and therapies to improve symptoms and life expectancy once organ damage has already occurred. Therapies targeting enzyme activity
Enzyme replacement therapy is designed to provide the enzyme the patient is missing as a result of a genetic malfunction. This treatment is not a cure, but can partially prevent disease progression, and potentially reverse some symptoms. As of March 2022, two medical drugs based on enzyme replacement therapy are available for Fabry disease:
Agalsidase alfa, sold under the brand name Replagal by the company Takeda (since its acquisition of the company Shire), is a recombinant form of alpha-galactosidase A It received approval in the EU in 2001. FDA approval was applied for the United States. However, Shire withdrew their application for approval in the United States in 2012, citing that the agency will require additional clinical trials before approval. As of March 2022, Replagal has not received FDA approval. | 0-1
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Cannabis is mostly used recreationally or as a medicinal drug, although it may also be used for spiritual purposes. In 2013, between 128 and 232 million people used cannabis (2.7% to 4.9% of the global population between the ages of 15 and 65). It is the most commonly used illegal drug in the world, though it is legal in some jurisdictions, with the highest use among adults (as of 2018) in Zambia, the United States, Canada, and Nigeria.While cannabis plants have been grown since at least the 3rd millennium BCE, evidence suggests that it was being smoked for psychoactive effects at least 2,500 years ago in the Pamir Mountains, Asia. Since the early 20th century, cannabis has been subject to legal restrictions. The possession, use, and cultivation of cannabis is illegal in most countries. In 2013, Uruguay became the first country to legalize recreational use of cannabis. Other countries to do so are Canada, Georgia, Malta, Mexico, and South Africa. In the United States, the recreational use of cannabis is legal in 19 states, two territories, and the District of Columbia, though the drug remains federally illegal. Uses
Medical
Medical cannabis, or medical marijuana, refers to the use of cannabis to treat disease or improve symptoms; however, there is no single agreed-upon definition (e.g., cannabinoids derived from cannabis and synthetic cannabinoids are also used). The rigorous scientific study of cannabis as a medicine has been hampered by production restrictions and by the fact that it is classified as an illegal drug by many governments. | They have also been shown to protect mice from a lethal challenge with several TBE-virus isolates obtained over a period of more than 30 years from all over Europe and the Asian part of the former Soviet Union. In addition, it has been demonstrated that antibodies induced by vaccination of human volunteers neutralized all tested isolates. Pregnancy and breastfeeding
The vaccine appears to be safe during pregnancy, but because of insufficient data the vaccine is only recommended during pregnancy and breastfeeding when it is considered urgent to achieve protection against TBE infection and after careful consideration of risks versus benefits. Schedule
Two to three doses are recommended depending on the formulation. Typically one to three months should occur between the first doses followed by five to twelve months before the final dose. Additional doses are then recommended every three to five years. A study from 2006 suggests that the FSME-Immun/Ticovac and Encepur are interchangeable for booster vaccination, but cautions against change during the primary immunization course. History
The first vaccine against TBE was prepared in 1937 in the brains of mice. Some 20 years later TBE vaccines derived from cell cultures (chicken embryo fibroblast cells) were developed and used for active immunization in humans in the former Soviet Union. Later, a purified, inactivated virus vaccine was developed which proved to be more immunogenic than previous TBE vaccines. Society and culture
Economics
Per dose it costs between £50 and £70 in the United Kingdom. Brand names
Brand names of the vaccines include Encepur N, FSME-Immun CC and Ticovac, Encevir-Neo, Klesh-E-Vak. | 0-1
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Two common methods to help are electroconvulsive therapy and repetitive transcranial magnetic stimulation (rTMS). Electroconvulsive therapy or ECT has been shown to reduce psychotic symptoms associated with schizophrenia, mania, and depression, and is often used in psychiatric hospitals. Transcranial magnetic stimulation when used to treat auditory hallucinations in patients with schizophrenia is done at a low frequency of 1 Hertz to the left temporoparietal cortex. History
Ancient history
Presentation
In the ancient world, auditory hallucinations were often viewed as either a gift or curse by God or the gods (depending on the specific culture). According to the Greek historian Plutarch, during the reign of Tiberius (A.D. 14–37), a sailor named Thamus heard a voice cry out to him from across the water, "Thamus, are you there? When you reach Palodes, take care to proclaim that the great god Pan is dead. "The oracles of ancient Greece were known to experience auditory hallucinations while breathing in certain neurologically active vapors (such as the smoke from bay leaves), while the more pervasive delusions and symptomatology were often viewed as possession by demonic forces as punishment for misdeeds. Treatments
Treatment in the ancient world is ill-documented, but there are some cases of therapeutics being used to attempt treatment, while the common treatment was sacrifice and prayer in an attempt to placate the gods. During the Middle Ages, those with auditory hallucinations were sometimes subjected to trepanning or trial as a witch. | Pipecolic acidemia is a very rare autosomal recessive metabolic disorder that is caused by a peroxisomal defect. Pipecolic acidemia can also be an associated component of Refsum disease with increased pipecolic acidemia (RDPA), as well as other peroxisomal disorders, including both infantile and adult Refsum disease, and Zellweger syndrome.The disorder is characterized by an increase in pipecolic acid levels in the blood, leading to neuropathy and hepatomegaly. See also
AASDHPPT
PHYH
References
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History
The first known mention of this disease is from a 1700 BCE Egyptian papyrus, which advises: "... Thou shouldest give a recipe, an ointment of great protection; acacia leaves, ground, titurated and cooked together. Smear a strip of fine linen there-with and place in the anus, that he recovers immediately." In 460 BCE, the Hippocratic corpus discusses a treatment similar to modern rubber band ligation: "And hemorrhoids in like manner you may treat by transfixing them with a needle and tying them with very thick and woolen thread, for application, and do not foment until they drop off, and always leave one behind; and when the patient recovers, let him be put on a course of Hellebore." Hemorrhoids may have been described in the Bible, with earlier English translations using the now-obsolete spelling "emerods".Celsus (25 BCE – 14 CE) described ligation and excision procedures and discussed the possible complications. Galen advocated severing the connection of the arteries to veins, claiming it reduced both pain and the spread of gangrene. The Susruta Samhita (4th–5th century BCE) is similar to the words of Hippocrates, but emphasizes wound cleanliness. In the 13th century, European surgeons such as Lanfranc of Milan, Guy de Chauliac, Henri de Mondeville, and John of Ardene made great progress and development of the surgical techniques.In medieval times, hemorrhoids were also known as Saint Fiacres curse after a sixth-century saint who developed them following tilling the soil. | Current prescribing guidelines in the United States list only the treatment of androgen deficiency in males and breast cancer in females as indications.Fluoxymesterone is less effective in inducing masculinization than testosterone, but is useful for maintaining established masculinization in adults. Available forms
Fluoxymesterone is available in the form of 2, 5, and 10 mg oral tablets. Non-medical uses
Fluoxymesterone is used for physique- and performance-enhancing purposes by competitive athletes, bodybuilders, and powerlifters. Side effects
Side effects that have been associated with fluoxymesterone include acne, edema, seborrhea/seborrheic dermatitis, alopecia, hirsutism, voice deepening, virilization in general, flushing, gynecomastia, breast pain, menstrual disturbances, hypogonadism, testicular atrophy, clitoral enlargement, penile enlargement, priapism, increased aggressiveness, prostate enlargement, cardiovascular toxicity, and hepatotoxicity, among others. Pharmacology
Pharmacodynamics
As an AAS, fluoxymesterone is an agonist of the androgen receptor (AR), similarly to androgens like testosterone and DHT. It is a substrate for 5α-reductase like testosterone, and so is potentiated in so-called "androgenic" tissues like the skin, hair follicles, and prostate gland via transformation into 5α-dihydrofluoxymesterone. As such, fluoxymesterone has a relatively poor ratio of anabolic to androgenic activity similarly to testosterone and methyltestosterone. However, fluoxymesterone is nonetheless proportionally less androgenic and more anabolic than methyltestosterone and testosterone.Fluoxymesterone has been reported to be non-aromatizable due to steric hindrance by its C11β hydroxyl group, and hence is not considered to have a propensity for producing estrogenic effects such as gynecomastia or fluid retention. | 0-1
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Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies. Stage 2: Mild reduction in GFR (60–89 mL/min/1.73 m2) with kidney damage. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies. Stage 3: Moderate reduction in GFR (30–59 mL/min/1.73 m2):. British guidelines distinguish between stage 3A (GFR 45–59) and stage 3B (GFR 30–44) for purposes of screening and referral. Stage 4: Severe reduction in GFR (15–29 mL/min/1.73 m2) Preparation for kidney replacement therapy. Stage 5: Established kidney failure (GFR <15 mL/min/1.73 m2), permanent kidney replacement therapy, or end-stage kidney disease.The term "non-dialysis-dependent chronic kidney disease" (NDD-CKD) is a designation used to encompass the status of those persons with an established CKD who do not yet require the life-supporting treatments for kidney failure known as kidney replacement therapy (RRT, including maintenance dialysis or kidney transplantation). The condition of individuals with CKD, who require either of the two types of kidney replacement therapy (dialysis or transplant), is referred to as the end-stage kidney disease (ESKD). Hence, the start of the ESKD is practically the irreversible conclusion of the NDD-CKD. Even though the NDD-CKD status refers to the status of persons with earlier stages of CKD (stages 1 to 4), people with advanced stage of CKD (stage 5), who have not yet started kidney replacement therapy, are also referred to as NDD-CKD. | Most agree that nephrology referral is required by Stage 4 CKD (when eGFR/1.73m2 is less than 30 mL/min; or decreasing by more than 3 mL/min/year).It may also be useful at an earlier stage (e.g. CKD3) when urine albumin-to-creatinine ratio is more than 30 mg/mmol, when blood pressure is difficult to control, or when hematuria or other findings suggest either a primarily glomerular disorder or secondary disease amenable to specific treatment. Other benefits of early nephrology referral include proper education regarding options for kidney replacement therapy as well as pre-emptive transplantation, and timely workup and placement of an arteriovenous fistula in those people with chronic kidney disease opting for future hemodialysis. Renal replacement therapy
At stage 5 CKD, kidney replacement therapy is usually required, in the form of either dialysis or a kidney transplant. In CKD numerous uremic toxins accumulate in the blood. Even when ESKD (largely synonymous with CKD5) is treated with dialysis, the toxin levels do not go back to normal as dialysis is not that efficient. Similarly, after a kidney transplant, the levels may not go back to normal as the transplanted kidney may not work 100%. If it does, the creatinine level is often normal. The toxins show various cytotoxic activities in the serum and have different molecular weights, and some of them are bound to other proteins, primarily to albumin. Uremic toxins are classified into three groups as small water-soluble solutes, middle molecular-weight solutes, and protein-bound solutes. | 11
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This prevents the batsman from playing shots on the leg side, whilst most of the off side is covered by fielders. The goal is to slow the scoring and frustrate the batsmen into an opportunity for a catch. The opposite of leg theory. Offer the light
Under historical rules, offering the light was the act of the umpires giving the batsmen the choice of whether or not to leave the field during times of bad light. Offering the light has disappeared from the game since 2010, the decision of whether or not to leave the field for bad light is made solely by the umpires. Olympic
Five consecutive ducks. The term alludes to the five interlocking Olympic rings. See also Audi. On side
see leg side. The opposite of off side. On a length
a delivery bowled on a good length. On strike
the batsman currently facing the bowling attack is said to be on strike. On the [shot name]
used to describe the type of shot that fielders are placed in order to intercept. For example, "three men on the hook" means three fielders who are placed behind square leg to catch the ball if the hook shot is used. "On the drive" is a similar term used for any type of drive, so generally within a straight V in front of the batsman. On the up
a batsman playing a shot, usually a drive, to a ball that is quite short and has already risen to knee height or more as the shot is played. | It has been reported in elderly but is vanishingly rare. It is most prevalent in Caucasians, and affects males twice as often as females. In other populations too the prevalence in males is slightly more than in females.LCH is usually a sporadic and non-hereditary condition but familial clustering has been noted in limited number of cases. Hashimoto-Pritzker disease is a congenital self-healing variant of Hand-Schüller-Christian disease. Culture
In the 10th episode of season 3 of House entitled "Merry Little Christmas", the primary patient is a girl with dwarfism who has a variety of symptoms, who is ultimately diagnosed with Langerhans cell histiocytosis. Also in the 5th episode, season 1 of "The Good Doctor", Dr. Murphy tries to diagnose Langerhans cell histiocytosis in a boy with a previously diagnosed osteosarcoma.In an episode of Mystery Diagnosis, "The Woman Who Saw Pink", Brooke Rohrer has experiencing symptoms of abdominal pain, was diagnosed with Langerhans cell histiocytosis. Nomenclature
Langerhans cell histiocytosis is occasionally misspelled as "Langerhan" or "Langerhans" cell histiocytosis, even in authoritative textbooks. The name, however, originates back to its discoverer, Paul Langerhans. References
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Vollum 1B is widely believed to have been isolated from William A. Boyles, a 46-year-old scientist at the US Army Biological Warfare Laboratories at Camp (later Fort) Detrick, Maryland, who died in 1951 after being accidentally infected with the Vollum strain. US Air Force researchers have developed a vaccine strain to produce an improved anthrax vaccine which requires a minimal number of injections to achieve and maintain long-term immunity. It is designated as the Alls/Gifford (Curlicue) strain. Society and culture
Site cleanup
Anthrax spores can survive for very long periods of time in the environment after release. Chemical methods for cleaning anthrax-contaminated sites or materials may use oxidizing agents such as peroxides, ethylene oxide, Sandia Foam, chlorine dioxide (used in the Hart Senate Office Building), peracetic acid, ozone gas, hypochlorous acid, sodium persulfate, and liquid bleach products containing sodium hypochlorite. Nonoxidizing agents shown to be effective for anthrax decontamination include methyl bromide, formaldehyde, and metam sodium. These agents destroy bacterial spores. All of the aforementioned anthrax decontamination technologies have been demonstrated to be effective in laboratory tests conducted by the US EPA or others.Decontamination techniques for Bacillus anthracis spores are affected by the material with which the spores are associated, environmental factors such as temperature and humidity, and microbiological factors such as the spore species, anthracis strain, and test methods used.A bleach solution for treating hard surfaces has been approved by the EPA. Chlorine dioxide has emerged as the preferred biocide against anthrax-contaminated sites, having been employed in the treatment of numerous government buildings over the past decade. | Anthrax in livestock grazing on open range where they mix with wild animals still occasionally occurs in the United States and elsewhere.Many workers who deal with wool and animal hides are routinely exposed to low levels of anthrax spores, but most exposure levels are not sufficient to develop anthrax infections. A lethal infection is reported to result from inhalation of about 10,000–20,000 spores, though this dose varies among host species. Little documented evidence is available to verify the exact or average number of spores needed for infection. Mode of infection
Anthrax can enter the human body through the intestines (ingestion), lungs (inhalation), or skin (cutaneous) and causes distinct clinical symptoms based on its site of entry. In general, an infected human is quarantined. However, anthrax does not usually spread from an infected human to an uninfected human. If the disease is fatal to the persons body, though, its mass of anthrax bacilli becomes a potential source of infection to others and special precautions should be used to prevent further contamination. Inhalational anthrax, if left untreated until obvious symptoms occur, is usually fatal.Anthrax can be contracted in laboratory accidents or by handling infected animals, their wool, or their hides. It has also been used in biological warfare agents and by terrorists to intentionally infect as exemplified by the 2001 anthrax attacks. Mechanism
The lethality of the anthrax disease is due to the bacteriums two principal virulence factors: the poly-D-glutamic acid capsule, which protects the bacterium from phagocytosis by host neutrophils, and the tripartite protein toxin, called anthrax toxin. | 11
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He writes, "the roots of child abuse lie not in parental psycho-pathology or in socio-environmental stress (though their influences cannot be discounted) but in a sick culture which denigrates and depersonalizes, which reduces children to property, to sexual objects so that they become the legitimate victims of both adult violence and lust". Worldwide
Child abuse is an international public health crisis. Poverty and substance use disorders are common social problems worldwide, and no matter the location, show a similar trend in the correlation to child abuse. Differences in cultural perspectives play a significant role in how children are treated. Laws reflect the populations views on what is acceptable - for example whether child corporal punishment is legal or not.A study conducted by members from several Baltic and Eastern European countries, together with specialists from the United States, examined the causes of child abuse in the countries of Latvia, Lithuania, Macedonia and Moldova. In these countries, respectively, 33%, 42%, 18% and 43% of children reported at least one type of child abuse. According to their findings, there was a series of correlations between the potential risk factors of parental employment status, alcohol abuse, and family size within the abuse ratings. In three of the four countries, parental substance use was considerably correlated with the presence of child abuse, and although it was a lower percentage, still showed a relationship in the fourth country (Moldova). Each country also showed a connection between the father not working outside of the home and either emotional or physical child abuse. | A study on child abuse sought to determine: the forms of child abuse perpetrated on children with disabilities; the extent of child abuse; and the causes of child abuse of children with disabilities. A questionnaire on child abuse was adapted and used to collect data in this study. Participants comprised a sample of 31 pupils with disabilities (15 children with vision impairment and 16 children with hearing impairment) selected from special schools in Botswana. The study found that the majority of participants were involved in doing domestic chores. They were also sexually, physically and emotionally abused by their teachers. This study showed that children with disabilities were vulnerable to child abuse in their schools.Substance use disorder can be a major contributing factor to child abuse. One U.S. study found that parents with documented substance use, most commonly alcohol, cocaine, and heroin, were much more likely to mistreat their children, and were also much more likely to reject court-ordered services and treatments. Another study found that over two-thirds of cases of child maltreatment involved parents with substance use disorders. This study specifically found relationships between alcohol and physical abuse, and between cocaine and sexual abuse. Also, parental stress caused by substance increases the likelihood of the minor exhibiting internalizing and externalizing behaviors. Although the abuse victim does not always realize the abuse is wrong, the internal confusion can lead to chaos. Inner anger turns to outer frustration. Once aged 17/18, drink and drugs are used to numb the hurt feelings, nightmares, and daytime flashbacks. | 11
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An opioid overdose is toxicity due to excessive consumption of opioids, such as morphine, codeine, heroin, fentanyl, tramadol, and methadone. This preventable pathology can be fatal if it leads to respiratory depression, a lethal condition that can cause hypoxia. Other symptoms include insufficient breathing, small pupils (with the exception of pethidine, where there may be dilated pupils), and unconsciousness, however its onset can depend on the method of ingestion, the dosage and individual risk factors. Although there were over 110,000 deaths in 2017 due to opioids, individuals who survived also faced adverse complications, including permanent brain damage.Opioid overdoses are diagnosed based on symptoms and examination. Risk factors for opioid overdose include high levels of opioid dependence, use of opioids via injection, high dosed opioid usage, having a mental disorder or having a predisposition for one, and use of opioids in combination with other substances, such as alcohol, benzodiazepines, or cocaine. Dependence on prescription opioids can occur from their use to treat chronic pain in individuals. Additionally, if following a period of detoxification, which allows the tolerance level to fall, the risk of overdose upon return to use is high.Initial treatment of an overdose involves supporting the persons breathing and providing oxygen to reduce the risk of hypoxia. Naloxone is then recommended to those who cannot reverse the opioids effects through breathing. Giving naloxone via nasal administration or as an injection into a muscle has shown to be equally effective. | Usually, these polyps are asymptomatic but gastric polyps may be the cause of dyspepsia, heartburn, bleeding from the upper gastrointestinal tract, and, rarely, gastric outlet obstruction while colorectal polyps may be the cause of rectal bleeding, anemia, constipation, diarrhea, weight loss, and abdominal pain.Individuals with chronic H. pylori infection have an increased risk of acquiring a cancer that is directly related to this infection. These cancers are stomach adenocarcinoma, less commonly diffuse large B-cell lymphoma of the stomach, or extranodal marginal zone B-cell lymphomas of the stomach, or, more rarely, of the colon, rectum, esophagus, or ocular adenexa (i.e. orbit, conjunctiva, and/or eyelids). The signs, symptoms, pathophysiology, and diagnoses of these cancers are given in the cited linkages. Microbiology
Morphology
Helicobacter pylori is a helix-shaped (classified as a curved rod, not spirochaete) Gram-negative bacterium about 3 μm long with a diameter of about 0.5 μm . H. pylori can be demonstrated in tissue by Gram stain, Giemsa stain, haematoxylin–eosin stain, Warthin–Starry silver stain, acridine orange stain, and phase-contrast microscopy. It is capable of forming biofilms and can convert from spiral to a possibly viable but nonculturable coccoid form.Helicobacter pylori has four to six flagella at the same location; all gastric and enterohepatic Helicobacter species are highly motile owing to flagella. The characteristic sheathed flagellar filaments of Helicobacter are composed of two copolymerized flagellins, FlaA and FlaB. Physiology
Helicobacter pylori is microaerophilic – that is, it requires oxygen, but at lower concentration than in the atmosphere. | 0-1
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Vitamin intake recommendations made by several countries are that intakes of 14–18 mg/day are sufficient to meet the needs of healthy adults. Niacin or nicotinamide (niacinamide) are used for prevention and treatment of pellagra, a disease caused by lack of the vitamin. When niacin is used as a medicine to treat elevated cholesterol and triglycerides, daily doses range from 500 to 3,000 mg/day. High-dose nicotinamide does not have this medicinal effect. Vitamin deficiency
Severe deficiency of niacin in the diet causes the disease pellagra, characterized by diarrhea, sun-sensitive dermatitis involving hyperpigmentation and thickening of the skin (see image), inflammation of the mouth and tongue, delirium, dementia, and if left untreated, death. Common psychiatric symptoms include irritability, poor concentration, anxiety, fatigue, loss of memory, restlessness, apathy, and depression. The biochemical mechanism(s) for the observed deficiency-caused neurodegeneration are not well understood, but may rest on: A) the requirement for nicotinamide adenine dinucleotide (NAD+) to suppress the creation of neurotoxic tryptophan metabolites, B) inhibition of mitochondrial ATP generation, resulting in cell damage; C), activation of the poly (ADP-ribose) polymerase (PARP) pathway, as PARP is a nuclear enzyme involved in DNA repair, but in the absence of NAD+ can lead to cell death; D) reduced synthesis of neuro-protective brain-derived neurotrophic factor or its receptor tropomyosin receptor kinase B; or E) changes to genome expression directly due to the niacin deficiency.Niacin deficiency is rarely seen in developed countries, and it is more typically associated with poverty, malnutrition or malnutrition secondary to chronic alcoholism. | The reason given: "Based on the collective evidence from several large cardiovascular outcome trials, the Agency has concluded that the totality of the scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL-cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events." The drug company discontinued the drugs. Contraindications
Prescription immediate release (Niacor) and extended release (Niaspan) niacin are contraindicated for people with either active or a history of liver disease because both, but especially Niaspan, have been associated with instances of serious, on occasion fatal, liver failure. Both products are contraindicated for people with existing peptic ulcer disease, or other bleeding problems because niacin lowers platelet count and interferes with blood clotting. Both products are also contraindicated for women who are pregnant or expecting to become pregnant because safety during pregnancy has not been evaluated in human trials. These products are contraindicated for women who are lactating because it is known that niacin is excreted into human milk, but the amount and potential for adverse effects in the nursing infant are not known. Women are advised to either not nurse their child or discontinue the drug. High-dose niacin has not been tested or approved for use in children under 16 years. Adverse effects
The most common adverse effects of medicinal niacin (500–3000 mg) are flushing (e.g., warmth, redness, itching or tingling) of the face, neck and chest, headache, abdominal pain, diarrhea, dyspepsia, nausea, vomiting, rhinitis, pruritus and rash. | 11
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An example is the 1999 Athens earthquake in Greece, in which many middle class people became homeless, with some of them living in containers, especially in the Nea Ionia earthquake survivors container city provided by the government; in most cases, their only property that survived the quake was their car. Such people are known in Greece as seismopathis, meaning earthquake-struck.War or armed conflict can create refugees fleeing the violence. Whether they be either domestic or foreign to the country, the number of migrants can outstrip the supply of affordable housing, leaving some section of this population to be homeless. Foster care
Transitions from foster care and other public systems can also impact homelessness; specifically, youth who have been involved in, or are a part of the foster care system, are more likely to become homeless. Most leaving the system have no support and no income, making it nearly impossible to break the cycle, and forcing them to live on the streets. There is also a lack of shelter beds for youth; various shelters have strict and stringent admissions policies. Choice
Although uncommon, some choose to be homeless as a personal lifestyle choice. There are different reasons why someone would choose to become homeless. They may not want to contribute to a capitalist society, which includes having a job, spending and owing money, and paying taxes to the government. The main aspect of freeganism is anti-consumerism, and avoiding spending excessive amounts of money at all costs. | I can’t go round in a raincoat and fedora looking over my life saying I did it my way — well, for 10 minutes in some American bar over a gin and tonic you might be able to get away with it. But Sid Vicious’s rendition takes in everybody; everybody is messed up like that, everybody is the mad hero of his own drama. It explodes the whole culture this self-presentation can take place in, so it completes the song for me. The 1986 film Sid and Nancy features a scene where Gary Oldman, portraying Vicious, performs his version of "My Way" while filming the songs music video.Viciouss version of this song appears in Martin Scorseses 1990 film GoodFellas, where it plays over the end credits. Margaret Mackie and Jamie Lee Morley
In December 2019 footage of Margaret Mackie, a resident of Northcare Suites Care Home in Edinburgh who suffers from dementia, performing "My Way" with staff member Jamie Lee Morley, went viral after being posted online by Mackies daughter.Morley later arranged to have the song professionally recorded and it was released in January 2020 as a charity single to raise funds for The Alzheimers Society and Dementia UK. The single peaked at number seven in the iTunes top 40 UK Pop Songs live chart and number five in the Amazon best seller chart. Yuzo Kayama
In Japan, Yuzo Kayama who is usually called the Japanese Frank Sinatra, performed My Way in 2008 in English. | 0-1
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The virus was also found in the eye of one patient in 2014, two months after it was cleared from his blood. Otherwise, people who have recovered are not infectious.The potential for widespread infections in countries with medical systems capable of observing correct medical isolation procedures is considered low. Usually when someone has symptoms of the disease, they are unable to travel without assistance.Dead bodies remain infectious; thus, people handling human remains in practices such as traditional burial rituals or more modern processes such as embalming are at risk. 69% of the cases of Ebola infections in Guinea during the 2014 outbreak are believed to have been contracted via unprotected (or unsuitably protected) contact with infected corpses during certain Guinean burial rituals.Health-care workers treating people with Ebola are at greatest risk of infection. The risk increases when they do not have appropriate protective clothing such as masks, gowns, gloves and eye protection; do not wear it properly; or handle contaminated clothing incorrectly. This risk is particularly common in parts of Africa where the disease mostly occurs and health systems function poorly. There has been transmission in hospitals in some African countries that reuse hypodermic needles. Some health-care centres caring for people with the disease do not have running water. | In 2015, a rapid antigen test which gives results in 15 minutes was approved for use by WHO. It is able to confirm Ebola in 92% of those affected and rule it out in 85% of those not affected. Differential diagnosis
Early symptoms of EVD may be similar to those of other diseases common in Africa, including malaria and dengue fever. The symptoms are also similar to those of other viral haemorrhagic fevers such as Marburg virus disease, Crimean–Congo haemorrhagic fever, and Lassa fever.The complete differential diagnosis is extensive and requires consideration of many other infectious diseases such as typhoid fever, shigellosis, rickettsial diseases, cholera, sepsis, borreliosis, EHEC enteritis, leptospirosis, scrub typhus, plague, Q fever, candidiasis, histoplasmosis, trypanosomiasis, visceral leishmaniasis, measles, and viral hepatitis among others.Non-infectious diseases that may result in symptoms similar to those of EVD include acute promyelocytic leukaemia, haemolytic uraemic syndrome, snake envenomation, clotting factor deficiencies/platelet disorders, thrombotic thrombocytopenic purpura, hereditary haemorrhagic telangiectasia, Kawasaki disease, and warfarin poisoning. Prevention
Vaccines
An Ebola vaccine, rVSV-ZEBOV, was approved in the United States in December 2019. It appears to be fully effective ten days after being given. It was studied in Guinea between 2014 and 2016. More than 100,000 people have been vaccinated against Ebola as of 2019. Infection control
Caregivers
People who care for those infected with Ebola should wear protective clothing including masks, gloves, gowns and goggles. The U.S. Centers for Disease Control (CDC) recommend that the protective gear leaves no skin exposed. | 11
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Hyperdontia is the condition of having supernumerary teeth, or teeth that appear in addition to the regular number of teeth (32 in the average adult). They can appear in any area of the dental arch and can affect any dental organ. The opposite of hyperdontia is hypodontia, where there is a congenital lack of teeth, which is a condition seen more commonly than hyperdontia. The scientific definition of hyperdontia is "any tooth or odontogenic structure that is formed from tooth germ in excess of usual number for any given region of the dental arch." The additional teeth, which may be few or many, can occur on any place in the dental arch. Their arrangement may be symmetrical or non-symmetrical. Signs and symptoms
The presence of a supernumerary tooth, particularly when seen in young children, is associated with a disturbance of the maxillary incisor region. This commonly results in the impaction of the incisors during the mixed dentition stage. The study debating this also considered many other factors such as: the patients age, number, morphology, growth orientation and position of the supernumerary tooth. Alongside this issue, the presence of an extra tooth can impede the eruption of adjacent additional or normal teeth. Therefore, the presence of a supernumerary tooth when found must be approached with the appropriate treatment plan, incorporating the likelihood of incisal crowding. In some individuals, the additional teeth can erupt far from the dental arch, within the maxillary sinus. The extra teeth may also migrate to a different location after development. | There is a considerable difference between males and females in the prevalence of these teeth in permanent dentition; hyperdontia is twice as common in males as in females. However, this approximation varies in terms of location, other associating syndromes that may be present, and the ethnicity of the individual. In terms of ethnicity, it can be seen that hyperdontia is in fact less common in European than in Asian populations. There is evidence to show that an individual is more likely to have hyperdontia if other members of their family also have the condition. References
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The first hyaluronan biomedical product, Healon, was developed in the 1970s and 1980s by Pharmacia, and approved for use in eye surgery (i.e., corneal transplantation, cataract surgery, glaucoma surgery, and surgery to repair retinal detachment). Other biomedical companies also produce brands of hyaluronan for ophthalmic surgery.Native hyaluronic acid has a relatively short half-life (shown in rabbits) so various manufacturing techniques have been deployed to extend the length of the chain and stabilise the molecule for its use in medical applications. The introduction of protein-based cross-links, the introduction of free-radical scavenging molecules such as sorbitol, and minimal stabilisation of the HA chains through chemical agents such as NASHA (non-animal stabilised hyaluronic acid) are all techniques that have been used to preserve its shelf life.In the late 1970s, intraocular lens implantation was often followed by severe corneal edema, due to endothelial cell damage during the surgery. It was evident that a viscous, clear, physiologic lubricant to prevent such scraping of the endothelial cells was needed.The name "hyaluronan" is also used for a salt. Other animals
Hyaluronan is used in treatment of articular disorders in horses, in particular those in competition or heavy work. It is indicated for carpal and fetlock joint dysfunctions, but not when joint sepsis or fracture are suspected. It is especially used for synovitis associated with equine osteoarthritis. It can be injected directly into an affected joint, or intravenously for less localized disorders. It may cause mild heating of the joint if directly injected, but this does not affect the clinical outcome. | Melanonychia is a black or brown pigmentation of the normal nail plate, and may be present as a normal finding on many digits in Afro-Caribbeans, as a result of trauma, systemic disease, or medications, or as a postinflammatory event from such localized events as lichen planus or fixed drug eruption. : 790 : 665 There are two types, longitudinal and transverse melanonychia. : 671 Longitudinal melanonychia may be a sign of subungual melanoma (acral lentiginous melanoma), although there are other diagnoses such as chronic paronychia, onychomycosis, subungual hematoma, pyogenic granuloma, glomus tumour, subungual verruca, mucous cyst, subungual fibroma, keratoacanthoma, carcinoma of the nail bed, and subungual exostosis. See also
Nail anatomy
List of cutaneous conditions
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US prescribing recommendations warn against the concurrent use of alcohol and/or other central nervous system depressants, but to date there have been no studies to assess the effects of azelastine nasal spray on the CNS in humans. More recent studies have shown similar degrees of somnolence (approx. 2%) compared with placebo treatment. The most common side effect is a bitter taste (about 20% of people). Due to this, the manufacturer has produced another formulation of azelastine with sucralose. The problem of bitter taste may also be reduced by correct application of the nasal spray (i.e. slightly tipping the head forward and not inhaling the medication too deeply), or alternatively using the azelastine/sucralose formulation.In addition, anosmia (loss in the ability to smell) can occur with nasal spray antihistamines (including both formulations of azelastine). Pharmacology
Pharmacodynamics
Azelastine has a triple mode of action:
Anti-histamine effect,
Mast-cell stabilizing effect and
Anti-inflammatory effect. Pharmacokinetics
The systemic bioavailability of azelastine is approximately 40% when administered intranasally. Maximum plasma concentrations (Cmax) are observed within 2–3 hours. The elimination half life, steady-state volume of distribution and plasma clearance are 22 h, 14.5 L/kg and 0.5 L/h/kg respectively (based on intravenous and oral administration data). Approximately 75% of an oral dose is excreted in feces. Pharmacokinetics of orally administered azelastine are not affected by age, gender or hepatic impairment. Metabolism
Azelastine is oxidatively metabolized by the cytochrome P450 family into its active metabolite, desmethylazelastine, and two inactive carboxylic acid metabolites. Chemical properties
The chemical nomenclature of azelastine is (±)-1-(2H)-phthalazinone, 4-[(4-chlorophenyl) methyl]-2-(hexahydro-1-methyl-1H-azepin-4-yl)-monohydrochloride. It is white, almost odorless with a bitter taste. References
External links
"Azelastine". | Calcium supplements are therefore often required to prevent symptoms of hypocalcemia and to restore lost bone mass.The patient is placed in a semi-Fowler position and the neck is extended. An abbreviated Kocher incision is made and the platysma muscle is dissected horizontally. The strap muscles are released off of the thyroid gland. Then the thyroid gland is mobilized and the parathyroid arterial blood supply is suture ligated. The entire parathyroid adenoma is identified and dissected out. Intraoperative PTH monitoring can begin at this time and will show falling PTH levels if the entire adenoma has been resected. Complications
While mild hypocalcemia is common after partial parathyroidectomy, some people experience persistently prolonged low calcium levels. This is called hungry bone syndrome. Despite the reactivation of unresected parathyroid glands producing normal to elevated levels of PTH, serum calcium continues to be low. The balance between calcium influx and efflux within the bone continues to be disrupted, favoring the former. The bone is said to be "hungry" as it consumes minerals without regard to PTH; calcium, magnesium, and phosphate continue to be deposited into the bones, resulting in hypocalcemia, hypomagnesemia, and hypophosphatemia. Prolonged calcium supplementation may be required. Hungry bone syndrome is particularly common in people who are on long-term regular dialysis. See also
List of surgeries by type
References
External links
"How is parathyroid surgery performed?". American Association of Endocrine Surgeons. Retrieved 11 May 2019. "Parathyroid gland removal". Medical Encyclopedia. Medline Plus. 3 December 2018. Retrieved 8 December 2018. | 0-1
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Another less common verbal response in the United States and Canada to anothers sneeze is "Gesundheit", which is a German word that means, appropriately, "good health". Several hypotheses exist for why the custom arose of saying "bless you" or "God bless you" in the context of sneezing:
Some say it came into use during the plague pandemics of the 14th century. Blessing the individual after showing such a symptom was thought to prevent possible impending death due to the lethal disease. In Renaissance times, a superstition was formed claiming ones heart stopped for a very brief moment during the sneeze; saying bless you was a sign of prayer that the heart would not fail. It has also been stated that one says "(God) bless you" so that one does not catch the flu, cold, or any other forms of sickness.Other cultures have similar traditions:
In China, after a person sneezes they often say "百岁!" which translates to "may you live one hundred years!" the pronunciation is similar to "bless you" in English. pronunciation: [Bai Sui]
In Iran, it is common to respond to sneezing with the Persian phrase عافیت باشه âfiyat bâše, which translates to "health", similar to common European expressions. Indian culture is to respond with Krishna, similar to a blessing in western cultures. In Italy after a person sneezes the people present respond with the word "salute" (meaning: health). The louder the sneeze the more emphatic the response. In Slovakia, after a person sneezes, it is proper to say "Na zdravie!" which means "For health! | Culture
In Indian culture, especially in northern parts of India, Bengali (Bangladesh and Bengal of India) culture and also in Iran, it has been a common superstition that a sneeze taking place before the start of any work was a sign of impending bad interruption. It was thus customary to pause in order to drink water or break any work rhythm before resuming the job at hand in order to prevent any misfortune from occurring. Contrarily, in Polish culture, especially in the Kresy Wschodnie borderlands, a popular belief persists that sneezes may be an inauspicious sign that, depending on the local version, either someone unspecified or ones mother-in-law speaks ill of the person sneezing at that moment. In other regions, however, this superstition concerns hiccups rather than sneezing. As with other Catholic countries, such as Mexico, Italy, or Ireland, the remnants of pagan culture are fostered in Polish peasant idiosyncratic superstitions. The practice among Islamic culture, in turn, has largely been based on various prophetic traditions and the teachings of the prophet Muhammad. An example of this is Al-Bukhaaris narrations from Abu Hurayrah that Muhammad once said:
When one of you sneezes, let him say, "Al-hamdu-Lillah" (Praise be to God), and let his brother or companion say to him, "Yarhamuk Allah" (May God have mercy on you). If he says, "Yarhamuk-Allah", then let [the sneezer] say, "Yahdeekum Allah wa yuslihu baalakum" (May God guide you and rectify your condition). Verbal responses
In English-speaking countries, one common verbal response to another persons sneeze is "[May God] bless you". | 11
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This is part of a normal process in which bacteria from the environment start to grow on a babys skin. It is unknown whether the immune response that causes erythema toxicum neonatorum is helpful to the baby. Recent research indicates an association with Demodex mites infestation (demodicosis). Diagnosis
Health professionals can diagnose erythema toxicum neonatorum with a skin exam. Most cases of erythema toxicum neonatorum can be diagnosed without further testing. If more testing is needed to make a diagnosis, the contents of a lesion can be examined under a microscope. A health professional may make a small cut into a pus-filled lesion and collect a swab of pus for testing. Lesions caused by erythema toxicum neonatorum contain eosinophils and other immune cells. These cells can be seen under a microscope when a special stain is applied to the sample.Since the appearance of erythema toxicum neonatorum varies, it may be confused with other newborn rashes. Some newborn infections cause bumps or boils, which may look like erythema toxicum neonatorum. Bacterial infections, including Staphylococcus and Streptococcus infections, almost always cause additional symptoms. These symptoms may be severe, and they are usually not limited to rash. Bacterial rashes can be diagnosed by testing pus from a lesion along with a blood sample. Bacteria can be seen under a microscope with a special stain or may be found on a culture. Fungal infection with Candida may also cause a similar rash in newborns, but it usually causes additional symptoms like thrush. | : 86 This form of acanthosis nigricans is more likely to involve mucous membranes (25–50% of cases) Malignant acanthosis nigricans that may either precede (18%), accompany (60%), or follow (22%) the onset of an internal cancer. : 506 Malignancy-associated acanthosis nigricans is usually rapid in onset and may be accompanied by skin tags, multiple seborrheic keratoses, or tripe palms. : 676
Acral acanthotic anomaly
Acral acanthotic anomaly refers to a variant of acanthosis nigricans limited to the elbows, knees, knuckles, and dorsal surfaces of the feet, in the absence of any other findings, in otherwise healthy individuals. While the etiology remains unknown, its presence does not suggest a likelihood of malignancy. Pathophysiology
Acanthosis nigricans is caused by increased activation of growth factor receptor proteins, usually due to endocrine dysfunction. This is most commonly insulin-mediated activation of IGF receptors on keratinocytes, as a result of hyperinsulinaemia or insulin resistance, as seen in diabetes mellitus.Factors involved in the development of acanthosis nigricans include:
Increased circulating insulin. This activates keratinocyte IGF receptors, particularly IGF-1. At high concentrations, insulin may also displace IGF-1 from insulin-like growth factor-binding protein (IGFBP). Increased circulating IGF may lead to keratinocyte and dermal fibroblast proliferation. In hereditary forms of acanthosis nigricans, fibroblast growth factor receptor (FGFR) defects
Increased transforming growth factor (TGF), which appears to be the mechanism for malignancy-associated acanthosis nigricans. TGF acts on epidermal tissue via the epidermal growth factor receptor (EGFR). | 0-1
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Over a five- to ten-year period, this vasculopathy (blood vessel pathology) results in vision loss and destructive brain lesions with neurologic deficits and death. Although brain and eye disease are universally present in patients with RVCL, the disease is truly a multi-system disorder characterized by chronic kidney disease, liver disease, and frequently other manifestations including gastrointestinal disease, osteonecrosis, and hypothyroidism. Diagnosis
Differential diagnosis
Treatment
Currently, there is no therapy that is proven to prevent the blood vessel deterioration. In 2021, Dr. Jonathan Miner of the University of Pennsylvania (Penn) in Philadelphia, and the Hospital of the University of Pennsylvania (Penn Medicine), initiated a clinical trial of crizanlizumab for RVCL. The University of Pennsylvania also sponsors RVCL patient support groups, and collaborates with the RVCL Research Center at Washington University (WashU) on clinical trials and longitudinal studies. Miner also established a large RVCL Research Center, which is conducting clinical trials, performing basic research, and developing novel personalized therapies for RVCL. This includes small molecular inhibitors (to be taken as pills) and gene therapy approaches, with the goal of fully correcting the disease-causing mutation. Developing these personalized therapies is a challenging process that will take years. History
1985–1988: CRV (Cerebral Retinal Vasculopathy) was discovered by multiple investigators including Dr. Gil Grand, Dr. John P. Atkinson, and colleagues at Washington University School of Medicine (WashU). | The normal function of the TREX1 gene is to provide instructions for making the 3-prime repair exonuclease 1 enzyme. This enzyme is a DNA exonuclease, which means it trims molecules of DNA by removing DNA building blocks (nucleotides) from the ends of the molecules. In this way, it breaks down unneeded DNA molecules or fragments that may be generated during genetic material in preparation for cell division, DNA repair, cell death, and other processes. Changes (mutations) to the TREX1 gene can result in a range of conditions, one of which is RVCL. The mutant TREX1 protein is produced and mislocalized. Haploinsufficiency of TREX1 does not explain the disease, since the parents of patients with Aicairdi-Goutieres syndrome, a disease characterized by insufficient TREX1 activity, are completely healthy with only one functional TREX1 allele. Different mutations in the TREX1 gene have also been identified in people with disorders involving the immune system. These disorders include a chronic inflammatory disease called Aicardi-Goutieres syndrome, as well as systemic lupus erythematosus (SLE), including a rare form of SLE called chilblain lupus that mainly affects the skin. Those diseases, which are inflammatory, may have a completely distinct mechanism compared with that of RVCL. The TREX1 gene is located on chromosome 3: base pairs 48,465,519 to 48,467,644
Pathogenesis
The main pathologic process centers on small blood vessels that prematurely "drop out" and disappear. The retina of the eye and white matter of the brain appear to be among the most sensitive to this pathologic process. | 11
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Immature DCs are therefore considered to be part of the innate phase of pulpal immune response.Persistent infection leads to the activation of adaptive immunity. A transition to an adaptive immune response will take place in the dental pulp as the caries and bacteria approach the pulp. Antigens are recognized individually and lines of lymphocytes are developed to produce specific antibodies which attach to the recognized cells and initiate their destruction. Phagocytes remove the remains. B cells and T cells are the major lymphocytes involved.A variety of cytokines have been observed in the pulp. Patients with symptomatic and asymptomatic irreversible pulpitis have been shown to have an almost 23-fold increase in the cytokine IL-8 in the pulp. Cytokines in the pulp interact with each other. The ultimate effect on pulpal inflammation and healing is dependent upon the integrated actions of these inflammatory mediators.In addition to the lymphocytes, macrophages also provide defense against certain intracellular pathogens. Activated macrophages can function as class II antigen-presenting cells, similar to pulpal dendritic and B cells. In addition, activated macrophages secrete many inflammatory mediators.Macrophages in the pulp become activated after receiving two signals. The first is a priming stimulus and the second is an activating signal. The priming stimulus is secreted by activated T-helper cells. The activating stimulus may include bacterial lipopolysaccharides, muramyl dipeptide, and other chemical mediators.Macrophages are professional phagocytes in innate immune responses. | There are 3 general types:
Thermal: Agents are applied to increase or decrease the temperature of a tooth and stimulate a pulp sensory response.Cold tests: Most commonly, ethyl chloride is sprayed onto a small ball of cotton wool and is applied to the tooth, which produces intense cold. Alternatively, CO2 snow and other refrigerants such as dichlorodifluoromethane (DDM) have been shown to be effective. Heat tests: Gutta percha can be heated and directly applied to the tooth to produce heat. Electrical pulp test: Electric pulp testing (EPT) has been available for over a century and is used by dentists worldwide. It is used to determine the health of the pulp and pulp-related pain.EPT is based on the stimulation of sensory nerves in the pulp. It does not provide information on vascular supply to the pulp. The probe tip of the test device is placed directly onto the tooth surface and an electrical stimulus is produced. This stimulus causes an ionic change across the neural membrane, inducing an action potential in the myelinated nerves. The threshold of pain is determined by increasing the voltage. A tingling sensation is felt once the voltage reaches the pain threshold. This threshold level varies between patients, and is affected by factors such as age, pain perception, tooth surface conduction and resistance. The requirements of an EPT are appropriate application method, careful interpretation of the results, and an appropriate stimulus. EPT must be done with tooth isolation and conduction media. | 11
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This combination of MHC and antigen attracts a matching helper T cell, which releases lymphokines and activates the B cell. As the activated B cell then begins to divide, its offspring (plasma cells) secrete millions of copies of the antibody that recognizes this antigen. These antibodies circulate in blood plasma and lymph, bind to pathogens expressing the antigen and mark them for destruction by complement activation or for uptake and destruction by phagocytes. Antibodies can also neutralize challenges directly, by binding to bacterial toxins or by interfering with the receptors that viruses and bacteria use to infect cells.Newborn infants have no prior exposure to microbes and are particularly vulnerable to infection. Several layers of passive protection are provided by the mother. During pregnancy, a particular type of antibody, called IgG, is transported from mother to baby directly through the placenta, so human babies have high levels of antibodies even at birth, with the same range of antigen specificities as their mother. Breast milk or colostrum also contains antibodies that are transferred to the gut of the infant and protect against bacterial infections until the newborn can synthesize its own antibodies. This is passive immunity because the fetus does not actually make any memory cells or antibodies—it only borrows them. This passive immunity is usually short-term, lasting from a few days up to several months. In medicine, protective passive immunity can also be transferred artificially from one individual to another. | Many of the classical molecules of the adaptive immune system (for example, immunoglobulins and T-cell receptors) exist only in jawed vertebrates. A distinct lymphocyte-derived molecule has been discovered in primitive jawless vertebrates, such as the lamprey and hagfish. These animals possess a large array of molecules called Variable lymphocyte receptors (VLRs) that, like the antigen receptors of jawed vertebrates, are produced from only a small number (one or two) of genes. These molecules are believed to bind pathogenic antigens in a similar way to antibodies, and with the same degree of specificity. Manipulation by pathogens
The success of any pathogen depends on its ability to elude host immune responses. Therefore, pathogens evolved several methods that allow them to successfully infect a host, while evading detection or destruction by the immune system. Bacteria often overcome physical barriers by secreting enzymes that digest the barrier, for example, by using a type II secretion system. Alternatively, using a type III secretion system, they may insert a hollow tube into the host cell, providing a direct route for proteins to move from the pathogen to the host. These proteins are often used to shut down host defenses.An evasion strategy used by several pathogens to avoid the innate immune system is to hide within the cells of their host (also called intracellular pathogenesis). Here, a pathogen spends most of its life-cycle inside host cells, where it is shielded from direct contact with immune cells, antibodies and complement. | 11
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Often psychotherapy teaches coping skills while allowing the teens or children to explore feelings and events in a safe environment.Severe depression, low global functioning, higher scores on suicidality scales, co-existing anxiety, distorted thought processes and feelings of hopelessness are characteristics of adolescent depression that are associated with a poor response to psychotherapy. If there is concomitant family conflict then interpersonal therapy is more effective than cognitive therapy. Talk therapy is one of the best forms of therapy, as the depressed person finds a solace in the one whom he/she is talking to. Through this means, the counselor is able to know and understood fully the mind of the depressed individual. Many people are depressed and simply needs the right person to talk to. This is where the talk therapy comes in as a very helpful solution to those who are in need of it. Cognitive therapy
Cognitive therapy aims to change harmful ways of thinking and reframe negative thoughts in a more positive way. Aims of cognitive therapy include various steps of patient learning. During cognitive behavioral therapy, children and adolescents with depression work with therapists to learn about their diagnosis, how to identify and reshape negative thought patterns, and how to increase engagement in enjoyable activities. CBT-trained therapists work with individuals, families, and groups. The approach can be used to help anyone irrespective of ability, culture, race, gender, or sexual preference. It can be applied with or without concurrent psychopharmacological medication, depending on the severity or nature of each patients problem. | In the 1990s, the National Institute of Mental Health (NIMH) found that up to 7% of adolescents who develop major depressive disorder may commit suicide as young adults. Such statistics demonstrate the importance of interventions by family and friends, the importance of early diagnosis, and treatment by medical staff, in order to prevent suicide amongst at-risk youth. However, some data showed an opposite conclusion. Most depression symptoms are reported more frequently by females; such as sadness (reported by 85.1% of women and 54.3% of men) and crying (approximately 63.4% of women and 42.9% of men). Women have a higher probability to experience depression than men with the prevalences of 19.2% and 13.5% respectively. Risk factor
Risk factors for adolescent depression include female sex, a family history of depression, a personal history of trauma, family conflict, minority sexual orientation, or having a chronic medical illness. There tends to be higher prevalence rates and more severe symptoms in adolescent girls when compared to adolescent boys. These higher rates are also applicable in older adolescents when compared to younger adolescents. This may be due to hormonal fluctuations may that make adolescent women to be more vulnerable to depression. The fact that increased prevalence of depression correlates with hormonal changes in women, particularly during puberty, suggests that female hormones may be a trigger for depression. The gender gap in depression between adolescent men and women is mostly due to young womens lower levels of positive thinking, need for approval, and self-focusing negative conditions. | 11
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2
NaNO
2
⟶
Na
2
O
+
NO
+
NO
2
{\displaystyle {\ce {2 NaNO2 -> Na2O + NO + NO2}}}
Sodium nitrite can also be used in the production of nitrous acid:
2
NaNO
2
+
H
2
SO
4
⟶
2
HNO
2
+
Na
2
SO
4
{\displaystyle {\ce {2NaNO2 + H2SO4 ->2 HNO2 + Na2SO4}}}
The nitrous acid then, under normal conditions, decomposes:
2
HNO
2
⟶
NO
2
+
NO
+
H
2
O
{\displaystyle {\ce {2 HNO2 -> NO2 + NO + H2O}}}
The resulting nitrogen dioxide hydrolyzes to a mixture of nitric and nitrous acids:
2
NO
2
+
H
2
O
⟶
HNO
3
+
HNO
2
{\displaystyle {\ce {2 NO2 + H2O -> HNO3 + HNO2}}}
Isotope labelling 15N
In organic synthesis isotope enriched sodium nitrite-15N can be used instead of normal sodium nitrite as their reactivity is nearly identical in most reactions. | Urea, also known as carbamide-containing cream, is used as a medication and applied to the skin to treat dryness and itching such as may occur in psoriasis, dermatitis, or ichthyosis. It may also be used to soften nails.In adults side effects are generally few. It may occasionally cause skin irritation. Urea works in part by loosening dried skin. Preparations generally contain 5 to 50% urea.Urea containing creams have been used since the 1940s. It is on the World Health Organizations List of Essential Medicines. It is available over the counter. Medical uses
Urea cream is indicated for debridement and promotion of normal healing of skin areas with hyperkeratosis, particularly where healing is inhibited by local skin infection, skin necrosis, fibrinous or itching debris or eschar. Specific condition with hyperkeratosis where urea cream is useful include:
Dry skin and rough skin
Dermatitis
Psoriasis
Ichthyosis
Eczema
Keratosis
Keratoderma
Corns
Calluses
Damaged, ingrown and devitalized nails
Side effects
Common side effects of urea cream are:
Mild skin irritation
Temporary burning sensation
Stinging sensation
ItchingIn severe cases, there can be an allergic reaction with symptoms such as skin rash, urticaria, difficulty breathing and swelling of the mouth, face, lips, or tongue. Mechanism of action
Urea in low doses is a humectant while at high doses (above 20%) it causes breakdown of protein in the skin.Urea dissolves the intercellular matrix of the cells of the stratum corneum, promoting desquamation of scaly skin, eventually resulting in softening of hyperkeratotic areas. In nails, urea causes softening and eventually debridement of the nail plate. References
External links
"Urea". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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High levels of adrenaline and noradrenaline have a protective effect on the cardiac electrophysiology because they bind to beta 2 adrenergic receptors, which, when activated, extracellularly decrease potassium concentration.Hyperkalemic periodic paralysis is an autosomal dominant clinical condition where there is a mutation in gene located at 17q23 that regulates the production of protein SCN4A. SCN4A is an important component of sodium channels in skeletal muscles. During exercise, sodium channels would open to allow influx of sodium into the muscle cells for depolarization to occur. But in hyperkalemic periodic paralysis, sodium channels are slow to close after exercise, causing excessive influx of sodium and displacement of potassium out of the cells.Rare causes of hyperkalemia are discussed as follows. Acute digitalis overdose such as digoxin toxicity may cause hyperkalemia through the inhibition of sodium-potassium-ATPase pump. Massive blood transfusion can cause hyperkalemia in infants due to leakage of potassium out of the red blood cells during storage. Giving succinylcholine to people with conditions such as burns, trauma, infection, prolonged immobilisation can cause hyperkalemia due to widespread activation of acetylcholine receptors rather than a specific group of muscles. Arginine hydrochloride is used to treat refractory metabolic alkalosis. The arginine ions can enter cells and displace potassium out of the cells, causing hyperkalemia. Calcineurin inhibitors such as cyclosporine, tacrolimus, diazoxide, and minoxidil can cause hyperkalemia. Box jellyfish venom can also cause hyperkalemia. | Hyperkalemia is an elevated level of potassium (K+) in the blood. Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels above 5.5 mmol/L defined as hyperkalemia. Typically hyperkalemia does not cause symptoms. Occasionally when severe it can cause palpitations, muscle pain, muscle weakness, or numbness. Hyperkalemia can cause an abnormal heart rhythm which can result in cardiac arrest and death.Common causes of hyperkalemia include kidney failure, hypoaldosteronism, and rhabdomyolysis. A number of medications can also cause high blood potassium including spironolactone, NSAIDs, and angiotensin converting enzyme inhibitors. The severity is divided into mild (5.5–5.9 mmol/L), moderate (6.0–6.4 mmol/L), and severe (>6.5 mmol/L). High levels can be detected on an electrocardiogram (ECG). Pseudohyperkalemia, due to breakdown of cells during or after taking the blood sample, should be ruled out.Initial treatment in those with ECG changes is salts, such as calcium gluconate or calcium chloride. Other medications used to rapidly reduce blood potassium levels include insulin with dextrose, salbutamol, and sodium bicarbonate. Medications that might worsen the condition should be stopped and a low potassium diet should be started. Measures to remove potassium from the body include diuretics such as furosemide, potassium-binders such as polystyrene sulfonate and sodium zirconium cyclosilicate, and hemodialysis. Hemodialysis is the most effective method.Hyperkalemia is rare among those who are otherwise healthy. Among those who are hospitalized, rates are between 1% and 2.5%. | 11
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Lack of proper training of service providers, such as social workers, law enforcement, nurses, etc., about elder abuse, therefore the number of cases reported tend to be low. The subjective nature of elder abuse, which largely depends on ones interpretation. Another reason why there is a lack of accurate statistics is the debate of whether to include self-neglect or not. Many are unsure if it should be included since it does not involve another person as an abuser. Those opposed to the inclusion of self-neglect make the claim that it is a different form of abuse and thus, should not be included in the statistics. Due to this discrepancy and the others mentioned above, it is difficult to get accurate data concerning the abuse of the elderly. Prevention
Doctors, nurses, and other medical personnel can play a vital role in assisting elder abuse victims. Studies have shown that elderly individuals, on average, make 13.9 visits per year to a physician. Although there has been an increase in awareness of elder abuse over the years, physicians tend to only report 2% of elder abuse cases. Reasons for lack of reporting by physicians include a lack of current knowledge concerning state laws on elder abuse, concern about angering the abuser and ruining the relationship with the elderly patient, possible court appearances, lack of cooperation from elderly patients or families, and lack of time and reimbursement. Through education and training on elder abuse, health care professionals can better assist elder abuse victims. | Elder abuse (also called "elder mistreatment", "senior abuse", "abuse in later life", "abuse of older adults", "abuse of older women", and "abuse of older men") is "a single, or repeated act, or lack of appropriate action, occurring within any relationship where there is an expectation of trust, which causes harm or distress to an older person." This definition has been adopted by of the World Health Organization (WHO) from a definition put forward by Hourglass (formerly Action on Elder Abuse) in the UK. Laws protecting the elderly from abuse are similar to and related to laws protecting dependent adults from abuse. It includes harms by people, the older person knows, or has a relationship with, such as a spouse, partner, or family member; a friend or neighbor; or people that the older person relies on for services. Many forms of elder abuse are recognized as types of domestic violence or family violence since they are committed by family members. Paid caregivers have also been known to prey on their elderly patients. While a variety of circumstances are considered elder abuse, it does not include general criminal activities against older persons, such as home break-ins, "muggings" in the street, or "distraction burglary," where a stranger distracts an older person at the doorstep while another person enters the property to steal. The abuse of elders by caregivers is a worldwide issue. In 2002, WHO brought international attention to the issue of elder abuse. | 11
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Combined hepatitis A and B vaccine, is used to provide protection against hepatitis A and hepatitis B. It is given by injection into muscle.It is used in areas where hepatitis A and B are endemic, for travelers, people with hepatitis C or chronic liver disease, and those at high risk of sexually transmitted diseases.The combined vaccine is as safe and protective as if given as separate hepatitis A and B vaccines. It is generally well-tolerated. Common side effects are mild and include redness and pain at the injection site, where a small lump may appear. Feeling faint or tired, or a headache may occur. Other side effects include numbness, tingling, rash, bruising, abnormal bleeding such as from the nose or gums, weak muscle or pain. Severe side effects are rare and include an allergic reaction and seizures.It is widely available. Administration schedule
Routine Twinrix vaccination is administered by intramuscular injection in the deltoid area using a schedule of three separate doses at 0, 1, and 6 months ([minimum intervals: 4 weeks between doses 1 and 2, 5 months between doses 2 and 3]). In some circumstances, an accelerated dosing schedule of 0, 7 and 21 to 30 days followed by a booster at 12 months can be used and was shown to have similar efficacy as the traditional schedule. | Efficacy
The U.S. Centers for Disease Control and Prevention (CDC) reports that clinical trials found the following levels of protection against Hepatitis A and Hepatitis B one month after each dose:
A: 93.8%, 98.8%, 99.9%
B: 30.8%, 78.2%, 98.5%GlaxoSmithKline claims that its studies found 70% of subjects had antibodies against hepatitis B a month after just the first dose, however.Twinrix should not be used for postexposure prophylaxis, because no data are available on the efficacy of combination vaccine for prophylaxis after exposure to HAV. Availability
Twinrix is a brand manufactured by GlaxoSmithKline Biologicals. The full generic name is hepatitis A inactivated & hepatitis B (recombinant) vaccine. Twinrix is administered over three doses. The name was created because it is a mixture of two earlier vaccines — Havrix, an inactivated-virus Hepatitis A vaccine, and Engerix-B, a recombinant Hepatitis B vaccine. Twinrix first entered the market in early 1997.In the United States, Twinrix is approved by the Food and Drug Administration (FDA) for those aged 18 and older. In some countries outside the United States, notably Canada and in the European Union, Twinrix is known as Twinrix Adult or Ambirix and a pediatric formulation, called Twinrix Junior or Twinrix Paediatric, is available. Society and culture
Economics
By being a combination it may reduce administrative costs and achieve a better uptake of the vaccine. Names
Brand names include Twinrix, Twinrix Junior, Twinrix paediatric, Ambirix, and Bilive. References
External links
"Twinrix". Food and Drug Administration (FDA). 3 October 2019. | 11
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Several agents are used to temporarily lower K+ levels. The choice depends on the degree and cause of the hyperkalemia, and other aspects of the persons condition. Myocardial excitability
Calcium (calcium chloride or calcium gluconate) increases threshold potential through a mechanism that is still unclear, thus restoring normal gradient between threshold potential and resting membrane potential, which is elevated abnormally in hyperkalemia. A standard ampule of 10% calcium chloride is 10 mL and contains 6.8 mmol of calcium. A standard ampule of 10% calcium gluconate is also 10 mL but has only 2.26 mmol of calcium. Clinical practice guidelines recommend giving 6.8 mmol for typical EKG findings of hyperkalemia. This is 10 mL of 10% calcium chloride or 30 mL of 10% calcium gluconate. Though calcium chloride is more concentrated, it is caustic to the veins and should only be given through a central line. Onset of action is less than one to three minutes and lasts about 30–60 minutes. The goal of treatment is to normalise the EKG and doses can be repeated if the EKG does not improve within a few minutes.Some textbooks suggest that calcium should not be given in digoxin toxicity as it has been linked to cardiovascular collapse in humans and increased digoxin toxicity in animal models. Recent literature questions the validity of this concern. Temporary measures
Several medical treatments shift potassium ions from the bloodstream into the cellular compartment, thereby reducing the risk of complications. | Second-generation antihistamines such as loratadine and cetirizine are non-sedating and may also be effective in controlling pruritus in pregnant people.Knowing that oral antihistamines are generally ineffective, high-potency topical steroids are used to treat PUPPP, and ideally tapering it off after 7 days of therapy. Class I or II corticosteroid creams and ointments are used in more aggressive cases, and oral (systemic) corticosteroids can be used to treat very severe cases—although the benefits of a pregnant womans ingesting high-potency corticosteroids must be weighed carefully against possible (and mostly unknown) risks to the developing fetus or fetuses. The use of high-potency topical corticosteroids over 300 grams throughout the pregnancy may increase the risk of low birth weight for the baby. Rarely, in unusually persistent and distressing cases, some women have had their labor induced as soon as they are considered to be at term (37 weeks).When the pruritus is unbearable to the patient with PUPPP, oral prednisone in doses of 10 to 40 mg/day has been generally used for these type of severe cases. With this treatment, symptoms are usually relieved after 24 hours of the oral treatment. Sometimes, if the cases are too severe and the symptoms are extremely unbearable, early delivery can be discussed with the patient if the other treatments are ineffective. However, early delivery of the baby still does not guarantee that the symptoms will be gone. Luckily, in most cases, steroid treatment works efficiently and symptoms are generally greatly improved within several days. | 0-1
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A further distinction can be made between routine exposure and exposure required for emergency treatment, where a higher risk of oxygen toxicity may be justified to achieve a reduction of a more critical injury, particularly when in a relatively safe controlled and monitored environment. The Repex (repetitive exposure) method, developed in 1988, allows oxygen toxicity dosage to be calculated using a single dose value equivalent to 1 minute at atmospheric pressure called an Oxygen Tolerance Unit (OTU), is used to avoid toxic effects over several days of operetional exposure. Some dive computers will automatically track the dosage bases on depth and selected gas mixture. The limits allow a greater exposure when the person has not been exposed recently, and daily allowable dose decreases with an increase in consecutive days with exposure. These values may not be fully supported by current data. A more recent proposal uses a simple power equation, Toxicity Index (TI) = t2 × PO2c, where t is time and c is the power term. This was derived from the chemical reactions producing reactive oxygen or nitrogen species, and has been shown to give good predictions for CNS toxicity with c = 6.8 and for pulmonary toxicity for c = 4.57.For pulmonary toxicity, time is in hours, and PO2 in atmospheres absolute, TI should be limited to 250. For CNS toxicity, time is in minutes, PO2 in atmospheres absolute, and a TI of 26,108 indicates a 1% risk. | This has led to the current recommendation by the Diving Committee of the Undersea and Hyperbaric Medical Society that a diver should be raised during the seizures clonic (convulsive) phase if the regulator is not in the divers mouth—as the danger of drowning is then greater than that of AGE—but the ascent should be delayed until the end of the clonic phase otherwise. Rescuers ensure that their own safety is not compromised during the convulsive phase. They then ensure that where the victims air supply is established it is maintained, and carry out a controlled buoyant lift. Lifting an unconscious body is taught by most recreational diver training agencies as an advanced skill, and for professional divers it is a basic skill, as it is one of the primary functions of the standby diver. Upon reaching the surface, emergency services are always contacted as there is a possibility of further complications requiring medical attention. The U.S. Navy has procedures for completing the decompression stops where a recompression chamber is not immediately available.The occurrence of symptoms of bronchopulmonary dysplasia or acute respiratory distress syndrome is treated by lowering the fraction of oxygen administered, along with a reduction in the periods of exposure and an increase in the break periods where normal air is supplied. Where supplemental oxygen is required for treatment of another disease (particularly in infants), a ventilator may be needed to ensure that the lung tissue remains inflated. | 11
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Patients should be questioned about their medication history, any history of pruritus or genital pain and history of dysphagia or odynophagia. Examination of entire cutaneous surface including the scalp, oral cavity and external genitalia need to be included. Wickhams striae often can be seen during microscopic examination of cutaneous lesions of lichen planus.To confirm the diagnosis of cutaneous lichen planus, a skin biopsy can be done. A punch biopsy of sufficient depth to the mid dermis is usually significant. Immunofluorescence studies are not always needed. Direct immunofluorescence (DIF) can be useful in patients with bullous lesions to differentiate the condition from an autoimmune vesiculobullous disease. Mouth
A diagnosis of oral lichen planus (LP) is confirmed through review of the patient history, physical examination, and histologic findings.The clinical evaluation should include a patient history that assesses the following:
History of LP involving other body sites or other skin disorders that may present with similar findings (e.g., autoimmune blistering diseases)
Presence of associated symptoms (e.g., pain, burning)
Medication the patients are taking within the few weeks to months after drug initiation e.g. antihypertensives, antidepressants, diuretics, antidiabetics, NSAIDs, etc. to evaluate for the possibility of an oral lichenoid drug eruption
History of dental restorations, use of dental appliances, or oral exposure to substances that may cause oral lichenoid contact eruptions (e.g. dental composites, cobalt chromium based dentures etc. )A full examination that includes the evaluation of the mucosal and cutaneous surfaces, including the vulva, vagina, penis, scalp, and nails should be performed. | About 50% of females with oral lichen planus were reported to have undiagnosed vulvar lichen planus.Some studies suggest that cutaneous lichen planus is more commonly found in men whilst oral lichen planus lesions are more commonly found in women. History
Lichen planus was first reported in 1869 by Erasmus Wilson.The origin of the word is believed to be from the Greek word Leichen, which means tree moss, and also from Latin word planus, which means flat and even surface. Dr Wilson explained the condition as an inflammatory disorder with unknown etiology. Initially, the characteristic surface markings or striae was described by Weyl in 1885. In 1895, Wickham further explained the characteristic of the lesion, now known as Wickham striae. Further on, Darier explained the presence of such characteristic markings by correlating with an increase thickness of the granular cell layer. The coexistence of oral, cervical and stomach lichen planus lesions were described by Guogerot and Burnier in 1937. A similar variant of mucosal lichen planus as the vulvovaginal-gingival syndrome with erosive lesions involving oral and vulvovaginal mucosa were introduced by Pelisse and colleagues in year 1982. Research
Apremilast is undergoing investigation as a potential treatment. Notes
References
External links
Lichen planus at Curlie | 11
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This usually happens with chronic obstruction of the bladder outlet or with diseases damaging the nerves supplying the urinary bladder. The urine stretches the bladder without the person feeling the pressure, and eventually, it overwhelms the ability of the urethral sphincter to hold it back. Mixed incontinence contains symptoms of multiple other types of incontinence. It is not uncommon in the elderly female population and can sometimes be complicated by urinary retention. Other types
Functional incontinence occurs when a person recognizes the need to urinate but cannot make it to the bathroom. The loss of urine may be large. There are several causes of functional incontinence including confusion, dementia, poor eyesight, mobility or dexterity, unwillingness to the toilet because of depression or anxiety or inebriation due to alcohol. Functional incontinence can also occur in certain circumstances where no biological or medical problem is present. For example, a person may recognize the need to urinate but may be in a situation where there is no toilet nearby or access to a toilet is restricted. Structural incontinence: Rarely, structural problems can cause incontinence, usually diagnosed in childhood (for example, an ectopic ureter). Fistulas caused by obstetric and gynecologic trauma or injury are commonly known as obstetric fistulas and can lead to incontinence. These types of vaginal fistulas include, most commonly, vesicovaginal fistula and, more rarely, ureterovaginal fistula. These may be difficult to diagnose. The use of standard techniques along with a vaginogram or radiologically viewing the vaginal vault with instillation of contrast media. | That order requires incontinence briefs funded by Medicaid to be given by Missouri to adults who would be institutionalized without them. Research
The effectiveness of different therapeutic approaches to treating urinary incontinence is not well studied for some medical conditions. For example, for people who experience urinary incontinence due to stroke, treatment approaches such as physical therapy, cognitive therapy, complementary medicine, and specialized interventions with experienced medical professionals are sometimes suggested, however it is not clear how effective these are at improving incontinence and there is no strong medical evidence to guide clinical practice. References
External links
Urinary incontinence at Curlie
Patient-centered information from the European Urological Association
Independent continence product advisor | 11
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In general, about 1-3% of the tick population carries R. rickettsii, even in areas where the majority of human cases are reported. Therefore, the risk of exposure to a tick carrying R. rickettsii is low.The disease is spread by the American dog tick (Dermacentor variabilis), Rocky Mountain wood tick (D. andersoni), brown dog tick (Rhipicephalus sanguineus), and Amblyomma sculptum. Not all of these are of equal importance, and most are restricted to certain geographic areas. The two major vectors of R. rickettsii in the United States are the American dog tick and the Rocky Mountain wood tick. American dog ticks are widely distributed east of the Rocky Mountains and they also occur in limited areas along the Pacific Coast. Dogs and medium-sized mammals are the preferred hosts of an adult American dog tick, although it feeds readily on other large mammals, including human beings. This tick is the most commonly identified species responsible for transmitting R. rickettsii to humans. Rocky Mountain wood ticks (D. andersoni) are found in the Rocky Mountain states and in southwestern Canada. The lifecycle of this tick may require up to three years for its completion. The adult ticks feed primarily on large mammals. The larvae and nymphs feed on small rodents.Other tick species have been shown to be naturally infected with R. rickettsii or serve as experimental vectors in the laboratory. These species are likely to play only a minor role in the ecology of R. rickettsii. | In cardiology, ventricular dyssynchrony is a difference in the timing, or lack of synchrony, of contractions in different ventricles in the heart. Large differences in timing of contractions can reduce cardiac efficiency and is correlated with heart failure. Types of dyssynchrony
Three chief presentations of dyssynchrony can occur:
Atrioventricular (AV) dyssynchrony occurs when there is an unfavorable difference in timing between atrial and ventricular contractions. Interventricular dyssynchrony occurs when there is a difference in timing between right ventricular (RV) and left ventricular (LV) Systole. Intraventricular dyssynchrony occurs when the timing in a sequence of activations and contractions of segments of the LV wall becomes abnormal. In all three types, changes in timing lead to changes in the dynamic behavior of the myocardial tissues, leading to mechanical dyssynchrony. All three presentations allow distinct and easily reproducible electrical signatures as illustrated by left and right bundle branch blocks, hemiblocks, etc. The concise measurement of the time and morphology of the QRS interval allows the interventional ability to manipulate this interval with biventricular pacemakers. It is important to distinguish ventricular dyssynchrony from ventricular dyssynergy. Dyssynergy refers to changes in relative strength of contractions, whereas dyssynchrony is a change in relative timing of contractions. Once again the terms inotropy and chronotropy apply to the pathology under examination. Biventricular pacing strongly favors chronotropy over inotropy. Diagnosis
Echocardiography and tissue Doppler echocardiography are both needed to fully diagnose the different types of ventricular dyssynchrony. Treatment
Recent studies suggest that cardiac resynchronization therapy can reduce the incidence of ventricular dyssynchrony and thus increase cardiac efficiency. | 0-1
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Without treatment the infantile form (which can typically be predicted by mutation analysis) of the disease is particularly lethal - in these cases time to get on treatment is critical, with evidence that days (not weeks or months) matter.Myozyme (alglucosidase alfa) is a recombinant form of the human enzyme acid alpha-glucosidase, and is also currently being used to replace the missing enzyme. In a study which included the largest cohort of patients with Pompe disease treated with enzyme replacement therapy (ERT) to date findings showed that Myozyme treatment clearly prolongs ventilator-free survival and overall survival in patients with infantile-onset Pompe disease as compared to an untreated historical control population. Furthermore, the study demonstrated that initiation of ERT prior to 6 months of age, which could be facilitated by newborn screening, shows great promise to reduce the mortality and disability associated with this devastating disorder. Taiwan and several states in the United States have started the newborn screening and results of such regimen in early diagnosis and early initiation of the therapy have dramatically improved the outcome of the disease; many of these babies have reached the normal motor developmental milestones.Another factor affecting the treatment response is generation of antibodies against the infused enzyme, which is particularly severe in Pompe infants who have complete deficiency of the acid alpha-glucosidase. Immune tolerance therapy to eliminate these antibodies has improved the treatment outcome.A Late Onset Treatment Study (LOTS) was published in 2010. | On June 14, 2007, the Canadian Common Drug Review issued their recommendations regarding public funding for Myozyme therapy. Their recommendation was to provide funding to treat a tiny subset of Pompe patients (Infants less one year of age with cardiomyopathy).On May 26, 2010, FDA approved Lumizyme, a similar version of Myozyme, for the treatment of late-onset Pompe disease. Lumizyme and Myozyme have the same generic ingredient (alglucosidase alfa) and manufacturer (Genzyme Corporation). The difference between these two products is in the manufacturing process. Myozyme is made using a 160-L bioreactor, while Lumizyme uses a 4000-L bioreactor. Because of the difference in the manufacturing process, the FDA claims that the two products are biologically different. Moreover, Lumizyme is FDA approved as replacement therapy for late-onset (noninfantile) Pompe disease without evidence of cardiac hypertrophy in people 8 years and older. Myozyme is FDA approved for replacement therapy for infantile-onset Pompe disease.In July 2021, the European Medicines Agency (EMA) recommended the authorization of avalglucosidase alfa. Avalglucosidase alfa (Nexviazyme) was approved for medical use in the United States in August 2021. Prognosis
The prognosis for individuals with Pompe disease varies according to the onset and severity of symptoms, along with lifestyle factors. | 11
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Adverse events
The most common adverse events reported in clinical studies were mild or moderate reactions involving the skin and appendages (primarily urticaria, rash, or pruritus), which occurred in 14 out of 42 patients. Three patients experienced a serious adverse event. Two patients had a severe allergic reaction (severe hives and a severe rash and pruritus) following treatment. One patient had a recurrent coagulopathy due to envenomation, which required re-hospitalisation and additional antivenin administration. In clinical trials, recurrent coagulopathy (the return of a coagulation abnormality after it has been successfully treated with antivenin), characterised by decreased fibrinogen, decreased platelets and elevated prothrombin time, occurred in approximately half of the patients studied. Recurrent coagulopathy may persist for one to two weeks or more. One patient discontinued CroFab therapy due to an allergic reaction. Patients with allergies to papain, chymopapain, other papaya extracts or the pineapple enzyme bromelain may also be at risk for an allergic reaction to CroFab. Cost
Leslie Boyer, Director of the VIPER Institute, who was on the team that developed CroFab, said they were "crestfallen" to discover that the wholesale price of Anascorp, their latest antivenom, was too high to be cost effective, even in the treatment of critically ill children. The industry website Fierce Pharma called the product a “drug launch disaster” and “one of the most bizarre marketing tales in the industry.” Boyer said that CroFab, a US drug whose sister product retailed in Mexico at $100, was resulting in bills to Arizona patients of between $7,900 and $39,652 per vial. | Crotalidae polyvalent immune fab, sold under the brandname CroFab, is a snake antivenin, indicated for minimal or moderate North American Crotalid (Rattlesnake, Copperhead and Cottonmouth/Water moccasin) snake envenomation. CroFab is composed of several monovalent Fragment antigen-binding proteins (Fab) derived from the blood of sheep immunized with one of four snake venom: Crotalus atrox (western diamondback rattlesnake), Crotalus adamanteus (Eastern diamondback rattlesnake), Crotalus scutulatus (Mojave rattlesnake), or Agkistrodon piscivorus (Cottonmouth or Water Moccasin). Each monospecific antivenin is purified from sheep serum, digested with the enzyme papain, and purified further resulting in specific Fab fragments. The resulting four different Fab preparations are mixed to formulate the final product. Background
It was developed by the Venom Immunochemistry, Pharmacology and Emergency Response (VIPER) Institute, University of Arizona, and commercialized by BTG plc (formerly Protherics PLC). As reported in the Washington Post in July 2015, this was the only commercially available antivenin in the United States for the treatment of venomous snakebites until the release of a competing product, ANAVIP. Treatment
Crotalid snakebites can range from mild to life-threatening, depending on the size and type of snake, the amount of venom injected and the location of the bite. This in turn determines the number of vials of CroFab that are required by the patient. Untreated, the snake venom can cause severe pain and tissue damage that can result in the loss of a limb or even death. Prompt (within six hours of snake bite) treatment with CroFab is recommended. Fab refers to Fragment Antigen-Binding, the active mechanism for this antivenom. | 11
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Discitis, or diskitis, is an infection in the intervertebral disc space that affects different age groups. In adults, it can lead to severe consequences, such as sepsis or epidural abscess, but it can also spontaneously resolve, especially in children under 8 years of age. Discitis occurs post-surgically in approximately 1–2 percent of patients after spinal surgery. Signs and symptoms
Symptoms include severe back pain, leading to lack of mobility. Some very young children may refuse to walk and arching of the back is possible. In post-operative situations, the symptoms occur within a week and result in severe low back pain or neck pain (depending on the surgical location). If untreated, the discitis may resolve on its own, causing spontaneous fusion of the intervertebral disc space, cause a chronic low grade infection, or progress to osteomyelitis and possibly even an epidural abscess. In case of concomitant inflammation of one or more vertebrae (in such cases usually involving the areas adjacent to the intervertebral disc spaces) the condition is called spondylodiscitis. Causes
There is debate as to the cause, although hematogenous seeding of the offending organism is favored as well as direct spread. It is important to differentiate between spontaneous discitis which is usually from hematologic spread from a urinary or respiratory infection versus that from a post-operative complication which usually involves skin flora such as staph aureus. It can be caused due to spinal tuberculosis and spread along spinal ligament to involve the adjacent anterior vertebral bodies, causing angulation of the vertebrae with subsequent kyphosis. | Schenck and Mahowald also discovered that none of the patients had any eating instability before their problems at night while sleeping. In their 1993 report, they summarized the major findings with the idea that women encompass at least two thirds of the patients and that the majority of these patients had become overweight. They also discovered that while the patients night-eating normally started during early adulthood, this wasnt always the case as it started as early as childhood to as late as middle adulthood. These patients not only had NSRED, but many of them had also had other nighttime behaviors such as sleep terrors for several years. This revolutionized the way people saw NSRED. With the technological age growing and more people becoming obese, Schenck and Mahowalds discovery of NSRED causing a large weight increase helped doctors more easily identify this disorder. As seen in Table 1 below, almost half of Schenck and Mahowalds patients were significantly obese. According to body mass indexs criteria, no patient was emaciated. Schenck and Mahowald said, "virtually all patients had accurate non-distorted appraisals of their body size, shape, and weight. Furthermore, unlike the patients in Stunkards series, none of our patients had problematic eating in the evening between dinner and bedtime; sleep onset insomnia was not present; and sleep latency was usually brief, apart from several patients with RLS." After realizing what was wrong with them, many of Schenck and Mahowalds patients with NSRED restricted their day eating and over exercised. | 0-1
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Pyridoxine, or Vitamin B6 may be used as adjunctive therapy in some cases, which may be referred to as Pyridoxine responsive seizures. History
It was discovered initially in 1936 but was fully named and documented by a Canadian pediatrician, John Campbell Rathbun (1915-1972), while examining and treating a baby boy with very low levels of alkaline phosphatase in 1948. The genetic basis of the disease was mapped out only some 40 years later. Hypophosphatasia is sometimes called Rathbuns syndrome after its principal documenter. See also
Alkaline phosphatase
Choline
References
Further reading
External links
Online Mendelian Inheritance in Man (OMIM): Adult Hypophosphatasia - 146300 | IGF-1 is responsible for most of the symptoms of acromegaly, and the normalization of its levels can control the symptoms.Long-term treatment studies with pegvisomant as a monotherapy have shown it to be safe, and effective. Research
Some studies show the potential of using pegvisomant as an anti-tumor treatment for certain types of cancers. References
External links
"Pegvisomant". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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The scavenger can be any reagent that will irreversibly react with water such as phthalic anhydride or titanium chloride. The temperature required for the reaction varies based upon choice of acid and water scavenger. The yield of this reaction is much higher: at least 55%. History
The pharmacological effects of the naturally-occurring analog aporphine in the blue lotus (Nymphaea caerulea) were known to the ancient Egyptians and Mayans, with the plant featuring in tomb frescoes and associated with entheogenic rites. It is also observed in Egyptian erotic cartoons, suggesting that they were aware of its erectogenic properties. The modern medical history of apomorphine begins with its synthesis by Arppe in 1845 from morphine and sulfuric acid, although it was named sulphomorphide at first. Matthiesen and Wright (1869) used hydrochloric acid instead of sulfuric acid in the process, naming the resulting compound apomorphine. Initial interest in the compound was as an emetic, tested and confirmed safe by London doctor Samuel Gee, and for the treatment of stereotypies in farmyard animals. Key to the use of apomorphine as a behavioural modifier was the research of Erich Harnack, whose experiments in rabbits (which do not vomit) demonstrated that apomorphine had powerful effects on the activity of rabbits, inducing licking, gnawing and in very high doses convulsions and death. Treatment of alcoholism
Apomorphine was one of the earliest used pharmacotherapies for alcoholism. | Opioid addiction
In his Deposition: Testimony Concerning a Sickness in the introduction to later editions of Naked Lunch (first published in 1959), William S. Burroughs wrote that apomorphine treatment was the only effective cure to opioid addiction he has encountered:
The apomorphine cure is qualitatively different from other methods of cure. I have tried them all. Short reduction, slow reduction, cortisone, antihistamines, tranquilizers, sleeping cures, tolserol, reserpine. None of these cures lasted beyond the first opportunity to relapse. I can say that I was never metabolically cured until I took the apomorphine cure... The doctor, John Yerbury Dent, explained to me that apomorphine acts on the back brain to regulate the metabolism and normalize the blood stream in such a way that the enzyme stream of addiction is destroyed over a period of four to five days. Once the back brain is regulated apomorphine can be discontinued and only used in case of relapse. He goes on to lament the fact that as of his writing, little to no research has been done on apomorphine or variations of the drug to study its effects on curing addiction, and perhaps the possibility of retaining the positive effects while removing the side effect of vomiting. Despite his claims throughout his life, Burroughs never really cured his addiction and was back to using opiates within years of his apomorphine "cure". However, he insisted on apomorphines effectiveness in several works and interviews. Society and culture
Apomorphine has a vital part in Agatha Christies detective story Sad Cypress. | 11
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Alternating hemiplegia (also known as crossed hemiplegia) is a form of hemiplegia that has an ipsilateral cranial nerve palsies and contralateral hemiplegia or hemiparesis of extremities of the body. The disorder is characterized by recurrent episodes of paralysis on one side of the body. There are multiple forms of alternating hemiplegia, Webers syndrome, middle alternating hemiplegia, and inferior alternating hemiplegia. This type of syndrome can result from a unilateral lesion in the brainstem affecting both upper motor neurons and lower motor neurons. The muscles that would receive signals from these damaged upper motor neurons result in spastic paralysis. With a lesion in the brainstem, this affects the majority of limb and trunk muscles on the contralateral side due to the upper motor neurons decussation after the brainstem. The cranial nerves and cranial nerve nuclei are also located in the brainstem making them susceptible to damage from a brainstem lesion. Cranial nerves III (Oculomotor), VI (Abducens), and XII (Hypoglossal) are most often associated with this syndrome given their close proximity with the pyramidal tract, the location which upper motor neurons are in on their way to the spinal cord. Damages to these structures produce the ipsilateral presentation of paralysis or palsy due to the lack of cranial nerve decussation (aside from the trochlear nerve) before innervating their target muscles. The paralysis may be brief or it may last for several days, many times the episodes will resolve after sleep. | Subepithelial mucinous corneal dystrophy (SMCD) is a rare form of corneal dystrophy. It was first described in 1993 by Feder et al. Anterior to Bowman layer, deposits of glycosaminoglycan were detected and identified as chondroitin-4-sulfate and dermatan sulfate. References
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Nodular vasculitis is a skin condition characterized by crops of small, tender, erythematous nodules on the legs, mostly on the calves and shins. Miroscopically there are epithelioid granulomas and vasculitis in the subcutaneous tissue, making it a form of panicullitis. Most of these cases are now thought to be manifestation of tuberculosis and indeed they respond well to anti-tuberculous treatment. See also
Panniculitis
List of cutaneous conditions
References
== External links == | "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. | 0-1
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It may also act as a norepinephrine reuptake inhibitor at higher therapeutic doses. Compared to amphetamine, tranylcypromine shows low potency as a dopamine releasing agent, with even weaker potency for norepinephrine and serotonin release.Tranylcypromine has also been shown to inhibit the histone demethylase, BHC110/LSD1. Tranylcypromine inhibits this enzyme with an IC50 < 2 μM, thus acting as a small molecule inhibitor of histone demethylation with an effect to derepress the transcriptional activity of BHC110/LSD1 target genes. The clinical relevance of this effect is unknown. Tranylcypromine has been found to inhibit CYP46A1 at nanomolar concentrations. The clinical relevance of this effect is unknown. Pharmacokinetics
Tranylcypromine reaches its maximum concentration (tmax) within 1–2 hours. After a 20 mg dose, plasma concentrations reach at most 50-200 ng/mL. While its half-life is only about 2 hours, its pharmacodynamic effects last several days to weeks due to irreversible inhibition of MAO.Metabolites of tranylcypromine include 4-hydroxytranylcypromine, N-acetyltranylcypromine, and N-acetyl-4-hydroxytranylcypromine, which are less potent MAO inhibitors than tranylcypromine itself. Amphetamine was once thought to be a metabolite of tranylcypromine, but has not been shown to be.Tranylcypromine inhibits CYP2A6 at therapeutic concentrations. Chemistry
Synthesis
History
Tranylcypromine was originally developed as an analog of amphetamine. Although it was first synthesized in 1948, its MAOI action was not discovered until 1959. | Many different treatments have been attempted, with limited success in certain patients: purine analogues (pentostatin, fludarabine, cladribine), chlorambucil, and various forms of combination chemotherapy regimens, including cyclophosphamide, doxorubicin, vincristine, prednisone (CHOP), etoposide, bleomycin (VAPEC-B). Alemtuzumab (Campath), an anti-CD52 monoclonal antibody that attacks white blood cells, has been used in treatment with greater success than previous options. In one study of previously treated people with T-PLL, people who had a complete response to alemtuzumab survived a median of 16 months after treatment.Some patients who successfully respond to treatment also undergo stem cell transplantation to consolidate the response. Prognosis
T-PLL is an extremely rare aggressive disease, and patients are not expected to live normal lifespans. Before the recent introduction of better treatments, such as alemtuzumab, the median survival time was 7.5 months after diagnosis. More recently, some patients have survived five years and more, although the median survival is still low. Epidemiology
About four men are diagnosed with this disease for every three women. Despite its overall rarity, it is also the most common type of mature T cell leukemia. References
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Skin nearby the lesion often shows evidence of solar damage characterized by notable pigmentary alterations, being yellow or pale in color with areas of hyperpigmentation; deep wrinkles, coarse texture, purpura and ecchymoses, dry skin, and scattered telangiectasias are also characteristic.Photoaging leads to an accumulation of oncogenic changes, resulting in a proliferation of mutated keratinocytes that can manifest as AKs or other neoplastic growths. With years of sun damage, it is possible to develop multiple AKs in a single area on the skin. This condition is termed field cancerization. The lesions are usually asymptomatic, but can be tender, itch, bleed, or produce a stinging or burning sensation. AKs are typically graded in accordance with their clinical presentation: Grade I (easily visible, slightly palpable), Grade II (easily visible, palpable), and Grade III (frankly visible and hyperkeratotic). Variants
Actinic keratoses can have various clinical presentations, often characterized as follows:
Classic (or common): Classic AKs present as white, scaly macules, papules or plaques of various thickness, often with surrounding erythema. They are usually 2–6mm in diameter but can sometimes reach several centimeters in diameter. Hypertrophic (or hyperkeratotic): Hypertrophic AKs (HAKs) appears as a thicker scale or rough papule or plaque, often adherent to an erythematous base. Classic AKs can progress to become HAKs, and HAKs themselves can be difficult to distinguish from malignant lesions. Atrophic: Atrophic AKs lack an overlying scale, and therefore appear as a nonpalpable change in color (or macule). They are often smooth and red and are less than 10mm in diameter. | Monocephalus is a genus of dwarf spiders that was first described by F. P. Smith in 1906. Species
As of May 2019 it contains two species:
Monocephalus castaneipes (Simon, 1884) – Europe
Monocephalus fuscipes (Blackwall, 1836) (type) – Europe
See also
List of Linyphiidae species (I–P)
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Eplerenone, sold under the brand name Inspra, is an aldosterone antagonist type of potassium-sparing diuretic that is used to treat chronic heart failure and high blood pressure, particularly for patients with resistant hypertension due to elevated aldosterone. It is a steroidal antimineralocorticoid of the spirolactone group and a selective aldosterone receptor antagonist (SARA). Eplerenone is more selective than spironolactone at the mineralocorticoid receptor relative to binding at androgen, progestogen, glucocorticoid, or estrogen receptors. Medical uses
Heart failure
Eplerenone reduces risk of death in patients with heart failure, particularly in patients with recent myocardial infarction (heart attack). Hypertension
Eplerenone lowers blood pressure in patients with primary hypertension. Eplerenone also reduces arterial stiffness and vascular endothelial dysfunction.For persons with resistant hypertension, eplerenone is safe and effective for reducing blood pressure, particularly in persons with resistant hypertension due to hyperaldosteronism. Central serous chorioretinopathy
Eplerenone is often prescribed for people with central serous chorioretinopathy (CSC). However, the most recent and largest randomized controlled trial showed that eplerenone has no significant effect on chronic CSC. Adverse effects
Common adverse drug reactions (ADRs) associated with the use of eplerenone include: hyperkalaemia, hypotension, dizziness, and reduced renal clearance. Eplerenone may have a lower incidence than spironolactone of sexual side effects such as feminization, gynecomastia, impotence, low sex drive and reduction of size of male genitalia. This is because other antimineralocorticoids have structural elements of the progesterone molecule, causing progestogenic and antiandrogenic outcomes. | The remainder is attributed to secondary causes: vascular problems, infections and various other conditions. History
The importance of severe headaches in the diagnosis of subarachnoid hemorrhage has been known since the 1920s, when London neurologist Charles Symonds described the clinical syndrome. The term "thunderclap headache" was introduced in 1986 in a report by John Day and Neil Raskin, neurologists at the University of California, San Francisco, in a report of a 42-year-old woman who had experienced several sudden headaches and was found to have an aneurysm that had not ruptured. References
Further reading
Dodick, DW (1 January 2002). "Thunderclap headache". Journal of Neurology, Neurosurgery & Psychiatry. 72 (1): 6–11. doi:10.1136/jnnp.72.1.6. PMC 1737692. PMID 11784817. Ju, Yo-El; Schwedt, Todd (29 March 2010). "Abrupt-Onset Severe Headaches". Seminars in Neurology. 30 (2): 192–200. doi:10.1055/s-0030-1249229. PMC 3558726. PMID 20352589. Ducros, A; Bousser, MG (9 January 2013). "Thunderclap headache". BMJ. 346 (jan08 15): e8557. doi:10.1136/bmj.e8557. PMID 23303883. S2CID 2537784. == External links == | 0-1
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As the respiratory muscles relax the air is expelled through the mouth, effectively "burping" the animal.There are a number of characteristics of hiccups that support this theory. The burping of a suckling infant may increase its capacity for milk by more than 15-25%, bringing a significant survival advantage. There is a strong tendency for infants to get hiccups, and although the reflex persists throughout life it decreases in frequency with age. The location of the sensory nerves that trigger the reflex suggests it is a response to a condition in the stomach. The component of the reflex that suppresses peristalsis in the esophagus while the airway is being actively blocked suggests the esophagus is involved. Additionally, hiccups are only described in mammals - the group of animals that share the trait of suckling their young. Phylogenetic hypothesis
An international respiratory research group composed of members from Canada, France, and Japan proposed that the hiccup is an evolutionary remnant of earlier amphibian respiration. Amphibians such as tadpoles gulp air and water across their gills via a rather simple motor reflex akin to mammalian hiccuping. The motor pathways that enable hiccuping form early during fetal development, before the motor pathways that enable normal lung ventilation form. Thus, the hiccup is evolutionarily antecedent to modern lung respiration. Additionally, this group (C. Straus et al.) points out that hiccups and amphibian gulping are inhibited by elevated CO2 and may be stopped by GABAB receptor agonists, illustrating a possible shared physiology and evolutionary heritage. | The Food and Drug Administration approved the vagus nerve stimulator in 1997 as a way to control seizures in some patients with epilepsy. "Persistent digital rectal massage has also been proven effective in terminating intractable hiccups. Folk remedies
There are many superstitious and folk remedies for hiccups, including headstanding, drinking a glass of water upside-down, being frightened by someone, breathing into a bag, eating a large spoonful of peanut butter and placing sugar on or under the tongue.Acupressure, either through actual function or placebo effect, may cure hiccups in some people. For example, one technique is to relax the chest and shoulders and find the deepest points of the indentations directly below the protrusions of the collarbones. The index or middle fingers are inserted into the indents and pressed firmly for sixty seconds as long, deep breaths are taken.A simple treatment involves increasing the partial pressure of CO2 and inhibiting diaphragm activity by holding ones breath or rebreathing into a paper bag. Other potential remedies suggested by NHS Choices include pulling the knees up to the chest and leaning forward, sipping ice-cold water and swallowing some granulated sugar.Drinking through a straw with the ears plugged is a folk remedy that can be successful. In 2021 a scientific tool with a similar basis was tested on 249 hiccups subjects; the results were published in the Journal of the American Medical Association (JAMA). This device is named FISST (Forced Inspiratory Suction and Swallow Tool) and branded as "HiccAway". | 11
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Burkitt lymphoma is a cancer of the lymphatic system, particularly B lymphocytes found in the germinal center. It is named after Denis Parsons Burkitt, the Irish surgeon who first described the disease in 1958 while working in equatorial Africa. The overall cure rate for Burkitt lymphoma in developed countries is about 90%, and it is worse in low-income countries. Burkitt lymphoma is uncommon in adults, in whom it has a worse prognosis. Classification
Burkitt lymphoma can be divided into three main clinical variants: the endemic, the sporadic, and the immunodeficiency-associated variants. By morphology (i.e., microscopic appearance), immunophenotype, and genetics, the variants of Burkitt lymphoma are alike. The endemic variant (also called "African variant") most commonly occurs in children living in malaria-endemic regions of the world (e.g., equatorial Africa, Brazil, and Papua New Guinea). Epstein–Barr virus (EBV) infection is found in nearly all patients. Chronic malaria is believed to reduce resistance to EBV, allowing it to take hold. The disease characteristically involves the jaw or other facial bone, distal ileum, cecum, ovaries, kidney, or breast. The sporadic type of Burkitt lymphoma (also known as "non-African") is the most common variant found in places where malaria is not prevalent such as North America and parts of Europe. The tumor cells have a similar appearance to the cancer cells of classical endemic Burkitt lymphoma. Sporadic lymphomas are rarely associated with the EBV. The jaw is less commonly involved in this variant. The abdominal region is the common site of involvement. | Epidemiology
As a non-Hodgkin lymphoma (NHL), Burkitt lymphoma makes up 1-5% of cases, and it is more common in males than females with a 3–4 to 1 ratio. The endemic variant mainly impacts areas with an increased prevalence of malaria and EBV in Africa and Papua New Guinea. For children less than 18 years of age from equatorial Africa, the annual incidence of Burkitt lymphoma is 4–5/100,000. Additionally, in equatorial Africa, 50% of tumors that are diagnosed during childhood as well as 90% of lymphoma cases can be attributed to Burkitt lymphoma. The peak incidence for endemic Burkitt lymphoma is from ages 4 to 7 with an average age of 6 years. The sporadic variant with an annual incidence 2-3/million is more commonly found in North America and Europe comprising 1-2% of adult lymphomas and 30–40% of NHL cases. This variant is 3.5 times more commonly found in males compared to females and it is more frequent in younger individuals. The sporadic variant has a peak incidence at 11 years of age in children, and diagnosis typically occurs from 3–12 years of age on average. For adults, 45 years was the median age that the sporadic Burkitt lymphoma was diagnosed. The immunodeficiency-associated variant predominantly impacts the HIV-infected population. For those in the United States and with AIDS, the incidence of this variant was found to be 22/100,000 person-years. | 11
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The presence of metastatic disease is the most important prognostic factor in Ewing Sarcoma with the 5 year survival rate being only 30% when metastasis is present at the time of diagnosis as compared to a 70% 5 year survival rate with no metastasis present. Another important prognostic factor is the location of the primary tumor; proximal tumors (located in the pelvis and sacrum) are worse prognostic indicators as compared to more distal tumors. Other factors associated with a poor prognosis include a large primary neoplasm, older age at diagnosis (older than 18 years of age) and increased lactate dehydrogenase (LDH) levels.Five-year survival for localized disease is greater than 70% after therapy. Prior to the use of multi-drug chemotherapy, long-term survival was less than 10%. The development of multi-disciplinary therapy with chemotherapy, irradiation, and surgery has increased current long-term survival rates in most clinical centers to greater than 50%. However, some sources state it is 25–30%.Retrospective research showed that two chemokine receptors, CXCR4 and CXCR7, can be used as molecular prognosis factors. People who express low levels of both chemokine receptors have the highest odds of long-term survival with >90% survival at five years post-diagnosis versus <30% survival at five years for patients with very high expression levels of both receptors. A recent study also suggested a role for SOX2 as an independent prognostic biomarker that can be used to identify patients at high risk for tumor relapse. Epidemiology
Ewing sarcomas represent 16% of primary bone sarcomas. | In analytical chemistry, EDTA is used in complexometric titrations and analysis of water hardness or as a masking agent to sequester metal ions that would interfere with the analyses. EDTA finds many specialised uses in the biomedical labs, such as in veterinary ophthalmology as an anticollagenase to prevent the worsening of corneal ulcers in animals. In tissue culture EDTA is used as a chelating agent that binds to calcium and prevents joining of cadherins between cells, preventing clumping of cells grown in liquid suspension, or detaching adherent cells for passaging. In histopathology, EDTA can be used as a decalcifying agent making it possible to cut sections using a microtome once the tissue sample is demineralised. EDTA is also known to inhibit a range of metallopeptidases, the method of inhibition occurs via the chelation of the metal ion required for catalytic activity. EDTA can also be used to test for bioavailability of heavy metals in sediments. However, it may influence the bioavailability of metals in solution, which may pose concerns regarding its effects in the environment, especially given its widespread uses and applications. EDTA is also used to remove crud (corroded metals) from fuel rods in nuclear reactors. Side effects
EDTA exhibits low acute toxicity with LD50 (rat) of 2.0 g/kg to 2.2 g/kg. It has been found to be both cytotoxic and weakly genotoxic in laboratory animals. Oral exposures have been noted to cause reproductive and developmental effects. | 0-1
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This system recognized differences in genetic, immunophenotype, molecular, and morphological features found through cytogenetic and molecular diagnostics tests. : 1531–1535 This subtyping helps determine the prognosis and the most appropriate treatment for each specific case of ALL. The WHO subtypes related to ALL are:
B-lymphoblastic leukemia/lymphoma
Not otherwise specified (NOS)
with recurrent genetic abnormalities
with t(9;22)(q34.1;q11.2);BCR-ABL1
with t(v;11q23.3);KMT2A rearranged
with t(12;21)(p13.2;q22.1); ETV6-RUNX1
with t(5;14)(q31.1;q32.3) IL3-IGH
with t(1;19)(q23;p13.3);TCF3-PBX1
with hyperdiploidy
with hypodiploidy
T-lymphoblastic leukemia/lymphoma
Acute leukemias of ambiguous lineage
Acute undifferentiated leukemia
Mixed phenotype acute leukemia (MPAL) with t(9;22)(q34.1;q11.2); BCR–ABL1
MPAL with t(v;11q23.3); KMT2A rearranged
MPAL, B/myeloid, NOS
MPAL, T/myeloid, NOS
MicroRNA signature
A systematic review of miRNA levels in pediatric B-ALL compared with controls revealed that miR-155 is the most frequently reported upregulated miRNA (followed by miR-146a, miR-181b, miR-222 and miR-708; two citations for miR-16, miR-21, miR-34a, miR-100, miR-128-1, miR-181a, miR-181c, miR-195, miR-210, miR-320a and miR-660), whereas the most frequently reported downregulated miRNA is miR-374a (two citations for miR-27a, miR-30c, miR-196b, miR-223 and miR-494). To date, there is no consensus miRNA signature and this is mainly attributed to different miRNA signatures across ALL subtypes and methodology of conducted studies. Treatment
The aim of treatment is to induce a lasting remission, defined as the absence of detectable cancer cells in the body (usually less than 5% blast cells in the bone marrow). Over the past several decades, there have been strides to increase the efficacy of treatment regimens, resulting in increased survival rates. Possible treatments for acute leukemia include chemotherapy, steroids, radiation therapy, intensive combined treatments (including bone marrow or stem cell transplants), targeted therapy, and/or growth factors. | Treatment of Patau syndrome focuses on the particular physical problems with which each child is born. Many infants have difficulty surviving the first few days or weeks due to severe neurological problems or complex heart defects. Surgery may be necessary to repair heart defects or cleft lip and cleft palate. Physical, occupational, and speech therapy will help individuals with Patau syndrome reach their full developmental potential. Surviving children are described as happy and parents report that they enrich their lives. Prognosis
Approximately 90% of infants with Patau syndrome die within the first year of life. Those children who do survive past 1 year of life are typically severely disabled with intellectual disability, seizures, and psychomotor issues. Children with the mosaic variation are usually affected to a lesser extent. In a retrospective Canadian study of 174 children with trisomy 13, median survival time was 12.5 days. One and ten year survival was 19.8% and 12.9% respectively, including those who underwent aggressive surgical intervention. History
Trisomy 13 was first observed by Thomas Bartholin in 1657, but the chromosomal nature of the disease was ascertained by Dr. Klaus Patau and Dr. Eeva Therman in 1960. The disease is named in Pataus honor.In England and Wales during 2008–09, there were 172 diagnoses of Patau syndrome (trisomy 13), with 91% of diagnoses made prenatally. There were 111 elective abortions, 14 stillbirth/miscarriage/fetal deaths, 30 outcomes unknown, and 17 live births. | 0-1
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Detection in biological fluids
Sildenafil and/or N-desmethylsildenafil, its major active metabolite, may be quantified in plasma, serum, or whole blood to assess pharmacokinetic status in those receiving the drug therapeutically, to confirm the diagnosis in potential poisoning victims, or to assist in the forensic investigation in a case of fatal overdose. Mechanism of action
Sildenafil protects cyclic guanosine monophosphate (cGMP) from degradation by cGMP-specific phosphodiesterase type 5 (PDE5) in the corpus cavernosum. Nitric oxide (NO) in the corpus cavernosum of the penis binds to guanylate cyclase receptors, which results in increased levels of cGMP, leading to smooth muscle relaxation (vasodilation) of the intimal cushions of the helicine arteries. This smooth muscle relaxation leads to vasodilation and increased inflow of blood into the spongy tissue of the penis, causing an erection. Robert F. Furchgott, Ferid Murad, and Louis Ignarro won the Nobel Prize in Physiology or Medicine in 1998 for their independent study of the metabolic pathway of nitric oxide in smooth muscle vasodilation. The molecular mechanism of smooth muscle relaxation involves the enzyme CGMP-dependent protein kinase, also known as PKG. This kinase is activated by cGMP and it phosphorylates multiple targets in the smooth muscle cells, namely myosin light chain phosphatase, RhoA, IP3 receptor, phospholipase C, and others. Overall, this results in a decrease in intracellular calcium and desensitizing proteins to the effects of calcium, engendering smooth muscle relaxation.Sildenafil is a potent and selective inhibitor of cGMP-specific phosphodiesterase type 5 (PDE5), which is responsible for degradation of cGMP in the corpus cavernosum. | Ciclesonide is a glucocorticoid used to treat asthma and allergic rhinitis. It is marketed under the brand names Alvesco for asthma and Omnaris, Omniair, Zetonna, and Alvesco for hay fever in the US and Canada. Side effects of the medication include headache, nosebleeds, and inflammation of the nose and throat linings.It was patented in 1990 and approved for medical use in 2005. The drug was approved for adults and children 12 and over by the US Food and Drug Administration in October 2006. It is on the World Health Organizations List of Essential Medicines. See also
Beclomethasone dipropionate
References
== Further reading == | 0-1
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For example, varicella zoster virus causes chickenpox in the acute phase; after recovery from chickenpox, the virus may remain dormant in nerve cells for many years, and later cause herpes zoster (shingles). Acute disease
An acute disease is a short-lived disease, like the common cold. Chronic disease
A chronic disease is one that lasts for a long time, usually at least six months. During that time, it may be constantly present, or it may go into remission and periodically relapse. A chronic disease may be stable (does not get any worse) or it may be progressive (gets worse over time). Some chronic diseases can be permanently cured. Most chronic diseases can be beneficially treated, even if they cannot be permanently cured. Clinical disease
One that has clinical consequences; in other words, the stage of the disease that produces the characteristic signs and symptoms of that disease. AIDS is the clinical disease stage of HIV infection. Cure
A cure is the end of a medical condition or a treatment that is very likely to end it, while remission refers to the disappearance, possibly temporarily, of symptoms. Complete remission is the best possible outcome for incurable diseases. Flare-up
A flare-up can refer to either the recurrence of symptoms or an onset of more severe symptoms. Progressive disease
Progressive disease is a disease whose typical natural course is the worsening of the disease until death, serious debility, or organ failure occurs. Slowly progressive diseases are also chronic diseases; many are also degenerative diseases. | Examples of the first-mentioned type are that Turner syndrome and DiGeorge syndrome are still often called by the "syndrome" name despite that they can also be viewed as disease entities and not solely as sets of signs and symptoms. Predisease
Predisease is a subclinical or prodromal vanguard of a disease. Prediabetes and prehypertension are common examples. The nosology or epistemology of predisease is contentious, though, because there is seldom a bright line differentiating a legitimate concern for subclinical/prodromal/premonitory status (on one hand) and conflict of interest–driven disease mongering or medicalization (on the other hand). Identifying legitimate predisease can result in useful preventive measures, such as motivating the person to get a healthy amount of physical exercise, but labeling a healthy person with an unfounded notion of predisease can result in overtreatment, such as taking drugs that only help people with severe disease or paying for drug prescription instances whose benefit–cost ratio is minuscule (placing it in the waste category of CMS "waste, fraud, and abuse" classification). Three requirements for the legitimacy of calling a condition a predisease are:
a truly high risk for progression to disease – for example, a pre-cancer will almost certainly turn into cancer over time
actionability for risk reduction – for example, removal of the precancerous tissue prevents it from turning into a potentially deadly cancer
benefit that outweighs the harm of any interventions taken – removing the precancerous tissue prevents cancer, and thus prevents a potential death from cancer. | 11
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Such uses include induction of anesthesia in high-risk patients such as those with hemorrhagic shock, anaphylactic shock, septic shock, severe bronchospasm, severe hepatic insufficiency, cardiac tamponade, and constrictive pericarditis; anesthesia in caesarian section; use of multiple anesthetics in burns; and as a supplement to regional anesthesia with incomplete nerve blocks. Depression
Esketamine is approved under the brand name Spravato in the form of a nasal spray added to a conventional antidepressant as a therapy for treatment-resistant depression (TRD) as well as major depressive disorder (MDD) associated with suicidal ideation or behavior in adults in the United States. In the clinical trials that led to approval of esketamine, TRD was defined as MDD with inadequate response to at least two different conventional antidepressants. The nasal spray formulation of esketamine used for depression delivers two sprays containing a total of 28 mg esketamine and doses of 56 mg (2 devices) to 84 mg (3 devices) are used. The recommended dosage of Spravato is 56 mg on day 1, 56 or 84 mg twice per week during weeks 1 to 4, 56 or 84 mg once per week during weeks 5 to 8, and 56 or 84 mg every 2 weeks or once weekly during week 9 and thereafter. Dosing is individualized to the least frequent dosing necessary to maintain response or remission. Spravato is administered under the supervision of a healthcare provider and patients are monitored for at least 2 hours during each treatment session. | A January 2021 meta-analysis reported that ketamine was similarly effective to esketamine in terms of antidepressant effect size (SMD for depression score of –1.1 vs. –1.2) but more effective than esketamine in terms of response and remission rates (RR = 3.01 vs. RR = 1.38 for response and RR = 3.70 vs. RR = 1.47 for remission). A September 2021 Cochrane review found that ketamine had an effect size (SMD) for depression at 24 hours of –0.87, with very low certainty, and that esketamine had an effect size (SMD) at 24 hours of –0.31, based on moderate-certainty evidence. However, these meta-analyses have involved largely non-directly-comparative studies with dissimilar research designs and patient populations. Only a single clinical trial has directly compared ketamine and esketamine for depression as of May 2021. This study reported similar antidepressant efficacy as well as tolerability and psychotomimetic effects between the two agents. However, the study was small and underpowered, and more research is still needed to better-characterize the comparative antidepressant effects of ketamine and esketamine. Preliminary research suggests that arketamine, the R(−) enantiomer of ketamine, may also have its own independent antidepressant effects and may contribute to the antidepressant efficacy of racemic ketamine, but more research likewise is needed to evaluate this possibility.In February 2019, an outside panel of experts recommended in a 14–2 vote that the FDA approve the nasal spray version of esketamine for TRD, provided that it be given in a clinical setting, with people remaining on site for at least two hours after. | 11
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In severe forms, psoriatic arthritis may progress to arthritis mutilans which on X-ray gives a "pencil-in-cup" appearance.Because prolonged inflammation can lead to joint damage, early diagnosis and treatment to slow or prevent joint damage is recommended. Causes
The exact causes are not yet known, however silica dust exposure has been identified in Australia and a number of genetic associations have been identified in a genome-wide association study of psoriasis and psoriatic arthritis including HLA-B27. Diagnosis
There is no definitive test to diagnose psoriatic arthritis. Symptoms of psoriatic arthritis may closely resemble other diseases, including rheumatoid arthritis. A rheumatologist (a physician specializing in autoimmune diseases) may use physical examinations, health history, blood tests and x-rays to accurately diagnose psoriatic arthritis. Factors that contribute to a diagnosis of psoriatic arthritis include the following:
Psoriasis in the patient, or a family history of psoriasis or psoriatic arthritis. A negative test result for rheumatoid factor, a blood factor associated with rheumatoid arthritis. Arthritis symptoms in the distal Interphalangeal articulations of hand (the joints closest to the tips of the fingers). This is not typical of rheumatoid arthritis. Ridging or pitting of fingernails or toenails (onycholysis), which is associated with psoriasis and psoriatic arthritis. Radiologic images demonstrating degenerative joint changes.Other symptoms that are more typical of psoriatic arthritis than other forms of arthritis include enthesitis (inflammation in the Achilles tendon (at the back of the heel) or the plantar fascia (bottom of the feet)), and dactylitis (sausage-like swelling of the fingers or toes). | Caffeine/ergotamine (trade name Cafergot) is the proprietary name of a medication consisting of ergotamine tartrate and caffeine. This combination is used for the treatment of headaches, such as migraine headache. Use
Correct timing of use is important. Cafergot is an abortive headache treatment, which prevents the development of the headache, rather than a treatment for an established headache. The medication should be administered at the first sign of headache. There exist some limitations as to the maximum number of tablets that can be taken per day per week. Different sources of drug information may carry different information, and patients are encouraged to ask their pharmacist or prescriber about such details. Cafergot is currently available as a generic drug (ergotamine tartrate/caffeine)
Mechanism of action
According to a topic review on UpToDate, "ergotamine and dihydroergotamine (DHE 45) bind to 5HT 1b/d receptors, just as triptans do." This along with binding to other serotonergic and dopaminergic receptors is their presumed mechanism of action in treating migraine. Adverse effects
Because the vasoconstrictive effects of ergotamine and caffeine are not selective for the brain, adverse effects due to systemic vasoconstriction can occur. Cold feet or hands, angina pectoris, myocardial infarction, or dizziness are some examples. == References == | 0-1
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Both are potent inhibitors of CYP2D6 (which is also the chief enzyme responsible for their metabolism) and CYP2C19, and mild to moderate inhibitors of CYP2B6 and CYP2C9. In vivo, fluoxetine and norfluoxetine do not significantly affect the activity of CYP1A2 and CYP3A4. They also inhibit the activity of P-glycoprotein, a type of membrane transport protein that plays an important role in drug transport and metabolism and hence P-glycoprotein substrates such as loperamide may have their central effects potentiated. This extensive effect on the bodys pathways for drug metabolism creates the potential for interactions with many commonly used drugs.Its use should also be avoided in those receiving other serotonergic drugs such as monoamine oxidase inhibitors, tricyclic antidepressants, methamphetamine, amphetamine, MDMA, triptans, buspirone, ginseng, dextromethorphan (DXM), linezolid, tramadol, serotonin–norepinephrine reuptake inhibitors, and other SSRIs due to the potential for serotonin syndrome to develop as a result.Fluoxetine may also increase the risk of opioid overdose in some instances, in part due to its inhibitory effect on cytochrome P-450. Similar to how fluoxetine can effect the metabolization of dextromethorphan, it may cause medications like oxycodone to not be metabolized at a normal rate, thus increasing the risk of serotonin syndrome as well as resulting in an increased concentration of oxycodone in the blood, which may lead to accidental overdose. | Sexual dysfunction
Sexual dysfunction, including loss of libido, erectile dysfunction, lack of vaginal lubrication, and anorgasmia, are some of the most commonly encountered adverse effects of treatment with fluoxetine and other SSRIs. While early clinical trials suggested a relatively low rate of sexual dysfunction, more recent studies in which the investigator actively inquires about sexual problems suggest that the incidence is >70%.On 11 June 2019, the Pharmacovigilance Risk Assessment Committee of the European Medicines Agency concluded that there is a possible causal association between SSRI use and long-lasting sexual dysfunction that persists despite discontinuation of SSRI, including fluoxetine, and that the labels of these drugs should be updated to include a warning. Antidepressant discontinuation syndrome
Fluoxetines longer half-life makes it less common to develop antidepressant discontinuation syndrome following cessation of therapy, especially when compared to antidepressants with shorter half-lives such as paroxetine. Although gradual dose reductions are recommended with antidepressants with shorter half-lives, tapering may not be necessary with fluoxetine. Pregnancy
Antidepressant exposure (including fluoxetine) is associated with shorter average duration of pregnancy (by three days), increased risk of preterm delivery (by 55%), lower birth weight (by 75 g), and lower Apgar scores (by <0.4 points). There is 30–36% increase in congenital heart defects among children whose mothers were prescribed fluoxetine during pregnancy, with fluoxetine use in the first trimester associated with 38–65% increase in septal heart defects. Suicide
In October 2004, the FDA added a black box warning to all antidepressant drugs regarding use in children. In 2006, the FDA included adults aged 25 or younger. | 11
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U.S. National Library of Medicine. | Dextromethorphan, an N-methyl-D-aspartate receptor antagonist, inhibits glutamatergic transmission in the regions of the brainstem and cerebellum, which are hypothesized to be involved in pseudobulbar symptoms, and acts as a sigma ligand, binding to the sigma-1 receptors that mediate the emotional motor expression. See also
Corticobulbar tract
Bulbar palsy, a similar syndrome caused by the damage of lower motor neurons. Motor neuron disease
References
== External links == | 0-1
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Prognosis
Fukuyama congenital muscular dystrophy has a poor prognosis. Most children with FCMD reach a maximum mobility at sitting upright and sliding. Due to the compounded effects of continually worsening heart problems, impaired mental development, problems swallowing and additional complications, children with FCMD rarely live through adolescence, the disorder proves fatal by age 20. See also
Congenital muscular dystrophy
Muscular dystrophy
References
Further reading
Aida, N.; Tamagawa, K.; Takada, K.; Yagishita, A.; Kobayashi, N.; Chikumaru, K.; Iwamoto, H. (1996-04-01). "Brain MR in Fukuyama congenital muscular dystrophy". American Journal of Neuroradiology. 17 (4): 605–613. ISSN 0195-6108. PMID 8730178. Saito, Fumiaki; Matsumura, Kiichiro (2011-01-01). "Fukuyama-type congenital muscular dystrophy and defective glycosylation of α-dystroglycan". Skeletal Muscle. 1: 22. doi:10.1186/2044-5040-1-22. ISSN 2044-5040. PMC 3156645. Fukuyama type muscular dystrophy at NIHs Office of Rare Diseases
== External links == | Dutasteride/tamsulosin, sold under the brand name Jalyn among others, is a medication produced by GlaxoSmithKline for the treatment of adult male symptomatic benign prostatic hyperplasia (BPH). It is a combination of two previously existing medications: dutasteride, brand name Avodart, and tamsulosin, brand name Flomax. It contains 0.5 mg of dutasteride and 0.4 mg of tamsulosin hydrochloride.Jalyn was the result of the CombAT (Combination of Avodart and Tamsulosin) trial of 2008. It was approved by the U.S. Food and Drug Administration (FDA) on June 14, 2010. In June 2011, the FDA approved a label change warning of "Increased Risk of High-grade Prostate Cancer" from Jalyn. References
External links
"Dutasteride mixture with tamsulosin". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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: 16 Roasting converts the zinc sulfide concentrate to zinc oxide:
2
ZnS
+
3
O
2
→
t
o
2
ZnO
+
2
SO
2
{\displaystyle {\ce {2ZnS + 3O2 ->[t^o] 2ZnO + 2SO2}}}
The sulfur dioxide is used for the production of sulfuric acid, which is necessary for the leaching process. | A variety of zinc compounds are commonly used, such as zinc carbonate and zinc gluconate (as dietary supplements), zinc chloride (in deodorants), zinc pyrithione (anti-dandruff shampoos), zinc sulfide (in luminescent paints), and dimethylzinc or diethylzinc in the organic laboratory. Characteristics
Physical properties
Zinc is a bluish-white, lustrous, diamagnetic metal, though most common commercial grades of the metal have a dull finish. It is somewhat less dense than iron and has a hexagonal crystal structure, with a distorted form of hexagonal close packing, in which each atom has six nearest neighbors (at 265.9 pm) in its own plane and six others at a greater distance of 290.6 pm. The metal is hard and brittle at most temperatures but becomes malleable between 100 and 150 °C. Above 210 °C, the metal becomes brittle again and can be pulverized by beating. Zinc is a fair conductor of electricity. For a metal, zinc has relatively low melting (419.5 °C) and boiling points (907 °C). The melting point is the lowest of all the d-block metals aside from mercury and cadmium; for this reason among others, zinc, cadmium, and mercury are often not considered to be transition metals like the rest of the d-block metals.Many alloys contain zinc, including brass. Other metals long known to form binary alloys with zinc are aluminium, antimony, bismuth, gold, iron, lead, mercury, silver, tin, magnesium, cobalt, nickel, tellurium, and sodium. | 11
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This presentation is usually so suggestive of an infection that the majority of patients with COP have been treated with at least one failed course of antibiotics by the time the true diagnosis is made. Symptoms are usually subacute, occurring over weeks to months with dry cough (seen in 71% of people), dyspnea (shortness of breath)(62%) and fever (44%) being the most common symptoms. Causes
Pulmonary infection by bacteria, viruses and parasites
Drugs: antineoplastic drugs, erlotinib, amiodarone
Chemical exposure, most notably to diacetylVaping: On October 17, 2019, the American Journal of Clinical Pathology reported that lung biopsies from patients with vaping-associated pulmonary illness show acute lung injury patterns, including organizing pneumonia. Ionizing radiations
Inflammatory diseases
Systemic lupus
Rheumatoid arthritis (RA-associated COP)
Scleroderma
Bronchial obstruction
Proximal bronchial squamous cell carcinoma
SARS-CoV-2
Analysis of COVID-19 CT imaging along with postmortem lung biopsies and autopsies suggest that the majority of patients with COVID-19 pulmonary involvement also have secondary organizing pneumonia (OP) or its histological variant, acute fibrinous and organizing pneumonia, which are both well-known complications of viral infections. It was identified in 1985, although its symptoms had been noted before but not recognised as a separate lung disease. The risk of COP is higher for people with inflammatory diseases like lupus, dermatomyositis, rheumatoid arthritis, and scleroderma. It most commonly presents in the 5th or 6th decade of life and it is exceedingly rare in children. Pathophysiology
Organizing pneumonia is usually preceded by some type of lung injury that causes a localized denudation or disruption in continuity of the epithelial basal laminae of the type 1 alveolar pneumocytes that line the alveoli. | In medicine, myopathy is a disease of the muscle in which the muscle fibers do not function properly. This results in muscular weakness. Myopathy means muscle disease (Greek : myo- muscle + patheia -pathy : suffering). This meaning implies that the primary defect is within the muscle, as opposed to the nerves ("neuropathies" or "neurogenic" disorders) or elsewhere (e.g., the brain). Muscle cramps, stiffness, and spasm can also be associated with myopathy. Capture myopathy can occur in wild or captive animals, such as deer and kangaroos, and leads to morbidity and mortality. It usually occurs as a result of stress and physical exertion during capture and restraint. Muscular disease can be classified as neuromuscular or musculoskeletal in nature. Some conditions, such as myositis, can be considered both neuromuscular and musculoskeletal. Signs and symptoms
Common symptoms include muscle weakness, cramps, stiffness, and tetany. Systemic diseases
Myopathies in systemic disease results from several different disease processes including endocrine, inflammatory, paraneoplastic, infectious, drug- and toxin-induced, critical illness myopathy, metabolic, collagen related, and myopathies with other systemic disorders. Patients with systemic myopathies often present acutely or sub acutely. On the other hand, familial myopathies or dystrophies generally present in a chronic fashion with exceptions of metabolic myopathies where symptoms on occasion can be precipitated acutely. Most of the inflammatory myopathies can have a chance association with malignant lesion; the incidence appears to be specifically increased only in patients with dermatomyositis.There are many types of myopathy. ICD-10 codes are provided here where available. | 0-1
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An Apocrine nevus is an extremely rare cutaneous condition that is composed of hyperplastic mature apocrine glands. : 775
See also
Eccrine nevus
Seborrheic keratosis
List of cutaneous conditions
References
== External links == | Hyperacusis is the increased sensitivity to sound and a low tolerance for environmental noise. Definitions of hyperacusis can vary significantly; it can refer to normal noises being perceived as: loud, annoying, painful, fear-inducing, or a combination of those, and is often categorized into four subtypes: loudness, pain, annoyance, and fear.It can be a highly debilitating hearing disorder. Hyperacusis is often coincident with tinnitus. The latter is more common and there are important differences between their involved mechanisms.Little is known about the prevalence of hyperacusis, in part due to the degree of variation in the terms definition. Reported prevalence in children and adolescents ranges from 3% to 17%. Signs and symptoms
In hyperacusis, the symptoms are ear pain, annoyance, distortions, and general intolerance to many sounds that most people are unaffected by. Crying spells or panic attacks may result from the experience of hyperacusis. It may affect only one or both ears. Hyperacusis can also be accompanied by tinnitus. Hyperacusis can result in anxiety, stress and phonophobia. Avoidant behavior is often a response to prevent the effects of hyperacusis and this can include avoiding social situations. Loudness Hyperacusis
Hyperacusis is most often characterized by a sensitivity to sound, where the perception of loudness is much greater than for a typical person; it is often associated with certain volumes and/or frequencies. Hyperacusis can occur in children and adults, and can be either "short-term" in a duration of weeks to less than a year before recovery, or, less-commonly, "long-term", spanning years and in some cases becoming permanent. | 0-1
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They cover a spectrum of increasing symptom severity (staining, soilage, seepage and accidents). Rarely, minor FI in adults may be described as encopresis. Fecal leakage is a related topic to rectal discharge, but this term does not necessarily imply any degree of incontinence. Discharge generally refers to conditions where there is pus or increased mucus production, or anatomical lesions that prevent the anal canal from closing fully, whereas fecal leakage generally concerns disorders of IAS function and functional evacuation disorders which cause a solid fecal mass to be retained in the rectum. Solid stool incontinence may be called complete (or major) incontinence, and anything less as partial (or minor) incontinence (i.e. incontinence of flatus (gas), liquid stool and/or mucus).In children over the age of four who have been toilet trained, a similar condition is generally termed encopresis (or soiling), which refers to the voluntary or involuntary loss of (usually soft or semi-liquid) stool. The term pseudoincontinence is used when there is FI in children who have anatomical defects (e.g. enlarged sigmoid colon or anal stenosis). Encopresis is a term that is usually applied when there are no such anatomical defects present. The ICD-10 classifies nonorganic encopresis under "behavioural and emotional disorders with onset usually occurring in childhood and adolescence" and organic causes of encopresis along with FI. | A volume of lukewarm water is gently pumped into the colon via the anus. People can be taught how to perform this treatment in their own homes, but it does require special equipment. If the irrigation is efficient, stool will not reach the rectum again for up to 48 hours. By regularly emptying the bowel using transanal irrigation, controlled bowel function is often re-established to a high degree in patients with bowel incontinence and/or constipation. This enables control over the time and place of evacuation and development of a consistent bowel routine. However, persistent leaking of residual irrigation fluid during the day may occur and make this option unhelpful, particularly in persons with obstructed defecation syndrome who may have incomplete evacuation of any rectal contents. Consequently, the best time to carry out the irrigation is typically in the evening, allowing any residual liquid to be passed the next morning before leaving the home. Complications such as electrolyte imbalance and perforation are rare. The effect of transanal irrigation varies considerably. Some individuals experience complete control of incontinence, and other report little or no benefit. It has been suggested that if appropriate, people be offered home retrograde anal irrigation.Biofeedback (the use of equipment to record or amplify and then feed back activities of the body) is a commonly used and researched treatment, but the benefits are uncertain. | 11
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These values were lower than what was reported for 1975 as 14.6% and 13,8%, respectively, indicating a worldwide reduction in the extent of undernutrition. Causes
A person may be underweight due to genetics, improper metabolism of nutrients, lack of food (frequently due to poverty), drugs that affect appetite, illness (physical or mental) or the eating disorder anorexia nervosa.Being underweight is associated with certain medical conditions, including type 1 diabetes, hyperthyroidism, cancer, and tuberculosis. People with gastrointestinal or liver problems may be unable to absorb nutrients adequately. People with certain eating disorders can also be underweight due to one or more nutrient deficiencies or excessive exercise, which exacerbates nutrient deficiencies.A common belief is that healthy underweight individuals can ‘eat what they want’ and then burn it off either by high levels of activity or elevated metabolism. It has been shown however that individuals with BMI < 18.5 eat about 12% less calories than individuals with normal BMI (21.5 to 25) and they are 23% less physically active (by accelerometry). Problems
Being underweight can be a symptom of an underlying condition, in which case it is secondary. Unexplained weight loss may require a professional medical diagnosis.Being underweight can also cause other conditions, in which case it is primary. Severely underweight individuals may have poor physical stamina and a weak immune system, leaving them open to infection. | This can be done by eating a sufficient volume of sufficiently calorie-dense foods. Body weight may also be increased through the consumption of liquid nutritional supplements. Exercise
Another way for underweight people to gain weight is by exercising, since muscle hypertrophy increases body mass. Weight lifting exercises are effective in helping to improve muscle tone as well as helping with weight gain. Weight lifting has also been shown to improve bone mineral density, which underweight people are more likely to lack.Exercise is catabolic, which results in a brief reduction in mass. However, during recovery, anabolic overcompensation causes the muscles to grow, which results in an overall increase in mass. This can happen through an increase in muscle proteins, or through enhanced storage of glycogen in muscles. Exercise can also help stimulate the appetite of a person who is not inclined to eat. Appetite stimulants
Certain drugs may increase appetite either as their primary effect or as a side effect. Antidepressants, such as mirtazapine or amitriptyline, and antipsychotics, particularly chlorpromazine and haloperidol, as well as tetrahydrocannabinol (found in cannabis), all present an increase in appetite as a side effect. In states where it is approved, medicinal cannabis may be prescribed for severe appetite loss, such as that caused by cancer, AIDS, or severe levels of persistent anxiety. Other drugs or supplements which may increase appetite include antihistamines (such as diphenhydramine, promethazine or cyproheptadine). See also
Essential nutrient
List of phytochemicals in food
Body image
Emaciation
Malnutrition
Stunted growth
References
== External links == | 11
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In 1872, he investigated the later stages of pregnancy and noted that many pregnant women felt contractions without being near birth. He examined the prevalence of uterine contractions throughout pregnancy and determined that contractions that do not lead to labor are a normal part of pregnancy. == References == | An empyema () is a collection or gathering of pus within a naturally existing anatomical cavity. For example, pleural empyema is empyema of the pleural cavity. It must be differentiated from an abscess, which is a collection of pus in a newly formed cavity. The term is from Greek ἐμπύημα, "abscess". Classification
Empyema occurs in:
the pleural cavity (pleural empyema also known as pyothorax)
the thoracic cavity
the uterus (pyometra)
the appendix (appendicitis)
the meninges (subdural empyema)
the joints (septic arthritis)
the gallbladder
External links
Shen, K. Robert; Bribriesco, Alejandro; Crabtree, Traves; Denlinger, Chad; Eby, Joshua; Eiken, Patrick; Jones, David R.; Keshavjee, Shaf; Maldonado, Fabien; Paul, Subroto; Kozower, Benjamin (February 2017). "The American Association for Thoracic Surgery consensus guidelines for the management of empyema". The Journal of Thoracic and Cardiovascular Surgery. 153 (6): e129–e146. doi:10.1016/j.jtcvs.2017.01.030. PMID 28274565. | 0-1
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The hallmark of the period is Minnesotas adoption law of 1917, which mandated investigation of all placements and limited record access to those involved in the adoption.During the same period, the Progressive movement swept the United States with a critical goal of ending the prevailing orphanage system. The culmination of such efforts came with the First White House Conference on the Care of Dependent Children called by President Theodore Roosevelt in 1909, where it was declared that the nuclear family represented "the highest and finest product of civilization" and was best able to serve as primary caretaker for the abandoned and orphaned. As late as 1923, only two percent of children without parental care were in adoptive homes, with the balance in foster arrangements and orphanages. Less than forty years later, nearly one-third were in adoptive homes.Nevertheless, the popularity of eugenic ideas in America put up obstacles to the growth of adoption. There were grave concerns about the genetic quality of illegitimate and indigent children, perhaps best exemplified by the influential writings of Henry H. Goddard, who protested against adopting children of unknown origin, saying,
Now it happens that some people are interested in the welfare and high development of the human race; but leaving aside those exceptional people, all fathers and mothers are interested in the welfare of their own families. The dearest thing to the parental heart is to have the children marry well and rear a noble family. | Jasmine Whitbread, chief executive of Save the Children said: "The vast majority of the children currently on their own still have family members alive who will be desperate to be reunited with them and will be able to care for them with the right support. Taking children out of the country would permanently separate thousands of children from their families—a separation that would compound the acute trauma they are already suffering and inflict long-term damage on their chances of recovery." Rehoming in the United States
With the increase in adoption rates over the many decades, the United States has been faced with a new morally questionable practice: rehoming. This is the act of caregivers posting an advertisement when they do not feel the child should be in their care any longer. Investigation of the childs new housing situation is not required in this practice, and this has created an underground market, one where child traffickers can thrive. There is a lack of regulation surrounding this practice and current legislation contradicts each other, making this harder to combat. When a parent adopts a child, they may not have been aware that the child has special needs and thus, are not equipped to help this child. The child may act out or not fit in with the family so the family turns to rehoming. Rehoming is not adoption and because of that, the government does not have to be notified and adoption agencies are not involved. Thus, re-homing is a prime target for child and sex traffickers. | 11
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Typically, the sensitivity is to proteins in the white, rather than the yolk.Milk from cows, goats, or sheep is another common food allergen, and many affected people are also unable to tolerate dairy products such as cheese. A small portion of children with a milk allergy, roughly 10%, have a reaction to beef because it contains small amounts of protein that are also present in cows milk.Seafood is one of the most common sources of food allergens; people may be allergic to proteins found in fish or to different proteins found in shellfish (crustaceans and mollusks).Other foods containing allergenic proteins include soy and wheat, and to a lesser frequency, fruits, vegetables, maize, spices, synthetic and natural colors, and chemical additives.Balsam of Peru, which is in various foods, is in the "top five" allergens most commonly causing patch test reactions in people referred to dermatology clinics. Other than oral ingestion
Sensitization can occur through the gastrointestinal tract, respiratory tract and possibly the skin. Damage to the skin in conditions such as eczema has been proposed as a risk factor for sensitization.While the most obvious route for an allergic exposure is oral ingestion, some reactions are possible through external exposure. Peanut allergies are much more common in adults who had oozing and crusted skin rashes as infants. Airborne particles in a farm- or factory-scale peanut shelling or crushing environment, or from cooking, can produce respiratory effects in exposed allergic individuals. | Does the amino acid sequence of the transferred proteins resemble the sequence of known allergenic proteins? Are the transferred proteins resistant to digestion - a trait shared by many allergenic proteins? Genes approved for animal use can be restricted from human consumption due to potential for allergic reactions. In 1998 Starlink brand corn restricted to animals was detected in the human food supply, leading to first a voluntary and then a FDA mandated recall. There are requirements in some countries and recommendations in others that all foods containing GMO ingredients be so labeled, and that there be a post-launch monitoring system to report adverse effects (much there exists in some countries for drug and dietary supplement reporting). Restaurants
In the US, the FDA Food Code states that the person in charge in restaurants should have knowledge about major food allergens, cross-contacts, and symptoms of food allergy
reactions. Restaurant staff, including wait staff and kitchen staff, may not be adequately informed about allergenic ingredients, or the risk of cross-contact when kitchen utensils used to prepare food may have been in previous contact with an allergenic food. The problem may be compounded when customers have a hard time describing their food allergies or when wait staff have a hard time understanding those with food allergies when taking an order. Diagnosing issues
There exists both over-reporting and under-reporting of the prevalence of food allergies. | 11
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The bacteria invade nerve tissue in the brain, increasing the permeability of the blood–brain barrier and promoting the onset of Alzheimers. Individuals with a plethora of tooth plaque risk cognitive decline. Poor oral hygiene can have an adverse effect on speech and nutrition, causing general and cognitive health decline. Oral viruses
Herpes simplex virus (HSV) has been found in more than 70% of those aged over 50. HSV persists in the peripheral nervous system and can be triggered by stress, illness or fatigue. High proportions of viral-associated proteins in amyloid plaques or neurofibrillary tangles (NFTs) confirm the involvement of HSV-1 in Alzheimers disease pathology. NFTs are known as the primary marker of Alzheimers disease. HSV-1 produces the main components of NFTs. Diet
Diet is seen to be a modifiable risk factor for the development of dementia. Thiamine deficiency is identified to increase the risk of Alzheimers disease in adults. The role of thiamine in brain physiology is unique and essential for the normal cognitive function of older people. Many dietary choices of the elderly population, including the higher intake of gluten-free products, compromise the intake of thiamine as these products are not fortified with thiamine.The Mediterranean and DASH diets are both associated with less cognitive decline. A different approach has been to incorporate elements of both of these diets into one known as the MIND diet. These diets are generally low in saturated fats while providing a good source of carbohydrates, mainly those that help stabilize blood sugar and insulin levels. | Microstomia is a small mouth (micro- a combining form meaning small + -stomia a combining form meaning mouth = (abnormally) "small mouth" in Greek.) Congenital
It is a feature of many craniofacial syndromes, including Freeman–Sheldon syndrome and Sheldon-Hall syndromes (or distal arthrogryposis multiplex congenita). It may present with whistling-face feature, as well, as in Freeman-Sheldon syndrome. In this syndrome, it impairs alimentation and may require repeated oral surgeries (called commissurotomy) to improve function. Acquired
Microstomia can occur as a result of scarring due to many conditions. It is seen as complication of facial burns. It can also be a feature of systemic scleroderma. References
== External links == | 0-1
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It is used in combination with ethinylestradiol in birth control pills and in combination with estradiol in menopausal hormone therapy. Available forms
Norgestimate is available only in combination with the estrogens ethinylestradiol and estradiol. These formulations are for use by mouth and are indicated specifically for hormonal contraception and menopausal hormone therapy. Norgestimate is not available on its own (i.e., as a standalone medication). Contraindications
Side effects
Norgestimate has mostly been studied in combination with an estrogen, so the side effects of norgestimate specifically or on its own have not been well-defined.Side effects associated with the combination of ethinylestradiol and norgestimate in premenopausal women, with greater than or equal to 2% incidence over up to 24 menstrual cycles, include headache/migraine (33%), abdominal/gastrointestinal pain (7.8%), vaginal infection (8.4%), vaginal discharge (6.8%), breast issues (including breast pain, discharge, and enlargement) (6.3%), mood disorders (including depression and mood alterations) (5.0%), flatulence (3.2%), nervousness (2.9%), and rash (2.6%).Side effects associated with the combination of estradiol and norgestimate in postmenopausal women, with greater than or equal to 5% incidence over one year, include headache (23%), upper respiratory tract infection (21%), breast pain (16%), back pain (12%), abdominal pain (12%), flu-like symptoms (11%), arthralgia (9%), vaginal bleeding (9%), dysmenorrhea (8%), sinusitis (8%), vaginitis (7%), pharyngitis (7%), fatigue (6%), pain (6%), nausea (6%), viral infection (6%), flatulence (5%), tooth disorder (5%), myalgia (5%), dizziness (5%), depression (5%), and coughing (5%). | Other activities
Norgestimate and its active metabolites do not bind to other steroid hormone receptors besides the progesterone and androgen receptors and hence have no other off-target hormonal activity. This includes estrogenic, glucocorticoid, antimineralocorticoid, and neurosteroid activity. However, levonorgestrel has been found to inhibit 5α-reductase and hepatic cytochrome P450 enzymes in vitro to some extent. Pharmacokinetics
Norgestimate is rapidly and almost completely metabolized into its active metabolites, mainly norelgestromin (the primary active metabolite) and to a lesser extent levonorgestrel, upon oral ingestion. As a result, only very low concentrations (70 pg/mL) of norgestimate itself are detectable in the circulation, and only for about 6 hours after an oral dose. The oral bioavailability of norgestimate is unknown. This is due to the rapid and extensive metabolism of norgestimate, which makes determination of overall bioavailability difficult and necessitates methods other than area-under-the-curve (AUC) to do so. Peak levels of norelgestromin (3,500 pg/mL) are reached at approximately 2 hours following administration of norgestimate. Co-administration of norgestimate with a high-fat meal has been found to significantly decrease peak levels of norelgestromin, although the area-under-the-curve levels of norelgestromin are not significantly altered by food. Steady-state levels of norelgestromin and levonorgestrel are reached within 21 days of treatment with norgestimate. There is an approximate 2-fold accumulation in levels of norelgestromin and a non-linear approximate 8-fold accumulation in levels of levonorgestrel with continuous administration of norgestimate. The accumulation of levonorgestrel is thought to be a result of its high affinity for SHBG, which limits its biological activity. | 11
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Cholesterol metabolism primarily takes place in the liver, with significant amounts in the intestine as well. It should also be noted that cholesterol cannot pass the blood–brain barrier, thus within the brain, biosynthesis is the only source of cholesterol. In humans, cholesterol synthesis begins with the mevalonate pathway (see diagram), leading to the synthesis of farnesyl pyrophosphate (FPP). This pathway uses two acetyl-CoA and two NADPH to make mevalonate, which is metabolized to isopentenyl pyrophosphate (IPP) using three ATP. From there, three IPP are needed to make one FPP. The combination of two FPP leads to the formation of squalene; this represents the first committed step towards cholesterol biosynthesis. Squalene leads to the creation of lanosterol, from which there are multiple pathways that lead to cholesterol biosynthesis. The rate limiting step of cholesterol synthesis is the conversion of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) to mevalonate, this is an early step in the mevalonate pathway catalyzed by HMG-CoA reductase. Through a complicated series of reactions, lanosterol leads to the formation of zymosterol. As shown in a diagram to the right, it is at this point that the pathway diverges. In humans, the main pathway leading to cholesterol is known as the Kandutsch–Russell pathway. Zymosterol is metabolized to 5α-cholesta-7,24-dien-3β-ol, then to lathosterol, and then to 7-dehydrocholesterol, or 7-DHC. 7-DHC is the immediate precursor to cholesterol, and the enzyme DHCR7 is responsible for converting 7-DHC to cholesterol. DHCR7 reduces the double bond on carbon 7 of 7-DHC, leading to the unesterified product. | Vibratory angioedema is a form of physical urticaria that may be an inherited autosomal dominant trait, or may be acquired after prolonged exposure to occupational vibration. : 155
See also
Urticaria
Skin lesion
List of cutaneous conditions
== References == | 0-1
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For example, a 1000 Hz tone in an unaffected ear may be heard as a slightly different pitch in the opposite ear, or have an imperfect tonal quality in the affected ear. Biological explanation via theories of pitch of pure tones
There are two theories on the cause of diplacusis: place theory and temporal theory. Place theory posits that the cause is looking for the edge of the wave for the pitch and could explain diplacusis as a small differences between the two cochleas.Temporal theory posits that the cause is from looking at the phase locking to tell what the pitch is. This theory has a difficult time explaining diplacusis. There are some examples of pitch which do not have an "edge" on the basilar membrane, which this would account for—e.g., white noise, clicks, etc. Both theories are under debate. Effects of sensorineural hearing loss
Normal human ears can discriminate between two frequencies that differ by as little as 0.2%. If one ear has normal thresholds while the other has sensorineural hearing loss (SNHL), diplacusis may be present, as much as 15–20% (for example 200 Hz one ear => 240 Hz in the other). The pitch may be difficult to match because the SNHL ear hears the sound "fuzzy". Bilateral SNHL gives less diplacusis, but pitch distortions may persist. This may cause problems with music and speech understanding. Treatment
Treatment of diplacusis includes a full medical and audiological examination that may explain the nature of the problem. If needed, amplification may relieve the symptoms of diplacusis. | Therapy in helping the patient understand the cause of the symptom and tinnitus retraining may provide some relief. In at least some cases, amplification makes no difference and there is no treatment other than waiting for natural resolution. Some individuals may find the provided amplification also increases the audibility of their pitch discrepancy. If onset is linked to an underlying medical cause, i.e. sudden sensorineural hearing loss, appropriate medical treatment is recommended. Etymology
Diplacusis is from the Greek words "diplous" (double) and "akousis" (hearing). See also
Hearing
Hearing loss
Pitch (psychophysics)
Auditory system
External sources
Diplacusis: I. Historical Review
Turner, Christopher. "Perception of Pitch." Wendell Johnson Speech and Hearing Center, Iowa City. Dec. 2008. Plack et al. (ed.). Pitch : Neural coding and perception. Springer. 2005. == References == | 11
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Blisters are most common on the hands and feet, as these extremities are susceptible while walking, running, or performing repetitive motions, such as joystick manipulation whilst playing certain video games, certain sports (e.g., baseball pitching), digging with a shovel, playing guitar or bass, etc. Blisters form more easily on damp skin than on dry or soaked skin, and are more common in warm conditions. Less-aggressive rubbing over long periods of time may cause calluses to form rather than a blister. Both blisters and calluses can lead to more serious complications, such as foot ulceration and infection, particularly when sensation or circulation is impaired, as in the case of diabetes, neuropathy or peripheral artery disease (PAD). Burning
This type of blistering is one of the tools used to determine the degree of burns sustained. First and second degree burns may result in blistered skin; however, it is characteristic of second degree burns to blister immediately, whereas first degree burns can have blisters after a couple of days. Sunburn can also result in blisters. Blisters can also form on the hands and feet as a result of tissue damage incurred by frostbite. Chemical exposure
Sometimes, the skin will blister when it comes into contact with a cosmetic, detergent, solvent, or other chemical such as nickel sulfate, Balsam of Peru, or urushiol (poison ivy, poison oak, poison sumac). This is known as contact dermatitis. Blisters can also develop as a result of an allergic reaction to an insect bite or sting. | The β band consists of transferrin, low-density lipoproteins, and complement system proteins. The γ band is where the immunoglobulins appear, which is why they are also known as gammaglobulins. The majority of paraproteins appear in this band. Types
Paraproteinemias may be categorized according to the type of monoclonal protein found in blood:
Light chains only (or Bence Jones protein). This may be associated with multiple myeloma or AL amyloidosis. Heavy chains only (also known as "heavy chain disease");
Whole immunoglobulins. If immunoglobulins tend to precipitate within blood vessels with cold, that phenomenon takes the name of cryoglobulinaemia.The three types of paraproteins may occur alone or in combination in a given individual. Note that while most heavy chains or whole immunoglobulins remain within blood vessels, light chains frequently escape and are excreted by the kidneys into urine, where they take the name of Bence Jones protein.It is also possible for paraproteins (usually whole immunoglobulins) to form polymers by aggregating with each other; this takes the name of macroglobulinemia and may lead to further complications. For example, certain macroglobulins tend to precipitate within blood vessel with cold, a phenomenon known as cryoglobulinemia. Others may make blood too viscous to flow smoothly (usually with IgM pentamer macroglobulins), a phenomenon known as Waldenström macroglobulinemia.The most common type of paraproteinemia is monoclonal gammopathy of undetermined significance (MGUS). Another form, monoclonal gammopathy of renal significance (MGRS) results in kidney damage and chronic kidney disease due to the effects of monoclonal immunoglobulins. References
External links
Paraproteinaemia at patient.info. | 0-1
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Alternating hemiplegia (also known as crossed hemiplegia) is a form of hemiplegia that has an ipsilateral cranial nerve palsies and contralateral hemiplegia or hemiparesis of extremities of the body. The disorder is characterized by recurrent episodes of paralysis on one side of the body. There are multiple forms of alternating hemiplegia, Webers syndrome, middle alternating hemiplegia, and inferior alternating hemiplegia. This type of syndrome can result from a unilateral lesion in the brainstem affecting both upper motor neurons and lower motor neurons. The muscles that would receive signals from these damaged upper motor neurons result in spastic paralysis. With a lesion in the brainstem, this affects the majority of limb and trunk muscles on the contralateral side due to the upper motor neurons decussation after the brainstem. The cranial nerves and cranial nerve nuclei are also located in the brainstem making them susceptible to damage from a brainstem lesion. Cranial nerves III (Oculomotor), VI (Abducens), and XII (Hypoglossal) are most often associated with this syndrome given their close proximity with the pyramidal tract, the location which upper motor neurons are in on their way to the spinal cord. Damages to these structures produce the ipsilateral presentation of paralysis or palsy due to the lack of cranial nerve decussation (aside from the trochlear nerve) before innervating their target muscles. The paralysis may be brief or it may last for several days, many times the episodes will resolve after sleep. | The initial diagnosis is made based on the presence of neurologic and ophthalmic disease but the disease progresses differently in each patient so after initial diagnosis the patient should be monitored frequently in order to handle further complications resulting from the syndrome. Treatment
Medical treatment of hemiplegia can be separate into several different categories:: 779
prophylactic treatment by avoiding triggers and long-term drug treatment
acute management of the episodes
management of the epilepsy
sleep as a management technique.Seizure trigger include exposure to cold, emotional stress, fatigue, bathing, hyperthermia/hypothermia, and upper respiratory infection. A drug called flunarizine, which is a calcium channel blocker can help to reduce the severity and the length of attacks of the paralysis. Flunarizine
Many children affected by alternating hemiplegia also have epilepsy. Seizures may occur during an attack but more often occur between attacks. Anti-epilepsy drugs are given to prevent or lessen the seizures, but the drugs often dont work and have severe side effects that require the patient to discontinue use. Flunarizine, which blocks calcium channels, is an antiepilepsy drugs used in 50% of patients, and has been shown to shorten the duration of attacks as well as reducing the severity of the attacks. While Flunarizine does not stop the attacks, it is most common drug prescribed to treat those with alternating hemiplegia. : 779
Sleep and diet
Sleep is also used as a management technique. An early indication of an episode is tiredness so medication such as melatonin or Buccal midazolam can be administered to induce sleep and avoid the episode. | 11
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Multiple tumors (no viscera involvement)
Multiple tumors (no viscera involvement) typically occur as dozens to hundreds of mostly small tumors located in various areas such as the skin, muscles, and frontal eye socket, These tumors do not involve visceral organs, often take a benign course, and may regress spontaneously. Multiple tumors (with viscera involvement)
Multiple tumors (with viscera involvement) typically occur as dozens to hundreds of tumors located in the same sites as multiple tumors (no viscera involvement) but also occur in one or more visceral organs such as those in the gastrointestinal tract and upper respiratory tract and/or the heart, liver, cerebellum, rectum, parietal cortex of brain, and lung. This form of IMF, particularly in cases with tumors involving the gastrointestinal tract, heart, and/or lung, has a far higher morbidity and mortality than the other forms with death occurring in infants during the first weeks to 4 months of life in 30–70% of cases Death is typically due to a tumors compression of vital organs or tissues (e.g. blood vessels). However, there are uncommon cases of multiple tumors (with viscera involvement) that were not associated with serious symptoms, were observed without treatment, and over time showed spontaneous regressions of all or almost all of their tumors. Pathology
Microscopic histopathologic analyses of IMF tumor tissues commonly show repeated patterns of a central zone consisting of spindle-shaped cells lining capillaries and round-to-oval cells arranged around prominent "antler-shaped" vascular spaces all of which are surrounded by a peripheral zone of clustered smooth muscle-like cells. | Diagnosis
Techniques for the diagnosis of Page kidney are all imaging based, including abdominal x-ray, intravenous pyelography, angiography, renal doppler ultrasound, CT scan, and Magnetic resonance imaging (MRI). X-ray and pyelography may add in diagnosis, but are non-diagnostic when used alone. Additionally, pyelograms use potentially nephrotoxic contrast agents, further limiting their utility. Diagnosis is primarily made using ultrasound and CT. CT and MRI imaging can show the space occupying lesions but doppler ultrasound is needed to display the hemodynamic changes occurring in the kidney. Ultrasound is often the initial diagnostic test of choice but due to its low resolution further imaging may be necessary. Treatment
Surgical
Surgical treatment of Page kidney has evolved over time as newer techniques have become more popular. Open surgical procedures such as nephrectomy, which was once the treatment of choice have been replaced by less invasive options such as percutaneous drainage or endoscopic capsulotomy. Medical
Some cases of Page kidney will resolve spontaneously without need for surgical treatment. In this case, medical treatment focuses on symptomatic treatment of the hypertension with an angiotensin-converting enzyme inhibitor (ACEi) or an angiotensin receptor blocker (ARB). Adding a calcium channel blocker (CCB) or beta blocker to the ACEi or ARB has also been described. History
Irvine H. Page first demonstrated the Page kidney phenomena experimentally in animals in 1939. He found that wrapping one of the animals kidneys in cellophane produced hypertension that could be reversed after removal of the kidney. | 0-1
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Diagnosis
In terms of the clinical evaluation, clinical features are the classification method
Treatment
Management for this condition is symptom specific
Society and culture
Notable cases
Michael Berryman, American actor with hypohidrotic ectodermal dysplasia
Levi Hawken, New Zealand skateboarder and artist who became well known in 2011 in New Zealand for the "Nek minnit" viral video on YouTube
See also
List of cutaneous conditions
List of cutaneous conditions caused by mutations in keratins
References
== External links == | The study had several limitations; results were severely confounded by inherent differences between compliant and non-compliant women. == References == | 0-1
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Acromegaly is a disorder that results from excess growth hormone (GH) after the growth plates have closed. The initial symptom is typically enlargement of the hands and feet. There may also be an enlargement of the forehead, jaw, and nose. Other symptoms may include joint pain, thicker skin, deepening of the voice, headaches, and problems with vision. Complications of the disease may include type 2 diabetes, sleep apnea, and high blood pressure.Acromegaly is usually caused by the pituitary gland producing excess growth hormone. In more than 95% of cases the excess production is due to a benign tumor, known as a pituitary adenoma. The condition is not inherited from a persons parents. Acromegaly is rarely due to a tumor in another part of the body. Diagnosis is by measuring growth hormone after a person has consumed a glucose solution, or by measuring insulin-like growth factor I in the blood. After diagnosis, medical imaging of the pituitary is carried out to determine if an adenoma is present. If excess growth hormone is produced during childhood, the result is the condition gigantism rather than acromegaly, and it is characterized by excessive height.Treatment options include surgery to remove the tumor, medications, and radiation therapy. Surgery is usually the preferred treatment; the smaller the tumor, the more likely surgery will be curative. If surgery is contraindicated or not curative, somatostatin analogues or GH receptor antagonists may be used. Radiation therapy may be used if neither surgery nor medications are completely effective. | Primo Carnera (1906–1967), nicknamed the Ambling Alp, was an Italian professional boxer and wrestler who reigned as the boxing World Heavyweight Champion from 29 June 1933 to 14 June 1934. Maurice Tillet (1903–1954), Russian-born French professional wrestler, is better known by his ring name, the French Angel. Richard Kiel (1939–2014), actor, "Jaws" from two James Bond movies and Mr. Larson in Happy Gilmore
Pío Pico, the last Mexican Governor of California (1801–1894), manifested acromegaly without gigantism between at least 1847 and 1858. Some time after 1858, signs of the growth hormone-producing tumor disappeared along with all the secondary effects the tumor had caused in him. He looked normal in his 90s. His remarkable recovery is likely an example of spontaneous selective pituitary tumor apoplexy. Earl Nightingale (March 12, 1921 – March 25, 1989) was an American radio speaker and author, dealing mostly with the subjects of human character development, motivation, and meaningful existence. He was the voice during the early 1950s of Sky King, the hero of a radio adventure series, and was a WGN radio program host from 1950 to 1956. Nightingale was the author of The Strangest Secret, which economist Terry Savage has termed "…one of the great motivational books of all time." Nightingale’s daughter, Pamela, mentioned her father had acromegaly during a podcast about her father that aired in June 2022. | 11
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There have been no reported cases of decline in vision due to ONH. Neuroradiographic abnormalities
Estimates of cerebral malformations vary from 39% to 90% of children with ONH. Abnormalities evident via neuroradiography can include agenesis (absence) or hypoplasia of the corpus callosum, absence or incomplete development of the septum pellucidum, malformations of the pituitary gland, schizencephaly, cortical heterotopia, white matter hypoplasia, pachygyria, and holoprosencephaly. Hypoplasia of the corpus callosum, often in conjunction with other major malformations, is significantly associated with poor and delayed developmental outcome.ONH is often referred to as septo-optic dysplasia, a term that refers to agenesis of the septum pellucidum. It is now clear that the absence of the septum pellucidum does not correlate with the associated symptoms of ONH. Hypothalamic dysfunction
Dysfunction of the hypothalamus results in loss of regulation over behavior and function of the pituitary gland (master gland). Hypopituitarism is present in 75% to 80% of patients with ONH. The anterior pituitary gland contributes to growth, metabolism, and sexual development. The most common pituitary endocrinopathies are growth hormone (GH) deficiency (70%), hypothyroidism (43%), adrenal insufficiency (27%), and diabetes insipidus (5%).Absence of GH may often be indicated by short stature, although this is not always the case. Other indicators of GH deficiency may include hypoglycemic events (including seizures), prolonged jaundice, micropenis in boys, and delayed dentition. Testing for GH may involve blood tests (IGF-1 and IGFBP-3), growth hormone stimulation test, or bone age x-ray of the hand or wrist (or body for children younger than 2 years). | Although most patients with only optic nerve involvement lead normally productive lives, those with accompanying endocrine dysfunction or other midline cerebral abnormalities are more at risk for on-going intellectual and other disabilities. Epidemiology
Optic nerve hypoplasia (ONH) is a congenital condition in which the optic nerve is underdeveloped (small). Many times, de Morsier’s Syndrome or septo-optic dysplasia (SOD) is associated with ONH, however, it is possible to have ONH without any additional issues like SOD. SOD is a condition that can involve multiple problems in the midline structures of the brain, stemming from miswiring of the brain and central nervous system. Besides having small optic nerves, persons with ONH can have agenesis of the corpus callosum, absence of the septum pellucidum, maldevelopment of the anterior and posterior pituitary gland, and anomalies of the hypothalamus. Because of this, all children with ONH are at risk for developmental delays and hormonal deficiencies, regardless of severity of ONH, or whether abnormalities are visible by MRI. ONH is the single leading cause of permanent legal blindness in children in the western world. The incidence of ONH is increasing, although it is difficult to estimate the true prevalence. Between 1980 and 1999, the occurrences of ONH in Sweden increased four-fold to 7.2 per 100,000, while all other causes of childhood blindness had declined. In 1997, ONH overtook retinopathy of prematurity as the single leading cause of infant blindness in Sweden, with 6.3 in every 100,000 births diagnosed with ONH. | 11
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During chronic caffeine use, caffeine-induced dopamine release within the nucleus accumbens core is markedly reduced due to drug tolerance. Enzyme targets
Caffeine, like other xanthines, also acts as a phosphodiesterase inhibitor. As a competitive nonselective phosphodiesterase inhibitor, caffeine raises intracellular cyclic AMP, activates protein kinase A, inhibits TNF-alpha and leukotriene synthesis, and reduces inflammation and innate immunity. Caffeine also affects the cholinergic system where it is a moderate inhibitor of the enzyme acetylcholinesterase. Pharmacokinetics
Caffeine from coffee or other beverages is absorbed by the small intestine within 45 minutes of ingestion and distributed throughout all bodily tissues. Peak blood concentration is reached within 1–2 hours. It is eliminated by first-order kinetics. Caffeine can also be absorbed rectally, evidenced by suppositories of ergotamine tartrate and caffeine (for the relief of migraine) and of chlorobutanol and caffeine (for the treatment of hyperemesis). However, rectal absorption is less efficient than oral: the maximum concentration (Cmax) and total amount absorbed (AUC) are both about 30% (i.e., 1/3.5) of the oral amounts.Caffeines biological half-life – the time required for the body to eliminate one-half of a dose – varies widely among individuals according to factors such as pregnancy, other drugs, liver enzyme function level (needed for caffeine metabolism) and age. In healthy adults, caffeines half-life is between 3 and 7 hours. The half-life is decreased by 30-50% in adult male smokers, approximately doubled in women taking oral contraceptives, and prolonged in the last trimester of pregnancy. | According to a 2020 study in the United States, coffee is the major source of caffeine intake in middle-aged adults, while soft drinks and tea are the major sources in adolescents. Energy drinks are more commonly consumed as a source of caffeine in adolescents as compared to adults. Beverages
Coffee
The worlds primary source of caffeine is the coffee "bean" (the seed of the coffee plant), from which coffee is brewed. Caffeine content in coffee varies widely depending on the type of coffee bean and the method of preparation used; even beans within a given bush can show variations in concentration. In general, one serving of coffee ranges from 80 to 100 milligrams, for a single shot (30 milliliters) of arabica-variety espresso, to approximately 100–125 milligrams for a cup (120 milliliters) of drip coffee. Arabica coffee typically contains half the caffeine of the robusta variety. In general, dark-roast coffee has very slightly less caffeine than lighter roasts because the roasting process reduces caffeine content of the bean by a small amount. Tea
Tea contains more caffeine than coffee by dry weight. A typical serving, however, contains much less, since less of the product is used as compared to an equivalent serving of coffee. Also contributing to caffeine content are growing conditions, processing techniques, and other variables. Thus, teas contain varying amounts of caffeine.Tea contains small amounts of theobromine and slightly higher levels of theophylline than coffee. Preparation and many other factors have a significant impact on tea, and color is a very poor indicator of caffeine content. | 11
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In sacralization, the L5-S1 intervertebral disc may be thin and narrow. This abnormality is found by X-ray.Sacralization of L6 means L6 attaches to S1 via a rudimentary joint. This L6-S1 joint creates additional motion, increasing the potential for motion-related stress and lower back pain/conditions. This condition can usually be treated without surgery, injecting steroid medication at the pseudoarticulation instead. Additionally, if L6 fuses to another vertebra this is increasingly likely to cause lower back pain. The presence of a sixth vertebra in the space where five vertebrae normally reside also decreases the flexibility of the spine and increases the likelihood of injury. Hemivertebrae
Hemivertebrae are wedge-shaped vertebrae and therefore can cause an angle in the spine (such as kyphosis, scoliosis, and lordosis). Among the congenital vertebral anomalies, hemivertebrae are the most likely to cause neurologic problems. The most common location is the midthoracic vertebrae, especially the eighth (T8). Neurologic signs result from severe angulation of the spine, narrowing of the spinal canal, instability of the spine, and luxation or fracture of the vertebrae. Signs include rear limb weakness or paralysis, urinary or fecal incontinence, and spinal pain. Most cases of hemivertebrae have no or mild symptoms, so treatment is usually conservative. Severe cases may respond to surgical spinal cord decompression and vertebral stabilization. Associations
Recognised associations are many and include:
Aicardi syndrome,
cleidocranial dysostosis,
gastroschisis 3,
Gorlin syndrome,
fetal pyelectasis 3,
Jarcho-Levin syndrome,
OEIS complex,
VACTERL association.The probable cause of hemivertebrae is a lack of blood supply causing part of the vertebrae not to form. | Associations
Vertebral anomalies is associated with an increased incidence of some other specific anomalies as well, 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 defects
References
== External links == | 11
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They are responsible for differentiating into a diverse group of cells that reach different areas of the body. The neural tube and neural crest are derived from the ectoderm; the neural tube goes on to form the brain and spinal cord, while the neural crest cells eventually go on to form various bones and cartilage of the skull and face by migrating through the pharyngeal arches. They also differentiate into the stria vascularis of the cochlea, the nerves and glia of the intestines (myenteric plexus), Schwann cells, which myelinate the peripheral nervous system to allow sufficient conductivity, odontoblasts, which produce dentin deep in the teeth, some neuroendocrine cells, connective tissue around the salivary, lacrimal, pituitary, thymus and thyroid glands, connective tissue of the eye, such as the stroma of the iris and cornea and the trabecular meshwork, and melanocytes, including those in the stroma of the iris that give rise to brown eye colour through melanin. Neural crest cells also have a role in muscle formation, including the wall muscle of certain cardiac arteries. Causes of subtypes
Type 1 is caused by an autosomal dominant mutation in the gene PAX3. PAX3, or paired box 3, is a transcription factor that has a role in maintaining an open window of time for certain neural crest cells (such as those of the head and eyes) to divide and migrate before their terminal differentiation (i.e. to maintain them in the stem-cell state). | A pinealoma is a tumor of the pineal gland, a part of the brain that produces melatonin. If a pinealoma destroys the cells of the pineal gland in a child, it can cause precocious puberty. Signs and symptoms
The pineal gland produces the hormone melatonin which plays a role in regulating circadian rhythms. A pinealoma may disrupt production of this hormone, and insomnia may result.Frequently, paralysis of upward gaze along with several ocular findings such as convergence retraction nystagmus and eyelid retraction also known as Colliers sign and Light Near Dissociation (pupil accommodates but doesnt react to light) are known collectively as Parinauds syndrome or Dorsal Mid-brain syndrome, are the only physical symptoms seen. This is caused by the compression of the vertical gaze center in the midbrain tectum at the level of the superior colliculus and cranial nerve III. Work-up usually includes Neuro-imaging as seen on the right.A pinealoma may cause interruption of hypothalamic inhibiting pathways, sometimes leading to beta-hCG secretion and consequent Leydigs cell stimulation (endocrine syndrome).Other symptoms may include hydrocephalus, gait disturbances, and precocious puberty. Cause
Pinealomas can be due to proliferation of primary pineocytes (pineocytomas, pineoblastomas), astrocytes (astrocytoma), or germ cells (germinoma). Germinomas are the most common tumor in the pineal gland. Diagnosis
Treatment
Prognosis
Of the different types of pinealomas, the type with the most favorable prognosis is the pineocytoma. References
External links
00322 at CHORUS | 0-1
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2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2018 Mar;49(3):e46-e110. [PubMed]
Musuka TD, Wilton SB, Traboulsi M, Hill MD. Diagnosis and management of acute ischemic stroke: speed is critical. CMAJ. 2015 Sep 08;187(12):887-93. [PMC free article] [PubMed]
Uno J, Kameda K, Otsuji R, Ren N, Nagaoka S, Kazushi M, Ikai Y, Gi H. Mechanical Thrombectomy for Acute Anterior Cerebral Artery Occlusion. World Neurosurg. 2018 Dec;120:e957-e961. [PubMed]
Allen CM. Differential diagnosis of acute stroke: a review. J R Soc Med. 1984 Oct;77(10):878-81. [PMC free article] [PubMed]
Guery D, Ong E, Nighoghossian N. Akinetic mutism reversibility after L-dopa therapy in unilateral left anterior cerebral artery infarction. Neurocase. 2017 Apr;23(2):171-172. [PubMed]
Notes
== External links == | In ophthalmology, accommodative excess (also known as excessive accommodation or accommodation excess) occurs when an individual uses more than normal accommodation (focusing on close objects) for performing certain near work. Accommodative excess has traditionally been defined as accommodation that is persistently higher than expected for the patients age. Modern definitions simply regard it as an inability to relax accommodation readily. Excessive accommodation is seen in association with excessive convergence also. Symptoms and signs
Blurring of vision due to pseudomyopia
Headache
Eye strain
Asthenopia
Trouble concentrating when reading
Causes
Causes related to refractive errors
Accommodative excess may be seen in the following conditions:
Hypermetropia: Young hypermetropes use excessive accommodation as a physiological adaptation in the interest of clear vision. Myopia: Young myopes performing excessive near work may also use excessive accommodation in association with excessive convergence. Astigmatism: Astigmatic eye may also be associated with accommodative excess. Presbyopia: Early presbyopic eye may also induce excessive accommodation. Improper or ill fitting spectacles: Use of improper or ill fitting spectacles may also cause use of excessive accommodation. Causes related to systemic drugs
Use of systemic drugs like Morphine, Digitalis, Sulfonamides, Carbonic anhydrase inhibitors may cause accommodative excess. Causes related to diseases
Unilateral excessive accommodation-Trigeminal neuralgia, and head trauma may cause ciliary spasm and may cause accommodative excess. Bilateral excessive accommodation-Diseases like Encephalitis, Syphilis, Head trauma, Influenza, Meningitis may cause ciliary spasm and bilateral excessive accommodation. Secondary to Convergence insufficiency
Accommodative excess may occur secondary to convergence insufficiency also. In convergence insufficiency near point of convergence will recede, and positive fusional vergence (PFV) will reduce. | 0-1
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The cone complement contains the types of cones (or their opsins) expressed by an individual. Causes
Color vision deficiencies can be classified as inherited or acquired. Inherited: inherited or congenital/genetic color vision deficiencies are most commonly caused by mutations of the genes encoding opsin proteins. However, several other genes can also lead to less common and/or more severe forms of color blindness. Acquired: color blindness that is not present at birth, may be caused by chronic illness, accidents, medication, chemical exposure or simply normal ageing processes. Genetics
Color blindness is typically an inherited genetic disorder. The most common forms of colorblindness are associated with the Photopsin genes, but the mapping of the human genome has shown there are many causative mutations that dont directly affect the opsins. Mutations capable of causing color blindness originate from at least 19 different chromosomes and 56 different genes (as shown online at the Online Mendelian Inheritance in Man [OMIM]). Genetics of red–green color blindness
By far the most common form of colorblindness is congenital red–green colorblindness (Daltonism), which includes protanopia/protanomaly and deuteranopia/deuteranomaly. These conditions are mediated by the OPN1LW and OPN1MW genes, respectively, both on the X chromosome. Protanopia and Deuteranopia (Dichromacy) could be caused by either a missing gene, or a mutation that renders the protein fully non-functional. Protanomaly and Deuteranomaly are caused by a mutation of the genes that causes the spectral sensitivity of the associated opsin proteins to shift towards the other. | Aromatic L-amino acid decarboxylase deficiency is a rare genetic disorder caused by mutations in the DDC gene, which encodes an enzyme called aromatic L-amino acid decarboxylase. Signs and symptoms
Babies with severe aromatic L-amino acid decarboxylase deficiency usually present during the first few months of life. Symptoms can include:
Hypotonia (floppiness)
Developmental delay
Oculogyric crises
Difficulty with initiating and controlling movements
Dystonia and dyskinesia
Gastointestinal dysmotility which can present at as vomiting, gastro-oesophageal reflux, diarrhoea and/or constipation
Autonomic symptoms including difficulties controlling temperature and blood sugar, excessive sweating and nasal congestionSome people may develop cerebral folate deficiency, because O-methylation of the excessive amounts of L-Dopa can deplete methyl donors such as S-adenosyl methionine and levomefolic acid. This deviation can be detected by measuring the levels of levomefolic acid in the cerebrospinal fluid, and can be corrected by folinic acid. Genetics
Aromatic L-amino acid decarboxylase deficiency is an autosomal recessive condition, meaning an individual needs to have two faulty copies of the DDC gene in order to be affected. Usually, one copy is inherited from each parent. Pathophysiology
The aromatic L-amino acid decarboxylase deficiency enzyme is involved in the synthesis of dopamine and serotonin, both of which are important neurotransmitters. Diagnosis
Once there is a clinical suspicion of the diagnosis, neurotransmitters can be analysed in cerebrospinal fluid from a lumbar puncture. If these show the pattern of abnormalities typical for aromatic L-amino acid decarboxylase deficiency, the diagnosis can be confirmed by genetic testing and/or measurement of enzyme activity. | 0-1
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An obstetrician may need to divide the anterior lying placenta. In such cases, blood loss is expected to be high and thus blood and blood products are always kept ready. In rare cases, hysterectomy may be required. Complications
Maternal
Antepartum hemorrhage
Malpresentation
Abnormal placentation
Postpartum hemorrhage
Placenta previa increases the risk of puerperal sepsis and postpartum hemorrhage because the lower segment to which the placenta was attached contracts less well post-delivery. Fetal
IUGR (15% incidence)
Hypoxia
Premature delivery
Death
Epidemiology
Placenta previa occurs approximately one of every 200 births globally. It has been suggested that rates of placenta previa are increasing due to increased rate of Caesarian section. Reasons for regional variation may include ethnicity and diet. Africa
Rates of placenta praevia in sub-Saharan Africa are the lowest in the world, averaging 2.7 per 1000 pregnancies. Despite a low prevalence, this disease has had a profound impact in Africa as it is linked with negative outcomes for both the mother and infant. The most common maternal outcome of placenta praevia is extreme blood loss before or after birth (antepartum hemorrhage and postpartum hemorrhage), which is a major cause of maternal and infant mortality in countries like Tanzania. Risk factors for placenta praevia among African women include prior pregnancies, prenatal alcohol consumption, and insufficient gynecologic care. In North Africa placenta praevia rates occur in 6.4 per 1000 pregnancies. Asia
Mainland China has the highest prevalence of placenta praevia in the world, measuring at an average of 12.2 per 1000 pregnancies. Specifically, placenta praevia is most common in Southeast Asia, though the reason for this has not yet been investigated. | According to the socioeconomic demographic in North America, Black women are more likely to come from low income areas and are thus more likely to develop placenta praevia.In Nova Scotia, infants born to pregnant woman who experience placenta praevia have a mortality rate 3–4 times higher than normal pregnancies. A couple of factors contribute to this rate, including length of time fetus was in the womb and mothers age. Infants that did survive experienced increased rates of birth defects, breathing problems, and blood abnormalities.Research suggests that the incidence of placenta praevia in the U.S. is increasing as a result of the increased rate of Caesarian sections. References
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About 50% of eating disorder cases are attributable to genetics. Other cases are due to external reasons or developmental problems. There are also other neurobiological factors at play tied to emotional reactivity and impulsivity that could lead to binging and purging behaviors.Epigenetics mechanisms are means by which environmental effects alter gene expression via methods such as DNA methylation; these are independent of and do not alter the underlying DNA sequence. They are heritable, but also may occur throughout the lifespan, and are potentially reversible. Dysregulation of dopaminergic neurotransmission due to epigenetic mechanisms has been implicated in various eating disorders. Other candidate genes for epigenetic studies in eating disorders include leptin, pro-opiomelanocortin (POMC) and brain-derived neurotrophic factor (BDNF).There has found to be a genetic correlation between anorexia nervosa and OCD, suggesting a strong etiology. First and second relatives of probands with OCD have a greater chance of developing anorexia nervosa as genetic relatedness increases. Psychological
Eating disorders are classified as Axis I disorders in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM-IV) published by the American Psychiatric Association. There are various other psychological issues that may factor into eating disorders, some fulfill the criteria for a separate Axis I diagnosis or a personality disorder which is coded Axis II and thus are considered comorbid to the diagnosed eating disorder. Axis II disorders are subtyped into 3 "clusters": A, B and C. The causality between personality disorders and eating disorders has yet to be fully established. | Additionally, traditional Fijian values would encourage a robust appetite and a widespread vigilance for and social response to weight loss. Individual efforts to reshape the body by dieting or exercise, thus traditionally was discouraged.However, studies conducted in 1995 and 1998 both demonstrated a link between the introduction of television in the country, and the emergence of eating disorders in young adolescent ethnic Fijian girls. Through the quantitative data collected in these studies there was found to be a significant increase in the prevalence of two key indicators of disordered eating: self-induced vomiting and high Eating Attitudes Test- 26. These results were recorded following prolonged television exposure in the community, and an associated increase in the percentage of households owning television sets. Additionally, qualitative data linked changing attitudes about dieting, weight loss and aesthetic ideas in the peer environment to Western media images. The impact of television was especially profound given the longstanding social and cultural traditions that had previously rejected the notions of dieting, purging and body dissatisfaction in Fiji. Additional studies in 2011 found that social network media exposure, independent of direct media and other cultural exposures, was also associated with eating pathology. Hong Kong
From the early- to-mid- 1990s, a variant form of anorexia nervosa was identified in Hong Kong. This variant form did not share features of anorexia in the West, notably "fat-phobia" and distorted body image. Patients attributed their restrictive food intake to somatic complaints, such as epigastric bloating, abdominal or stomach pain, or a lack of hunger or appetite. | 11
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Mast cell tryptase levels may be elevated if the attack was due to an acute allergic (anaphylactic) reaction. When the patient has been stabilized, particular investigations may clarify the exact cause; complement levels, especially depletion of complement factors 2 and 4, may indicate deficiency of C1-inhibitor. HAE type III is a diagnosis of exclusion consisting of observed angioedema along with normal C1 levels and function. The hereditary form (HAE) often goes undetected for a long time, as its symptoms resemble those of more common disorders, such as allergy or intestinal colic. An important clue is the failure of hereditary angioedema to respond to antihistamines or steroids, a characteristic that distinguishes it from allergic reactions. It is particularly difficult to diagnose HAE in patients whose episodes are confined to the gastrointestinal tract. Besides a family history of the disease, only a laboratory analysis can provide final confirmation. In this analysis, it is usually a reduced complement factor C4, rather than the C1-INH deficiency itself, that is detected. The former is used during the reaction cascade in the complement system of immune defense, which is permanently overactive due to the lack of regulation by C1-INH. Angioedema is classified as either hereditary or acquired. Acquired angioedema
Acquired angioedema (AAE) can be immunologic, nonimmunologic, or idiopathic. It is usually caused by allergy and occurs together with other allergic symptoms and urticaria. It can also occur as a side effect to certain medications, particularly ACE inhibitors. | Tracheal intubation is required in these situations to prevent respiratory arrest and risk of death.Sometimes, the cause is recent exposure to an allergen (e.g. peanuts), but more often it is either idiopathic (unknown) or only weakly correlated to allergen exposure.In hereditary angioedema (HAE), often no direct cause is identifiable, although mild trauma, including dental work and other stimuli, can cause attacks. There is usually no associated itch or urticaria, as it is not an allergic response. Patients with HAE can also have recurrent episodes (often called "attacks") of abdominal pain, usually accompanied by intense vomiting, weakness, and in some cases, watery diarrhea, and an unraised, nonitchy splotchy/swirly rash. These stomach attacks can last one to five days on average and can require hospitalization for aggressive pain management and hydration. Abdominal attacks have also been known to cause a significant increase in the patients white blood cell count, usually in the vicinity of 13,000 to 30,000. As the symptoms begin to diminish, the white count slowly begins to decrease, returning to normal when the attack subsides. As the symptoms and diagnostic tests are almost indistinguishable from an acute abdomen (e.g. perforated appendicitis) it is possible for undiagnosed HAE patients to undergo laparotomy (operations on the abdomen) or laparoscopy (keyhole surgery) that turns out to have been unnecessary.HAE may also cause swelling in a variety of other locations, most commonly the limbs, genitals, neck, throat and face. The pain associated with these swellings varies from mildly uncomfortable to agonizing pain, depending on its location and severity. | 11
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The symptoms of apathy and irritability are common between these two conditions. OPD is somewhat similar to temporal lobe epilepsy, as patients who have chronic epilepsy may also express aggressive behaviours. Another similar symptom between Temporal lobe epilepsy and OPD is epileptic seizures. The symptom of epileptic seizure has influence on patients personality that means it causes behavioural alterations. Temporal lobe epilepsy is associated with the hyperexcitability of the medial temporal lobe of patients. Treatment
Patients with OPD show a wide variety of sudden behavioural changes and dysfunctions. There is little information about the treatment of OPD. The pharmacological approach is the most common therapy among patients with OPD. However, the choice of drug therapy relies on the seriousness of patients situation and what symptoms are shown. The choice and administration of specific drugs contribute to the reduction of symptoms of OPD. For this reason, it is crucial for patients treatment to be assessed by clinical psychologists and psychiatrists before the administration of drugs. The dysfunctions in expression of behaviour of patients with OPD and the development of symptom of irritability, which are caused by aggressive and self-injurious behaviours, can be dealt with the administration of carbamazepine. Moreover, the symptoms of this disorder can be decreased by the administration of valproic acid. Also, emotional irritability and signs of depression can be dealt with the use of nortriptyline and low-dose thioridazine. Except from the symptom of irritability, patients express aggressive behaviours. For effective treatment of anger and aggression, carbamazepine, phenobarbital, benztropine and haloperidol may be used. | Grade 2: follicles have 6 to 15 centroblasts per hpf. Grade 3: follicles have >15 centroblasts per hpf. Grade 3A: Grade 3 in which the follicles contain predominantly centrocytes. Grade 3B: Grade 3 in which the follicles consist almost entirely of centroblasts.Grades 1 and 2 are regarded as low grade FL; Grade 3A is usually also regarded as low grade FL although some studies have regarded it as high grade FL; and Grade 3B is regarded as a highly aggressive FL in the t-FL category.In addition to grade 3B disease, histologic examinations may reveal other evidence of t-FL such as histologic findings consistent with FL and diffuse large cell lymphoma in the same tissue (referred to as composite lymphomas) or in separate tissues (referred to as (discordant lymphomas) or histologic findings similar to those found in Burkitt lymphoma, precursor B-cell lymphoblastic leukemia, plasmablastic lymphoma, the high grade subtype of B-cell lymphoma, Hodgkin lymphoma of the B-cell type, chronic lymphocytic leukemia/small cell lymphocytic lymphoma, or histiocytic sarcoma. Other findings indicating the presence of this transformation include rapid growth in size of lymph nodes, recently acquired or new B symptoms, recent development of FL lesions in non-nodal tissue, rapid rises in serum lactate dehydrogenase levels, and the presence of high levels of serum calcium. Differential diagnosis
FL may be confused with marginal zone B-cell lymphoma, mantle cell lymphoma, and the small lymphocytic lymphoma variant of chronic lymphocytic leukemia. | 0-1
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A 2018 systematic review reported that breast density with an estrogen plus oral progesterone was significantly increased in three studies and unchanged in two studies. Changes in breast density with progesterone appear to be less than with the compared progestins.In large short-term observational studies, estrogen alone and the combination of estrogen and oral progesterone have generally not been associated with an increased risk of breast cancer. Conversely, the combination of estrogen and almost any progestin, such as medroxyprogesterone acetate or norethisterone acetate, has been associated with an increased risk of breast cancer. The only exception among progestins is dydrogesterone, which has shown similar risk to that of oral progesterone. Breast cancer risk with estrogen and progestin therapy is duration-dependent, with the risk being significantly greater with more than 5 years of exposure relative to less than 5 years. In contrast to shorter-term studies, the longer-term observations (>5 years) of the French E3N study showed significant associations of both estrogen plus oral progesterone and estrogen plus dydrogesterone with higher breast cancer risk, similarly to estrogen plus other progestogens. Oral progesterone has very low bioavailability and has relatively weak progestogenic effects. The delayed onset of breast cancer risk with estrogen plus oral progesterone is potentially consistent with a weak proliferative effect of oral progesterone on the breasts. As such, a longer duration of exposure may be necessary for a detectable increase in breast cancer risk to occur. In any case, the risk remains lower than that with most progestins. | Pure crystalline progesterone was isolated in 1934 and its chemical structure was determined. Later that year, chemical synthesis of progesterone was accomplished. Shortly following its chemical synthesis, progesterone began being tested clinically in women. Injections and implants
In 1933 or 1934, Schering introduced progesterone in oil solution as a medication by intramuscular injection under the brand name Proluton. This was the first pharmaceutical formulation of progesterone to be marketed for medical use. It was initially a corpus luteum extract, becoming pure synthesized progesterone only subsequently. A clinical study of the formulation was published in 1933. Multiple formulations of progesterone in oil solution for intramuscular injection, under the brand names Proluton, Progestin, and Gestone, were available by 1936. A parenteral route was used because oral progesterone had very low activity and was thought to be inactive. Progesterone was initially very expensive due to the large doses required. However, with the start of steroid manufacturing from diosgenin in the 1940s, costs greatly decreased.Subcutaneous pellet implants of progesterone were first studied in women in the late 1930s. They were the first long-acting progestogen formulation. Pellets were reported to be extruded out of the skin within a few weeks at high rates, even when implanted beneath the deep fascia, and also produced frequent inflammatory reactions at the site of implantation. In addition, they were absorbed too slowly and achieved unsatisfactorily low progesterone levels. Consequently, they were soon abandoned, in favor of other preparations such as aqueous suspensions. | 11
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In the human body it is first converted to phenylbutyryl-CoA and then metabolized by mitochondrial beta-oxidation, mainly in the liver and kidneys, to the active form, phenylacetate. Phenylacetate conjugates with glutamine to phenylacetylglutamine, which is eliminated with the urine. It contains the same amount of nitrogen as urea, which makes it an alternative to urea for excreting nitrogen.A 5g tablet or powder of sodium phenylbutyrate taken by mouth can be detected in the blood within 15 minutes, and reaches peak concentration in the bloodstream within an hour. It is metabolized into phenylacetate within half an hour. See also
Glycerol phenylbutyrate
References
External links
"Sodium phenylbutyrate". Drug Information Portal. U.S. National Library of Medicine. | Protothecosis, otherwise known as Algaemia, is a disease found in dogs, cats, cattle, and humans caused by a type of green alga known as Prototheca that lacks chlorophyll and enters the human or animal bloodstream. It and its close relative Helicosporidium are unusual in that they are actually green algae that have become parasites. The two most common species are Prototheca wickerhamii and Prototheca zopfii. Both are known to cause disease in dogs, while most human cases are caused by P. wickerhami. Prototheca is found worldwide in sewage and soil. Infection is rare despite high exposure, and can be related to a defective immune system. In dogs, females and Collies are most commonly affected.The first human case was identified in 1964 in Sierra Leone. Cause
Prototheca has been thought to be a mutant of Chlorella, a type of single-celled green alga. However, while Chlorella contains galactose and galactosamine in the cell wall, Prototheca lacks these. Also, Chlorella obtains its energy through photosynthesis, while Prototheca is saprotrophic, feeding on dead and decaying organic matter. When Prototheca was first isolated from slime flux of trees in 1894, it was thought to be a type of fungus. Its size varies from 2 to 15 micrometres. Treatment
Treatment with amphotericin B has been reported. In cattle
Cattle can be affected by protothecal enteritis and mastitis. Protothecal mastitis is endemic worldwide, although most cases of infected herds have been reported in Germany, the United States, and Brazil. In dogs
Disseminated protothecosis is most commonly seen in dogs. | 0-1
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Other dermatophytes that may be involved are T. interdigitale, Epidermophyton floccosum, T. violaceum, Microsporum gypseum, T. tonsurans, and T. soudanense. A common outdated name that may still be reported by medical laboratories is Trichophyton mentagrophytes for T. interdigitale. The name T. mentagrophytes is now restricted to the agent of favus skin infection of the mouse; though this fungus may be transmitted from mice and their danders to humans, it generally infects skin and not nails. Other
Other causative pathogens include Candida and nondermatophytic molds, in particular members of the mold genus Scytalidium (name recently changed to Neoscytalidium), Scopulariopsis, and Aspergillus. Candida species mainly cause fingernail onychomycosis in people whose hands are often submerged in water. Scytalidium mainly affects people in the tropics, though it persists if they later move to areas of temperate climate. Other molds more commonly affect people older than 60 years, and their presence in the nail reflects a slight weakening in the nails ability to defend itself against fungal invasion. Nail injury and nail psoriasis can cause damaged toenails to become thick, discolored & brittle. Risk factors
Advancing age (usually over the age of 60) is the most common risk factor for onychomycosis due to diminished blood circulation, longer exposure to fungi, nails which grow more slowly and thicken, and reduced immune function increasing susceptibility to infection. Nail fungus tends to affect men more often than women and is associated with a family history of this infection. | Signs and symptoms
The most common symptom of a fungal nail infection is the nail becoming thickened and discoloured: white, black, yellow or green. As the infection progresses the nail can become brittle, with pieces breaking off or coming away from the toe or finger completely. If left untreated, the skin underneath and around the nail can become inflamed and painful. There may also be white or yellow patches on the nailbed or scaly skin next to the nail, and a foul smell. There is usually no pain or other bodily symptoms, unless the disease is severe. People with onychomycosis may experience significant psychosocial problems due to the appearance of the nail, particularly when fingers – which are always visible – rather than toenails are affected.Dermatophytids are fungus-free skin lesions that sometimes form as a result of a fungus infection in another part of the body. This could take the form of a rash or itch in an area of the body that is not infected with the fungus. Dermatophytids can be thought of as an allergic reaction to the fungus. Causes
The causative pathogens of onychomycosis are all in the fungus kingdom and include dermatophytes, Candida (yeasts), and nondermatophytic molds. Dermatophytes are the fungi most commonly responsible for onychomycosis in the temperate western countries; while Candida and nondermatophytic molds are more frequently involved in the tropics and subtropics with a hot and humid climate. Dermatophytes
When onychomycosis is due to a dermatophyte infection, it is termed tinea unguium. Trichophyton rubrum is the most common dermatophyte involved in onychomycosis. | 11
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Since traumatic events can increase cortisol production and HPA axis activity, one possibility is that the prevalence of higher than average activity in the HPA axis of people with BPD may simply be a reflection of the higher than average prevalence of traumatic childhood and maturational events among people with BPD. Estrogen
Individual differences in womens estrogen cycles may be related to the expression of BPD symptoms in female patients. A 2003 study found that womens BPD symptoms were predicted by changes in estrogen levels throughout their menstrual cycles, an effect that remained significant when the results were controlled for a general increase in negative affect. Developmental factors
Childhood trauma
There is a strong correlation between child abuse, especially child sexual abuse, and development of BPD. Many individuals with BPD report a history of abuse and neglect as young children, but causation is still debated. Patients with BPD have been found to be significantly more likely to report having been verbally, emotionally, physically, or sexually abused by caregivers of either sex. They also report a high incidence of incest and loss of caregivers in early childhood. Individuals with BPD were also likely to report having caregivers of both sexes deny the validity of their thoughts and feelings. Caregivers were also reported to have failed to provide needed protection and to have neglected their childs physical care. Parents of both sexes were typically reported to have withdrawn from the child emotionally and to have treated the child inconsistently. | Sexual abuse can be a particular trigger for suicidal behavior in adolescents with BPD tendencies. Sense of self
People with BPD tend to have trouble seeing their identity clearly. In particular, they tend to have difficulty knowing what they value, believe, prefer, and enjoy. They are often unsure about their long-term goals for relationships and jobs. This can cause people with BPD to feel "empty" and "lost". Self-image can also change rapidly from healthy to unhealthy. People with BPD may base their identity on others, leading to chameleon-like changes in identity. Cognitions
The often intense emotions people with BPD experience may make it difficult for them to concentrate. They may also tend to dissociate, which can be thought of as an intense form of "zoning out". Others can sometimes tell when someone with BPD is dissociating because their facial or vocal expressions may become flat or expressionless, or they may appear distracted and "numb" to emotional stimuli.Dissociation most often occurs in response to a painful event (or something that triggers the memory of a painful event). It involves the mind automatically redirecting attention away from the current event or situation or blocking it out entirely. This is done presumably to protect against - based on similar or related past experiences - what the mind perceives and forecasts as arousing intense negative emotions and unwanted behavioral impulses that the present emotive event might trigger. | 11
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Child abuse and neglect have been shown, in some cases, to cause important regions of the brain to fail to form or grow properly, resulting in impaired development. Structural brain changes as a result of child abuse or neglect include overall smaller brain volume, hippocampal atrophy, prefrontal cortex dysfunction, decreased corpus callosum density, and delays in the myelination of synapses. These alterations in brain maturation have long-term consequences for cognitive, language, and academic abilities. In addition, these neurological changes impact the amygdala and hypothalamic-pituitary-adrenal (HPA) axis which are involved in stress response and may cause PTSD symptoms. Poor physical health. In addition to possible immediate adverse physical effects, household dysfunction and childhood maltreatment are strongly associated with many chronic physical and psychological effects, including subsequent ill-health in childhood, adolescence and adulthood, with higher rates of chronic conditions, high-risk health behaviors and shortened lifespan. Adults who experienced abuse or neglect during childhood are more likely to have physical ailments such as allergies, arthritis, asthma, bronchitis, high blood pressure, and ulcers. There may be a higher risk of developing cancer later in life, as well as possible immune dysfunction. Exposure to violence during childhood is associated with shortened telomeres and with reduced telomerase activity. The increased rate of telomere length reduction correlates to a reduction in lifespan of 7 to 15 years. | Drugs bearing resemblance to codeine in effects due to close structural relationship are variations on the methyl groups at the 3 position including ethylmorphine, also known as codethyline (Dionine), and benzylmorphine (Peronine). While having no narcotic effects of its own, the important opioid precursor thebaine differs from codeine only slightly in structure. Pseudocodeine and some other similar alkaloids not currently used in medicine are found in trace amounts in opium as well. History
Codeine, or 3-methylmorphine, is an alkaloid found in the opium poppy, Papaver somniferum var. album, a plant in the family Papaveraceae. Opium poppy has been cultivated and utilized throughout human history for a variety of medicinal (analgesic, anti-tussive and anti-diarrheal) and hypnotic properties linked to the diversity of its active components, which include morphine, codeine and papaverine. Codeine is found in concentrations of 1% to 3% in opium prepared by the latex method from unripe pods of Papaver somniferum. The name codeine is derived from the Ancient Greek κώδεια (kṓdeia, "poppy head"). The relative proportion of codeine to morphine, the most common opium alkaloid at 4% to 23%, tends to be somewhat higher in the poppy straw method of preparing opium alkaloids. | 0-1
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Both the International Hyperhidrosis Society and the Canadian Hyperhidrosis Advisory Committee have published treatment guidelines for focal hyperhidrosis that are said to be evidence-based. Prescription medications called anticholinergics, often taken by mouth, are sometimes used in the treatment of both generalized and focal hyperhidrosis. Anticholinergics used for hyperhidrosis include propantheline, glycopyrronium bromide or glycopyrrolate, oxybutynin, methantheline, and benzatropine. Use of these drugs can be limited, however, by side-effects, including dry mouth, urinary retention, constipation, and visual disturbances such as mydriasis (dilation of the pupils) and cycloplegia. For people who find their hyperhidrosis is made worse by anxiety-provoking situations (public speaking, stage performances, special events such as weddings, etc. ), taking an anticholinergic medicine before the event may be helpful.Several anticholinergic drugs can reduce hyperhidrosis. Oxybutynin (brand name Ditropan) is one that has shown promise, although it can have side-effects, such as drowsiness, visual symptoms and dryness of the mouth and other mucous membranes. Glycopyrrolate is another drug sometimes used. It is said to be nearly as effective as oxybutynin, but has similar side-effects. In 2018, the U.S. Food and Drug Administration (FDA) approved a glycopyrronium bromide-containing disposable cloth (brand name Qbrexza) for the treatment of primary axillary hyperhidrosis.For peripheral hyperhidrosis, some chronic patients have found relief by simply ingesting crushed ice water. Ice water helps to cool excessive body heat during its transport through the blood vessels to the extremities, effectively lowering overall body temperature to normal levels within ten to thirty minutes. | For example, one prospective study of 196 women found a prevalence of 2.8% for atypical anorexia, compared to only 0.8% for anorexia nervosa by the age of 20. == References == | 0-1
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While those with congenital bicuspid aortic valve make up 30-40% of those presenting during adulthood and typically presenting earlier (ages 40+ to 50+) than those with tricuspid aortic valves (65+).Acute rheumatic fever post-inflammatory is the cause of less than 10% of cases. Rare causes of aortic stenosis include Fabry disease, systemic lupus erythematosus, Paget disease, high blood uric acid levels, and infection. Pathophysiology
The human aortic valve normally consists of three cusps or leaflets and has an opening of 3.0-4.0 square centimeters. When the left ventricle contracts, it forces blood through the valve into the aorta and subsequently to the rest of the body. When the left ventricle expands again, the aortic valve closes and prevents the blood in the aorta from flowing backward (regurgitation) into the left ventricle. In aortic stenosis, the opening of the aortic valve becomes narrowed or constricted (stenotic) (e.g., due to calcification). Degenerative (the most common variety), and bicuspid aortic stenosis both begin with damage to endothelial cells from increased mechanical stress. Inflammation is thought to be involved in the earlier stages of the pathogenesis of AS and its associated risk factors are known to promote the deposition of LDL cholesterol and lipoprotein(a), a highly damaging substance, into the aortic valve, causing significant damage and stenosis over time. Infiltration of inflammatory cells (macrophages, T lymphocytes), followed by the release of inflammatory mediators such as interleukin-1-beta and transforming growth factor beta-1 occurs. | As with one-to-one interventions, several digital interventions have also proven successful in children with generalized math learning difficulties. Räsänen and colleagues have found that games such as The Number Race and Graphogame-math can improve performance on number comparison tasks in children with generalized math learning difficulties.Several digital interventions have been developed for dyscalculics specifically. Each attempts to target basic processes that are associated with maths difficulties. Rescue Calcularis was one early computerized intervention that sought to improve the integrity of and access to the mental number line. Other digital interventions for dyscalculia adapt games, flash cards, and manipulables to function through technology.While each intervention claims to improve basic numerosity skills, the authors of these interventions do admit that repetition and practice effects may be a factor involved in reported performance gains. An additional criticism is that these digital interventions lack the option to manipulate numerical quantities. While the previous two games provide the correct answer, the individual using the intervention cannot actively determine, through manipulation, what the correct answer should be. Butterworth and colleagues argued that games like The Number Bonds, which allows an individual to compare different sized rods, should be the direction that digital interventions move toward. Such games use manipulation activities to provide intrinsic motivation toward content guided by dyscalculia research. One of these serious games is Meister Cody – Talasia, an online training that includes the CODY Assessment – a diagnostic test for detecting dyscalculia. | 0-1
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Approximately 50% of those with gestational choriocarcinoma have experienced molar pregnancy, approximately 25% developed the disease after a regular, term pregnancy, and other situations have included history of ectopic pregnancy, where the pregnancy does not occur in the uterus.Guidelines from the Federation of Gynecologists and Obstetricians (FIGO), Royal College of Obstetricians and Gynaecologists (RCOG), European Society for Medical Oncology (ESMO), and Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG) exist to evaluate risk and treatment of the disease. There are generally three levels of risk: low risk, high risk, and ultrahigh risk. The primary form of treatment is chemotherapy with one or more agents. Duration can go upwards of six weeks following return of human chorionic gonadotropin levels to the normal range. Depending on the risk of gestational trophoblastic disease (GTD) development, such as in certain people with mole pregnancies, chemotherapy has been used in a preventative manner in the past. However, this type of use is now advised against due to risk of toxicity and resistance to agents that may be needed in future treatment of the disease, on top of medical costs. Guidelines also detail options for salvage therapies in the situation of resistance to preferred choice of chemotherapy and surgical procedures possible in the situation of drug-resistant tumors. Signs and symptoms
Vaginal bleeding is a common symptom of gestational choriocarcinoma. In the event the gestational choriocarcinoma has already spread to other parts of the body, bleeding events in other organs may be the first symptom. | If the choriocarcinoma has metastasized to the lungs, one of the most common organs of metastasis, then symptoms may include abnormally quick breathing, coughing, and chest pain. However, it is also possible for there to be none of these symptoms and only a difference in biomarkers in an individual instead.Uterine enlargement as seen in an ultrasound can be a presenting sign of gestational choriocarcinoma. Transvaginal ultrasounds may also be used in screening for the disease, with the positron emission tomography (PET) scan, computed tomography (CT), and magnetic resonance imaging (MRI) in locations such as the abdomen, pelvis, and brain being other imaging options. Chest x-rays may also be used to see if gestational choriocarcinoma has potentially spread to the lungs.Human chorionic gonadotropin is a hormone produced by the trophoblast and can be measured in both urine and blood. Another option of measuring this biomarker level is through lumbar puncture, which can show fluid-to-serum ratio of human chorionic gonadotropic and reflect whether the disease has potentially spread to the central nervous system. Elevated or rising human chorionic gonadotropin can be a sign of gestational choriocarcinoma, though it is also used as a biomarker in other types of gestational trophoblastic diseases (GTD). It is useful not only for diagnosis but also for monitoring disease progression, treatment response, and potential of recurring gestational choriocarcinoma. | 11
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Most males have mild symptoms such as hypertelorism and a broad nasal base with bifid nose, but can also be a carrier of the mutation yet stay clinically unaffected. Genetics
CFND is a very rare X-linked malformation syndrome caused by mutations in the ephrin-B1 gene (EFNB1). The EFNB1 gene codes for a membrane-anchored ligand which can bind to an ephrin tyrosine-kinase receptor. This ephrin receptor is, amongst other things, responsible for the regulation of embryonic tissue-border formation, and is important for skeletal and craniofacial development. As the ephrin receptor and its EFNB1 ligand are both bound to the (trans)membrane of the cell its cascade is activated through cell-cell interactions. These cell-cell interactions are disturbed due to the presence of cells with the mutant EFNB1 gene, as a result causing incomplete tissue-border formation.Paradoxical to other X-linked conditions, with CFND the females are more severely affected than males. This is due to the process of X-inactivation in females, where at random either the maternal or paternal X-chromosome is inactivated in a cell. Due to this process, the body’s tissues contain either cells with normal EFNB1 or the mutated EFNB1. This is called a mosaic pattern. This mosaic pattern of cells interferes with the functionality of the cell-cell interactions, as a result causing the severe physical malformations in females.As with all X-linked conditions CFND has a preset chance of being passed down from parents to their offspring. Females have two X-chromosomes and males have one X-chromosome. | A torus palatinus (pl. tori palatini), or palatal torus (pl. palatal tori), is a bony protrusion on the palate. Palatal tori are usually present on the midline of the hard palate. Most palatal tori are less than 2 cm in diameter, but their size can change throughout life. Types
Sometimes, the tori are categorized by their appearance. Arising as a broad base and a smooth surface, flat tori are located on the midline of the palate and extend symmetrically to either side. Spindle tori have a ridge located at their midline. Nodular tori have multiple bony growths that each have their own base. Lobular tori have multiple bony growths with a common base. Cause
Although some research suggest palatal tori to be an autosomal dominant trait, it is generally believed that palatal tori are caused by several factors. They are more common in early adult life and can increase in size. In some older people, the size of the tori may decrease due to bone resorption. It is believed that tori of the lower jaw are the result of local stresses and not due solely to genetic influences. Treatment
Palatal tori are usually a clinical finding with no treatment necessary. It is possible for ulcers to form on the area of the tori due to repeated trauma. Also, the tori may complicate the fabrication of dentures. If removal of the tori is needed, surgery can be done to reduce the amount of bone present. Surgical removal
A maxillary torus is only removed in instances where it is problematic. | 0-1
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See also
Voodoo death
References
External links
Syncope (medicine) at Curlie
2004 European Society of Cardiology Guidelines on Management (Diagnosis and Treatment) of Syncope
2017 American College of Cardiology Guideline
Tilt table test
The San Francisco syncope rule
"Fainting". MedlinePlus. U.S. National Library of Medicine. | It is not recommended in people with lupus erythematosus. Use during pregnancy may result in harm to the baby. Penicillamine works by binding heavy metals; the resulting penicillamine–metal complexes are then removed from the body in the urine.Bone marrow suppression, dysgeusia, anorexia, vomiting, and diarrhea are the most common side effects, occurring in ~20–30% of the patients treated with penicillamine.Other possible adverse effects include:
Nephropathy
Hepatotoxicity
Membranous glomerulonephritis
Aplastic anemia (idiosyncratic)
Antibody-mediated myasthenia gravis and Lambert–Eaton myasthenic syndrome, which may persist even after its withdrawal
Drug-induced systemic lupus erythematosus
Elastosis perforans serpiginosa
Toxic myopathies
Unwanted breast growth
Oligospermia
Chemistry
Penicillamine is a trifunctional organic compound, consisting of a thiol, an amine, and a carboxylic acid. It is structurally similar to the α-amino acid cysteine, but with geminal dimethyl substituents α to the thiol. Like most amino acids, it is a colorless solid that exists in the zwitterionic form at physiological pH. Penicillamine is a chiral drug with one stereogenic center and exist as a pair of enantiomers. Refer the image for the structure of penicillamine enantiomers. The (S)-enantiomer, the eutomer, is antiarthritic while the distomer (R)-penicillamine is extremely toxic. Of its two enantiomers, L-penicillamine (having R absolute configuration) is toxic because it inhibits the action of pyridoxine (also known as vitamin B6). That enantiomer is a metabolite of penicillin but has no antibiotic properties itself. A variety of penicillamine–copper complex structures are known. History
John Walshe first described the use of penicillamine in Wilsons disease in 1956. | 0-1
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Due to the low incidence rate of oral cancer, studies have not been able to conduct quality studies to prove the association between the two, however future larger studies may aid in the identification of individuals at a higher risk.Systemic implications
Periodontal disease (PD) can be described as an inflammatory condition affecting the supporting structures of the teeth. Studies have shown that PD is associated with higher levels of systemic inflammatory markers such as Interleukin-6 (IL-6), C-Reactive Protein (CRP) and Tumor Necrosis Factor (TNF). To compare, elevated levels of these inflammatory markers are also associated with cardiovascular disease and cerebrovascular events such as ischemic strokes.The presence of a wide spectrum inflammatory oral diseases can increase the risk of an episode of stroke in an acute or chronic phase. Inflammatory markers, CRP, IL-6 are known risk factors of stroke. Both inflammatory markers are also biomarkers of PD and found to be an increased level after daily activities, such as mastication or toothbrushing, are performed. Bacteria from the periodontal pockets will enter the bloodstream during these activities and the current literature suggests that this may be a possible triggering of the aggravation of the stroke process.Other mechanisms have been suggested, PD is a known chronic infection. It can aid in the promotion of atherosclerosis by the deposition of cholesterol, cholesterol esters and calcium within the subendothelial layer of vessel walls. Atherosclerotic plaque that is unstable may rupture and release debris and thrombi that may travel to different parts of the circulatory system causing embolization and therefore, an ischemic stroke. | It is often possible to manage these symptoms with specific behavioral techniques. Another evolutionary psychology view is that some forms of fainting are non-verbal signals that developed in response to increased inter-group aggression during the paleolithic. A non-combatant who has fainted signals that she or he is not a threat. This would explain the association between fainting and stimuli such as bloodletting and injuries seen in blood-injection-injury type phobias such as needle phobia as well as the gender differences.Much of this pathway was discovered in animal experiments by Bezold (Vienna) in the 1860s. In animals, it may represent a defence mechanism when confronted by danger ("playing possum"). Situational syncope
Syncope may be caused by specific behaviors including coughing, urination, defecation, vomiting, swallowing (deglutition), and following exercise. Manisty et al. note: "Deglutition syncope is characterised by loss of consciousness on swallowing; it has been associated not only with ingestion of solid food, but also with carbonated and ice-cold beverages, and even belching." Fainting can occur in "cough syncope" following severe fits of coughing, such as that associated with pertussis or "whooping cough." Neurally mediated syncope may also occur when an area in the neck known as the carotid sinus is pressed. A normal response to carotid sinus massage is reduction in blood pressure and slowing of the heart rate. Especially in people with hypersensitive carotid sinus syndrome this response can cause syncope or presyncope. | 0-1
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UV-A radiation (wavelength 320–400 nm) reaches more deeply into the skin and can lead to the generation of reactive oxygen species, which in turn can damage cell membranes, signaling proteins, and nucleic acids. UV-B radiation (wavelength 290–320 nm) causes thymidine dimer formation in DNA and RNA, leading to significant cellular mutations. In particular, mutations in the p53 tumor suppressor gene have been found in 30–50% of AK lesion skin samples.UV radiation has also been shown to cause elevated inflammatory markers such as arachidonic acid, as well as other molecules associated with inflammation. Eventually, over time these changes lead to the formation of AKs. Several predictors for increased AK risk from UV radiation have been identified:
Extent of sun exposure: Cumulative sun exposure leads to an increased risk for development of AKs. In one U.S. study, AKs were found in 55% of fair-skinned men with high cumulative sun exposure, and in only 19% of fair-skinned men with low cumulative sun exposure in an age-matched cohort (the percents for women in this same study were 37% and 12% respectively). Furthermore, the use of sunscreen (SPF 17 or higher) has been found to significantly reduce the development of AK lesions, and also promotes the regression of existing lesions. History of sunburn: Studies show that even a single episode of painful sunburn as a child can increase an individuals risk of developing AK as an adult. Six or more painful sunburns over the course of a lifetime was found to be significantly associated with the likelihood of developing AK. | Skin pigmentation
Melanin is a pigment in the epidermis that functions to protect keratinocytes from the damage caused by UV radiation; it is found in higher concentrations in the epidermis of darker-skinned individuals, affording them protection against the development of AKs. Fair-skinned individuals have a significantly increased risk of developing AKs when compared to olive-skinned individuals (odds ratios of 14.1 and 6.5, respectively), and AKs are uncommon in dark-skinned people of African descent. Other phenotypic features seen in fair-skinned individuals that are associated with an increased propensity to develop AKs include:
Freckling
Light hair and eye color
Propensity to sunburn
Inability to tan
Other risk factors
Immunosuppression: People with a compromised immune system from medical conditions (such as AIDS) or immunosuppressive therapy (such as chronic immunosuppression after organ transplantation, or chemotherapy for cancer) are at increased risk for developing AKs. They may develop AK at an earlier age or have an increased number of AK lesions compared to immunocompetent people. Human papillomavirus (HPV): The role of HPV in the development of AK remains unclear, but evidence suggests that infection with the betapapillomavirus type of HPV may be associated with an increased likelihood of AK. Genodermatoses: Certain genetic disorders interfere with DNA repair after sun exposure, thereby putting these individuals at higher risk for the development of AKs. Examples of such genetic disorders include xeroderma pigmentosum and Bloom syndrome. Balding: AKs are commonly found on the scalps of balding men. | 11
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Pregnancy is the time during which one or more offspring develops (gestates) inside a womans uterus (womb). A multiple pregnancy involves more than one offspring, such as with twins. Pregnancy usually occurs by sexual intercourse, but can also occur through assisted reproductive technology procedures. A pregnancy may end in a live birth, a miscarriage, an induced abortion, or a stillbirth. Childbirth typically occurs around 40 weeks from the start of the last menstrual period (LMP), a span known as the gestational age. This is just over nine months. Counting by fertilization age, the length is about 38 weeks. Pregnancy is "the presence of an implanted human embryo or fetus in the uterus"; implantation occurs on average 8–9 days after fertilization. An embryo is the term for the developing offspring during the first seven weeks following implantation (i.e. ten weeks gestational age), after which the term fetus is used until birth.Signs and symptoms of early pregnancy may include missed periods, tender breasts, morning sickness (nausea and vomiting), hunger, implantation bleeding, and frequent urination. Pregnancy may be confirmed with a pregnancy test. Methods of birth control—or, more accurately, contraception—are used to avoid pregnancy. Pregnancy is divided into three trimesters of approximately three months each. The first trimester includes conception, which is when the sperm fertilizes the egg. The fertilized egg then travels down the Fallopian tube and attaches to the inside of the uterus, where it begins to form the embryo and placenta. | Head engagement, also called "lightening" or "dropping", occurs as the fetal head descends into a cephalic presentation. While it relieves pressure on the upper abdomen and gives a renewed ease in breathing, it also severely reduces bladder capacity resulting in a need to void more frequently, and increases pressure on the pelvic floor and the rectum. It is not possible to predict when lightening occurs. In a first pregnancy it may happen a few weeks before the due date, though it may happen later or even not until labor begins, as is typical with subsequent pregnancies.It is also during the third trimester that maternal activity and sleep positions may affect fetal development due to restricted blood flow. For instance, the enlarged uterus may impede blood flow by compressing the vena cava when lying flat, which is relieved by lying on the left side. Childbirth
Childbirth, referred to as labor and delivery in the medical field, is the process whereby an infant is born.A woman is considered to be in labour when she begins experiencing regular uterine contractions, accompanied by changes of her cervix—primarily effacement and dilation. While childbirth is widely experienced as painful, some women do report painless labours, while others find that concentrating on the birth helps to quicken labour and lessen the sensations. Most births are successful vaginal births, but sometimes complications arise and a woman may undergo a cesarean section. | 11
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