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Approximately 30%-79% of people with the disease display symptoms of abnormality of the retinal pigmentation, ataxia, muscular hypotonia or reduced tendon reflexes.The signs and symptoms of abetalipoproteinemia appear in the first few months of life (because pancreatic lipase is not active in this period). They can include failure to gain weight and grow at the expected rate (failure to thrive); diarrhea; abnormal spiny red blood cells (acanthocytosis); and fatty, foul-smelling stools (steatorrhea). The stool may contain large chunks of fat and/or blood. Infants often present with gastrointestinal problems caused by the poor fat absorption, which also contributes to steatorrhea. Other features of this disorder may develop later in childhood and often impair the function of the nervous system. They can include poor muscle coordination, difficulty with balance and movement (ataxia), and progressive degeneration of the retina (the light-sensitive layer in the posterior eye) that can progress to near-blindness (due to deficiency of vitamin A, retinol). Adults in their thirties or forties may have increasing difficulty with balance and walking. Many of the signs and symptoms of abetalipoproteinemia result from a severe vitamin deficiency, especially vitamin E deficiency, which typically results in eye problems with degeneration of the spinocerebellar and dorsal column tracts. Genetics
Mutations in the microsomal triglyceride transfer protein (MTTP) gene has been associated with this condition. (apolipoprotein B deficiency, a related condition, is associated with deficiencies of apolipoprotein B. )The MTTP gene provides instructions for making a protein called microsomal triglyceride transfer protein, which is essential for creating beta-lipoproteins. | These lipoproteins are both necessary for the absorption of fats, cholesterol, and fat-soluble vitamins from the diet and necessary for the efficient transport of these substances in the bloodstream. Most of the mutations in this gene lead to the production of an abnormally short microsomal triglyceride transfer protein, which prevents the normal creation of beta-lipoproteins in the body. MTTP-associated mutations are inherited in an autosomal recessive pattern, which means both copies of the gene must be faulty to produce the disease.The disease is extremely rare with approximately 100 reported cases worldwide since it was first identified by doctors Bassen and Kornzweig in 1950. Mechanism
Abetalipoproteinemia effects multiple physiological systems, the two most common being the nervous and the skeletal. Disruption of nervous function includes loss of reflexes, speech impairments, tremors or involuntary motor tics, or peripheral neuropathy (damage to the nerves outside of the brain and spinal cord). Peripheral neuropathy causes loss of sensation, weakness or numbness and pain in the extremities through stabbing, burning, or tingling sensations. Skeletal system developments often include lordosis, kyphoscoliosis, or pes cavus. Individuals often have abnormal bleeding due to the difficulty of forming clots.Additional complications of the diseases if not properly treated include blindness, mental deterioration, ataxia, loss of peripheral nerve function. Diagnosis
The initial workup of Abetalipoproteinemia typically consists of stool sampling, a blood smear, and a fasting lipid panel, though these tests are not confirmatory. As the disease is rare, though a genetics test is necessary for diagnosis, it is generally not done initially. | 11
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The right ventricle is most susceptible to injury due to its prominent location. The two primary consequences of traumatic injury to the heart are severe hemorrhaging and fluid buildup around the heart. Musculoskeletal
Musculoskeletal injuries affect the skeleton and the muscular system. Soft tissue injuries affect the skeletal muscles, ligaments, and tendons. Ligament and tendon injuries account for half of all musculoskeletal injuries. Ligament sprains and tendon strains are common injuries that do not require intervention, but the healing process is slow. Physical therapy can be used to assist reconstruction and use of injured ligaments and tendons. Torn ligaments or tendons typically require surgery. Skeletal muscles are abundant in the body and commonly injured when engaging in athletic activity. Muscle injuries trigger an inflammatory response to facilitate healing. Blunt trauma to the muscles can cause contusions and hematomas. Excessive tensile strength can overstretch a muscle, causing a strain. Strains may present with torn muscle fibers, hemorrhaging, or fluid in the muscles. Severe muscle injuries in which a tear extends across the muscle can cause total loss of function. Penetrative trauma can cause laceration to muscles, which may take an extended time to heal. Unlike contusions and strains, lacerations are uncommon in sports injuries.Traumatic injury may cause various bone fractures depending on the amount of force, direction of the force, and width of the area affected. Pathologic fractures occur when a previous condition weakens the bone until it can be easily fractured. | It is used to define the term major trauma (polytrauma), recognized when the ISS is greater than 15. The AIS Committee of the Association for the Advancement of Automotive Medicine designed and updates the scale. Mechanisms
Trauma
Traumatic injury is caused by an external object making forceful contact with the body, resulting in a wound. Major trauma is a severe traumatic injury that has the potential to cause disability or death. Serious traumatic injury most often occurs as a result of traffic collisions. Traumatic injury is the leading cause of death in people under the age of 45.Blunt trauma injuries are caused by the forceful impact of an external object. Injuries from blunt trauma may cause internal bleeding and bruising from ruptured capillaries beneath the skin, abrasion from scraping against the superficial epidermis, lacerated tears on the skin or internal organs, or bone fractures. Crush injuries are a severe form of blunt trauma damage that apply large force to a large area over a longer period of time. Penetrating trauma injuries are caused by external objects entering the tissue of the body through the skin. Low-velocity penetration injuries are caused by sharp objects, such as stab wounds, while high-velocity penetration injuries are caused by ballistic projectiles, such as gunshot wounds or injuries caused by shell fragments. Perforated injuries result in an entry wound and an exit wound, while puncture wounds result only in an entry wound. Puncture injuries result in a cavity in the tissue. Burns
Burn injury is caused by contact with extreme temperature, chemicals, or radiation. | 11
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Standing, also referred to as orthostasis, is a position in which the body is held in an erect ("orthostatic") position and supported only by the feet. Although seemingly static, the body rocks slightly back and forth from the ankle in the sagittal plane. The sagittal plane bisects the body into right and left sides. The sway of quiet standing is often likened to the motion of an inverted pendulum.Standing at attention is a military standing posture, as is stand at ease, but these terms are also used in military-style organisations and in some professions which involve standing, such as modeling. At ease refers to the classic military position of standing with legs slightly apart, not in as formal or regimented a pose as standing at attention. In modeling, model at ease refers to the model standing with one leg straight, with the majority of the weight on it, and the other leg tucked over and slightly around. Control
Standing posture relies on dynamic rather than static balance. The human center of mass is in front of the ankle, and unlike in tetrapods, the base of support is narrow, consisting of only two feet. A static pose would cause humans to fall forward onto the face. In addition, there are constant external perturbations, such as breezes, and internal perturbations that come from respiration. Erect posture requires adjustment and correction. There are many mechanisms in the body that are suggested to control this, e.g. a spring action in muscles, higher control from the nervous system or core muscles. | Humans begin to stand between 8 and 12 months of age. Spring action
Traditionally, such correction was explained by the spring action of the muscles, a local mechanism taking place without the intervention of the central nervous system (C.N.S.). Recent studies, however, show that this spring action by itself is insufficient to prevent a forward fall. Also, human sway is too complicated to be adequately explained by spring action. Nervous system
According to current theory, the nervous system continually and unconsciously monitors our direction and velocity. The vertical body axis alternates between tilting forward and backward. Before each tilt reaches the tipover point the nervous system counters with a signal to reverse direction. Sway also occurs in the hip and there is a slight winding and unwinding of the lower back.An analogy would be a ball that volleys back and forth between two players without touching the ground. The muscle exertion required to maintain an aligned standing posture is crucial but minimal. Electromyography has detected slight activity in the muscles of the calves, hips and lower back. Core muscles
The core muscles play a role in maintaining stability. The core muscles are deep muscle layers that lie close to the spine and provide structural support. The transverse abdominals wrap around the spine and function as a compression corset. The multifidi are intersegmental muscles. Dysfunction in the core muscles has been implicated in back pain. Expansion of pendulum model
Some investigators have replaced the ankle inverted pendulum analogy with a model of double linked pendulums involving both hip and ankle sway. | 11
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In most cases, patients going in for surgery experience nausea or vomiting that require medication before surgery. Antibiotics, along with pain medication, may be administered before appendectomies. After surgery
Hospital lengths of stay typically range from a few hours to a few days but can be a few weeks if complications occur. The recovery process may vary depending on the severity of the condition: if the appendix had ruptured or not before surgery. Appendix surgery recovery is generally a lot faster if the appendix did not rupture. It is important that people undergoing surgery respect their doctors advice and limit their physical activity so the tissues can heal faster. Recovery after an appendectomy may not require diet changes or a lifestyle change. The length of hospital stays for appendicitis varies on the severity of the condition. A study from the United States found that in 2010, the average appendicitis hospital stay was 1.8 days. For stays where the persons appendix had ruptured, the average length of stay was 5.2 days.After surgery, the patient will be transferred to a postanesthesia care unit, so his or her vital signs can be closely monitored to detect anesthesia- or surgery-related complications. Pain medication may be administered if necessary. After patients are completely awake, they are moved to a hospital room to recover. Most individuals will be offered clear liquids the day after the surgery, then progress to a regular diet when the intestines start to function correctly. | It has been hypothesized that this could be due to facial hypertrichosis.Hypertrichosis (often mistakenly classified as hirsutism) is a well documented condition in horses with a hormonal disorder of the hypothalamus, called Cushings disease. It is the most common endocrine disease of the middle-aged to older horse, often resulting in fatal laminitis. It can be successfully controlled by medications if diagnosed early. See also
Jesús Aceves, the first person with hypertrichosis to perform in the UK in thirty years. Stephan Bibrowski (1890–1932), known as Lionel the Lion-faced Man. Krao Farini (1876–1926), known as The Missing Link. Fedor Jeftichew (1868–1904), known as Jo-Jo the Dog-Faced Boy. Human Nature, a 2001 American-French film where one of the main characters has hypertrichosis. Fur: An Imaginary Portrait of Diane Arbus, a 2006 American film where one of the main characters has hypertrichosis. Milo, a 2012 (Netherlands) movie about a 10-year-old boy with hypersensitive skin. Moon of Desire, a 2014 Filipino TV drama with a girl that has hypertrichosis as the main protagonist. The True Adventures of Wolfboy, a 2019 Drama Movie about a 13-year-old boy that has hypertrichosis. References
External links
The Hairy Family of Burma | 0-1
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This theory of persistence in structural unemployment has been referred to as an example of path dependence or "hysteresis." Much technological unemployment, caused by the replacement of workers by machines might be counted as structural unemployment. Alternatively, technological unemployment might refer to the way in which steady increases in labour productivity mean that fewer workers are needed to produce the same level of output every year. The fact that aggregate demand can be raised to deal with the problem suggests that the problem is instead one of cyclical unemployment. As indicated by Okuns law, the demand side must grow sufficiently quickly to absorb not only the growing labour force but also the workers who are made redundant by the increased labour productivity. Seasonal unemployment may be seen as a kind of structural unemployment since it is linked to certain kinds of jobs (construction and migratory farm work). The most-cited official unemployment measures erase this kind of unemployment from the statistics using "seasonal adjustment" techniques. That results in substantial and permanent structural unemployment. Frictional unemployment
Frictional unemployment is the time period between jobs in which a worker searches for or transitions from one job to another. It is sometimes called search unemployment and can be voluntary, based on the circumstances of the unemployed individual. Frictional unemployment exists because both jobs and workers are heterogeneous, and a mismatch can result between the characteristics of supply and demand. Such a mismatch can be related to skills, payment, work-time, location, seasonal industries, attitude, taste, and a multitude of other factors. | Availability
Since 2009, lansoprazole has been available over the counter (OTC) in the U.S. as Prevacid 24HR and as Lansoprazole 24HR. In Australia, it is marketed by Pfizer as Zoton. Research
In vitro experiments have shown that lansoprazole binds to the pathogenic form of tau protein. As of 2015 laboratory studies were underway on analogs of lansoprazole to explore their use as potential PET imaging agents for diagnosing tauopathies including Alzheimers disease. References
External links
"Lansoprazole". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Estradiol was used as a positive control and raloxifene was used because it is in the same drug class as ospemifene. Multiple doses of oral ospemifene were tested. 10 mg/kg/day of Ospemifene was found to cause a greater increase in vaginal weight and vaginal epithelial height than 10 mg/kg/day of raloxifene. Vaginal weight had a 1.46x increase after a two-week treatment of 10 mg/kg/day of ospemifene. The number of progesterone receptors was increased in the vaginal stroma and epithelium, which indicates that ospemifene has "estrogenic activity. "Two 12-week phase 3 clinical trials were performed for ospemifene. One evaluated the effects of Ospemifene on vaginal tissue thickness, composition and vaginal pH. The other evaluated the effects of Ospemifene on vaginal tissue and on symptoms of dyspareunia. Between the two trials, 4 signs and symptoms were measured. These included three tissue-related signs, two of which represented histological changes in the vaginal tissue (change in percent parabasal cells and change in percent superficial cells) and the third was "change in vaginal pH". Dyspareunia was evaluated in one of the trials. It was defined as "change in most bothersome symptom" of discomfort during sexual activity and further limited to symptoms of either vaginal dryness or vaginal pain." Ospemifene produced more changes in vaginal tissue and greater reduction in dyspareunia symptoms than placebo. A dose-response also was observed in the trial; ospemifene 60 mg had greater efficacy than ospemifene 30 mg. Safety was also evaluated in these phase 3 trials. | These include, but are not limited to, thromboembolism, allergic reactions, fatigue, and headache, and others could occur. There are other additional adverse effects. Ospemifene is a selective estrogen receptor modulator. As such, many of the effects produced by estrogens are produced by ospemifene. The boxed warning of the medication indicates ospemifene may thicken the endometrium, which could lead to unusual bleeding and endometrial cancer. For women taking estrogens, concurrently taking a type of drug called a progestin has been shown to decrease the occurrence of endometrial hyperplasia. In theory, progestins may be expected to attenuate ospemifenes effects on endometrial thickening. However clinical trials confirming this have not been conducted. Like estrogens, ospemifene also may increase the risk for cardiovascular events, including "stroke, coronary heart disease, venous thromboembolism," and others. The risk of thrombotic and hemorrhagic strokes is given as 0.72 and 1.45 per 1,000 women, while that of deep vein thrombosis is estimated to be 1.45 per 1,000 women. The risks of these adverse events in women taking ospemifene are lower than those in women taking estrogen alone in the form of oral conjugated estrogens. Studies have not documented the relative risk compared with women taking estrogen/progestin therapy. Pharmacology
Pharmacodynamics
Ospemifene is "an estrogen agonist/antagonist that makes vaginal tissue thicker and less fragile resulting in a reduction in the amount of pain women experience with sexual intercourse." This medication should be used for the shortest amount of time possible due to associated adverse effects. | 11
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In response to a triggering impulse, the waves of depolarisation will spread through regions with shorter action potentials but block in regions with longer action potentials. This allows the depolarising wavefront to bend around areas of block, potentially forming a complete loop and self-perpetuating. The twisting pattern on the ECG can be explained by movement of the core of the re-entrant circuit in the form of a meandering spiral wave. Diagnosis
Diagnosing long QT syndrome is challenging. Whilst the hallmark of LQTS is prolongation of the QT interval, the QT interval is highly variable among both those who are healthy and those who have LQTS. This leads to overlap between the QT intervals of those with and without LQTS. 2.5% of those with genetically proven LQTS have a QT interval within the normal range. Conversely, given the normal distribution of QT intervals, a proportion of healthy people will have a longer QT interval than any arbitrary cutoff. Other factors beyond the QT interval should therefore be taken into account when making a diagnosis, some of which have been incorporated into scoring systems. Electrocardiogram
Long QT syndrome is principally diagnosed by measuring the QT interval corrected for heart rate (QTc) on a 12-lead electrocardiogram (ECG). Long QT syndrome is associated with a prolonged QTc, although in some genetically proven cases of LQTS this prolongation can be hidden, known as concealed LQTS. The QTc is less than 450 ms in 95% of normal males, and less than 460 ms in 95% of normal females. | Overall, every 10 ms increase in the corrected QT interval is associated with a 15% increase in arrhythmic risk.As the QT prolonging effects of both genetic variants and acquired causes of LQTS are additive, those with inherited LQTS are more likely to experience TdP if given QT prolonging drugs or if they experience electrolyte problems such as low blood levels of low potassium (hypokalaemia). Similarly, those taking QT prolonging medications are more likely to experience TdP if they have a genetic tendency to a prolonged QT interval, even it this tendency is concealed. Arrhythmias occur more commonly in drug-induced LQTS if the medication in question has been rapidly given intravenously, or if high concentrations of the drug are present in the persons blood. The risk of arrhythmias is also higher if the person receiving the drug has heart failure, is taking digitalis, or has recently been cardioverted from atrial fibrillation. Other risk factors for developing torsades de pointes among those with LQTS include female sex, increasing age, pre-existing cardiovascular disease, and abnormal liver or kidney function. Causes
There are several subtypes of long QT syndrome. These can be broadly split into those caused by genetic mutations which those affected are born with, carry throughout their lives, and can pass on to their children (inherited or congenital long QT syndrome), and those caused by other factors which cannot be passed on and are often reversible (acquired long QT syndrome). Inherited
Inherited, or congenital long QT syndrome, is caused by genetic abnormalities. | 11
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Latah, from Southeast Asia, is a condition in which abnormal behaviors result from a person experiencing a sudden shock. When surprised, the affected person typically engages in such behaviors as screaming, cursing, dance movements, and uncontrollable laughter, and will typically mimic the words or actions of those around them. Physical symptoms include an increased heart rate and profuse sweating, but no clear physiological source has been identified. Latah is considered a culture-specific startle disorder that was historically regarded as personal difference rather than an illness. Similar conditions have been recorded within other cultures and locations. For example, there are the so-called Jumping Frenchmen of Maine, imu among women of the Ainu people of Japan, mali-mali or silok among Filipinos, and bat-schi (บ้าจี้) among Thais; however, the connection among these syndromes is controversial. Earliest record
The earliest mention of latah is in J. R. Logans journal from 1849 when he traveled from Melaka to Naning. Though this is only a possible reference, by the 1860s, latah had been clearly identified in Malaya and Java. Seen first as merely a "cerebral affection", little was understood about latah during this time. OBriens notes from the early– to mid–1880s are the first gathering of information on latah recorded. He observed that latah was more common in women than men, and more likely to occur in more mature, rather than younger, women. | Promethazine is a first-generation antihistamine and antiemetic used to treat allergies, insomnia, and nausea. It may also help with some symptoms associated with the common cold and may also be used for sedating people who are agitated or anxious. Promethazine is available by mouth in syrup or tablet dosage forms, as a rectal suppository, or by injection into a muscle.Common side effects of promethazine include confusion and sleepiness; consumption of alcohol or other sedatives can make these symptoms worse. It is unclear if use of promethazine during pregnancy or breastfeeding is safe for the baby. Use of promethazine is not recommended in those less than two years old, due to potentially negative effects on breathing. Use of promethazine by injection into a vein is not recommended, due to potential skin damage. Promethazine is in the phenothiazine family of medications.Promethazine was made in the 1940s by a team of scientists from Rhône-Poulenc laboratories. It was approved for medical use in the United States in 1951. It is a generic medication and is available under many brand names globally. In 2019, it was the 174th most commonly prescribed medication in the United States, with more than 3 million prescriptions. Medical uses
Promethazine has a variety of medical uses, including:
Sedation
For nausea and vomiting associated with anesthesia or chemotherapy. It is commonly used postoperatively as an antiemetic. The antiemetic activity increases with increased dosing; however, side effects also increase, which often limits maximal dosing. | 0-1
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This can be represented in equation form as:
(
v
33
m
/
s
)
2
×
(
r
96.6
k
m
)
{\displaystyle \left({\frac {v}{33m/s}}\right)^{2}\times \left({\frac {r}{96.6km}}\right)\,}
where v is the storms wind speed and r is the radius of hurricane-force winds. | Laws
This method of dismissal is covered by Law 33 of the Laws of cricket which reads:
The striker is out Caught if a ball delivered by the bowler, not being a No ball, touches his/her bat without having previously been in contact with any fielder, and is subsequently held by a fielder as a fair catch,..., before it touches the wicket and ground.This means that the batsman cannot be out caught if:
The ball is called a no-ball or dead ball. The batsman does not hit the ball with his bat or a gloved hand holding the bat. The ball, having been hit, makes contact with the field before a fielder catches the ball. The ball does not remain under the control of the fielder. The ball is hit and lands beyond or on the boundary; (six runs). A fielder taking the catch makes contact with the boundary rope or the area outside the boundary, with any part of his body, equipment, when touching the ball. An airborne fielder taking the catch, having not previously legally touched the ball, had his last contact with the ground not entirely within the boundary.Note that if a batsman could be given out both caught and by another method, caught takes precedence, unless the other method is bowled.If a batsman is out caught, any runs scored off that delivery are voided. | 0-1
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Unlike mesoblastic nephroma, clear cell sarcoma of the kidney presents with metastasis, particularly to bone, in 5-6% of cases; it histology is diverse and has been mistaken for mesoblastic nephroma. One chromosomal translocations t,(10;17)(q22;p13), has been repeatedly reported to be associated with clear cell sarcoma of the kidney. Infantile myofibromatosis is a fibrous tumor of infancy and childhood most commonly presenting during the first 2 years of life as a single subcutaneous nodule of the head and neck region or less commonly as multiple lesions of skin, muscle, bone, and in ~33% of these latter cases, visceral organs. All of these lesions have an excellent prognosis and can regress spontaneously except for those in which there is visceral involvement where the prognosis is poor. While infantile myofibromatosis and classic mesoblastic nephroma have been suggested to be the same diseases because of their very similar histology, studies on the distribution of cell-type markers (i.e. cyclin D1 and Beta-catenin) indicate that they have different cellular origins. Treatment
Based on a survey of >800, surgical removal of the entire involved kidney plus the peri-renal fat appeared curative for the majority of all types of mesoblastic nephroma; the patient overall survival rate was 94%. Of the 4% of non-survivors, half were due to surgical or chemotherapeutic treatments. Another 4% of these patients suffered relapses, primarily in the local area of surgery rare cases of relapse due to lung or bone metastasis.. About 60% of these recurrent cases had a complete remission following further treatment. | Congenital mesoblastic nephroma, while rare, is the most common kidney neoplasm diagnosed in the first three months of life and accounts for 3-5% of all childhood renal neoplasms. This neoplasm is generally non-aggressive and amenable to surgical removal. However, a readily identifiable subset of these kidney tumors has a more malignant potential and is capable of causing life-threatening metastases. Congenital mesoblastic nephroma was first named as such in 1967 but was recognized decades before this as fetal renal hamartoma or leiomyomatous renal hamartoma. Presentation
Congenital mesoblastic nephroma typically (76% of cases) presents as an abdominal mass which is detected prenatally (16% of cases) by ultrasound or by clinical inspection (84% of cases) either at birth or by 3.8 years of age (median age ~1 month). The neoplasm shows a slight male preference. Concurrent findings include hypertension (19% of cases), polyhydramnios (i.e. excess of amniotic fluid in the amniotic sac) (15%), hematuria (11%), hypercalcemia (4%), and elevated serum levels of the kidney-secreted, hypertension-inducing enzyme, renin (1%). Congenital anomalies have been reported in 11 patients: 6 with genitourinary anomalies, 2 with gastrointestinal anomalies, 1 with hydrocephalus, and 1 with the Beckwith–Wiedemann syndrome. The vast majority of patients present with localized (i.e. non-metastatic) disease. Most patients disease is classified at presentation as stage I or II (i.e. localized), few patients present with stage III (i.e. locally advanced/infiltrating), and virtually no patients present with stage IV (metastases present or V (i.e. tumors in both kidneys) disease (see staging of renal cancer). | 11
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This is intended to reduce the incidence and severity of menopausal symptoms such as hot flushes and decreased bone mineral density that are secondary to estrogen deficiency. Pharmacokinetics
A single 40-mg oral dose of relugolix has been found to result in peak levels of relugolix of 29 ng/mL (47 nmol/L) after 1.5 hours. Steady-state levels are reached within 7 days with 40 mg/day relugolix administration. There is an approximate 2-fold accumulation of relugolix by 2 weeks of continuous administration. Food diminishes the oral bioavailability of relugolix by about 50%.Relugolix is a substrate for P-glycoprotein, which may have a limiting effect on its absorption and distribution. The plasma protein binding of relugolix is approximately 68 to 71% over a concentration range of 0.05 to 5 μg/mL.Relugolix is not a substrate for CYP3A4. The elimination half-life of relugolix is 36 to 65 hours across a dosage range of 20 to 180 mg/day. There is moderate to high interindividual variability in systemic exposure to relugolix.Relugolix is excreted mainly in feces (83%) and to a small degree in urine (4%). Only about 6% of a dose of relugolix is excreted unchanged. Chemistry
Relugolix is a non-peptide, small-molecule compound, and is structurally distinct from GnRH analogues. It is an N-phenylurea derivative. History
Relugolix was first described in 2004. It superseded sufugolix (developmental code name TAK-013), which was developed by the same researchers. Relugolix was approved for the treatment of uterine fibroids in Japan on 8 January 2019. | Legal status
On 24 February 2022, the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency adopted a positive opinion, recommending the granting of a marketing authorization for the medicinal product Orgovyx, intended for the treatment of prostate cancer. The applicant for this medicinal product is Myovant Sciences Ireland Limited. Research
Relugolix is under development by Myovant Sciences and Takeda for the treatment of uterine fibroids in countries besides Japan such as the United States. Relugolix is also under development for the treatment of endometriosis in the United States and other countries. References
Further reading
Markham, Anthony (April 2019). "Relugolix: First Global Approval". Drugs. 79 (6): 675–679. doi:10.1007/s40265-019-01105-0. ISSN 0012-6667. PMID 30937733. S2CID 89616869. Elsharoud, A.; Ali, M.; Al-Hendy, A. (2019). "Relugolix. GnRH (LHRH) receptor antagonist, Treatment of uterine fibroids, Treatment of endometriosis-related pain, Treatment of prostate cancer". Drugs of the Future. 44 (2): 131. doi:10.1358/dof.2019.44.2.2927590. ISSN 0377-8282. S2CID 87369995. Barra F, Seca M, Della Corte L, Giampaolino P, Ferrero S (August 2019). "Relugolix for the treatment of uterine fibroids". Drugs Today. 55 (8): 503–512. doi:10.1358/dot.2019.55.8.3020179. PMID 31461087. S2CID 201654739. External links
"Relugolix". Drug Information Portal. U.S. National Library of Medicine. Clinical trial number NCT03085095 for "A Study to Evaluate the Safety and Efficacy of Relugolix in Men With Advanced Prostate Cancer (HERO)" at ClinicalTrials.gov | 11
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Diuresis is usually complete within 6–8 hours of oral administration, but there is significant variation between individuals. Adverse effects
Furosemide also can lead to gout caused by hyperuricemia. Hyperglycemia is also a common side effect. The tendency, as for all loop diuretics, to cause low serum potassium concentration (hypokalemia) has given rise to combination products, either with potassium or with the potassium-sparing diuretic amiloride (Co-amilofruse). Other electrolyte abnormalities that can result from furosemide use include hyponatremia, hypochloremia, hypomagnesemia, and hypocalcemia.In the treatment of heart failure, many studies have shown that the long-term use of furosemide can cause varying degrees of thiamine deficiency, so thiamine supplementation is also suggested.Furosemide is a known ototoxic agent generally causing transient hearing loss but can be permanent. Reported cases of furosemide induced hearing loss appeared to be associated with rapid intravenous administration, high dosages, concomitant renal disease and coadministration with other ototoxic medication. However, a recently reported longitudinal study showed that participants treated with loop diuretics over 10 years were 40% more likely to develop hearing loss and 33% more likely of progressive hearing loss compared to participants who did not use loop diuretics. This suggests the long-term consequences of loop diuretics on hearing could be a more significant than previously thought and further research is required in this area. Other precautions include: nephrotoxicity, sulfonamide (sulfa) allergy, and increases free thyroid hormone effects with large doses. Interactions
Furosemide has potential interactions with these medications:
Aspirin and other salicylates
Other diuretics (e.g. ethacrynic acid, hydrochlorothiazide)
Synergistic effects with other antihypertensives (e.g. | Although it increases circulation to the kidneys, it does not help kidney function, and is not recommended for kidney disease.It is also used to treat congestive heart failure (pulmonary edema, pleural effusion, and/or ascites) in cats and dogs. It can also be used in an attempt to promote urine production in anuric or oliguric acute kidney failure. Horses
Furosemide is injected either intramuscularly or intravenously, usually 0.5-1.0 mg/kg twice/day, although less before a horse is raced. As with many diuretics, it can cause dehydration and electrolyte imbalance, including loss of potassium, calcium, sodium, and magnesium. Excessive use of furosemide will most likely lead to a metabolic alkalosis due to hypochloremia and hypokalemia. The drug should, therefore, not be used in horses that are dehydrated or experiencing kidney failure. It should be used with caution in horses with liver problems or electrolyte abnormalities. Overdose may lead to dehydration, change in drinking patterns and urination, seizures, gastrointestinal problems, kidney damage, lethargy, collapse, and coma. Furosemide should be used with caution when combined with corticosteroids (as this increases the risk of electrolyte imbalance), aminoglycoside antibiotics (increases risk of kidney or ear damage), and trimethoprim sulfa (causes decreased platelet count). It may also cause interactions with anesthetics, so its use should be related to the veterinarian if the animal is going into surgery, and it decreases the kidneys ability to excrete aspirin, so dosages will need to be adjusted if combined with that drug. Furosemide may increase the risk of digoxin toxicity due to hypokalemia. | 11
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Sinus pericranii (SP) is a rare disorder characterized by a congenital (or occasionally, acquired) epicranial venous malformation of the scalp. Sinus pericranii is an abnormal communication between the intracranial and extracranial venous drainage pathways. Treatment of this condition has mainly been recommended for aesthetic reasons and prevention of bleeding. Signs and symptoms
Sinus pericranii typically present as soft palpable masses along midline skull, which may fluctuate in size depending on body positioning. Classically, these lesions are not associated with color change of the overlying skin, such as with other vascular lesions such as hemangioma. Cause
The nature of this malformation remains unclear. Congenital, spontaneous, and acquired origins are accepted. The hypothesis of a spontaneous origin in the current case of SP is supported by no evidence of associated anomalies, such as cerebral aneurysmal venous malformations, systemic angiomas, venous angioma dural malformation, internal cerebral vein aneurysm, and cavernous hemangiomas. Mechanism
Sinus pericranii is a venous anomaly where a communication between the intracranial dural sinuses and dilated epicranial venous structures exists. That venous anomaly is a collection of nonmuscular venous blood vessels adhering tightly to the outer surface of the skull and directly communicating with intracranial venous sinuses through diploic veins. The venous collections receive blood from and drain into the intracranial venous sinuses. The varicosities are intimately associated with the periosteum, are distensible, and vary in size when changes in intracranial pressure occur. Diagnosis
Treatment
The surgical treatment involves the resection of the extracranial venous package and ligation of the emissary communicating vein. | In some cases of SP, surgical excision is performed for cosmetic reasons. The endovascular technique has been described by transvenous approach combined with direct puncture and the recently endovascular embolization with Onyx. See also
Mondors disease
List of cutaneous conditions
== References == | 11
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Genetic factors cause clefts in 20% to 50% of the cases and the remaining clefts are attributable to either environmental factors (such as teratogens) or gene-environment interactions. The polygenic/multifactorial inheritance model predicts that most individuals will be born without clefts; however with a number of genetic or environmental factors, it can result in cleft formation.The development of the face is coordinated by complex morphogenetic events and rapid proliferative expansion, and is thus highly susceptible to environmental and genetic factors, rationalising the high incidence of facial malformations. During the first six to eight weeks of pregnancy, the shape of the embryos head is formed. Five primitive tissue lobes grow:
If these tissues fail to meet, a gap appears where the tissues should have joined (fused). This may happen in any single joining site, or simultaneously in several or all of them. The resulting birth defect reflects the locations and severity of individual fusion failures (e.g., from a small lip or palate fissure up to a completely malformed face). The upper lip is formed earlier than the palate, from the first three lobes named a to c above. Formation of the palate is the last step in joining the five embryonic facial lobes, and involves the back portions of the lobes b and c. These back portions are called palatal shelves, which grow towards each other until they fuse in the middle. This process is very vulnerable to multiple toxic substances, environmental pollutants, and nutritional imbalance. | However, other thyroid diseases such as multinodular goitre, Hashimoto thyroiditis, thyroid adenoma, and thyroid carcinoma also retains the radiotracer because of high metabolic nature of these diseases. Thus, the final diagnosis always requires pathological examination of the tissue in question. Treatment
Parathyroid carcinoma is sometimes diagnosed during surgery for primary hyperparathyroidism. If the surgeon suspects carcinoma based on severity or invasion of surrounding tissues by a firm parathyroid tumor, aggressive excision is performed, including the thyroid and surrounding tissues as necessary.Agents such as calcimimetics (for example, cinacalcet) are used to mimic calcium and are able to activate the parathyroid calcium-sensing receptor (making the parathyroid gland "think" we have more calcium than we actually do), therefore lowering the calcium level, in an attempt to decrease the hypercalcemia. References
External links
Parathyroid cancer entry in the public domain NCI Dictionary of Cancer Terms
Parathyroid Carcinoma (Medscape eMedicine)
Cancer Management Handbook: Thyroid and Parathyroid Cancers
This article incorporates public domain material from the U.S. National Cancer Institute document: "Dictionary of Cancer Terms". | 0-1
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Some authors consider MS and its borderline forms to constitute a spectrum, differing only in chronicity, severity, and clinical course, while others consider them discretely different diseases.Typically, ADEM appears in children following an antigenic challenge and remains monophasic. Nevertheless, ADEM does occur in adults, and can also be clinically multiphasic.Problems for differential diagnosis increase due to the lack of agreement for a definition of multiple sclerosis. If MS were defined just by the separation in time and space of the demyelinating lesions as McDonald did, it would not be enough to make a difference, as some cases of ADEM satisfy these conditions. Therefore, some authors propose to establish the separation line in the shape of the lesions around the veins, being therefore "perivenous vs. confluent demyelination". The pathology of ADEM is very similar to that of MS with some differences. The pathological hallmark of ADEM is perivenular inflammation with limited "sleeves of demyelination". Nevertheless, MS-like plaques (confluent demyelination) can appearPlaques in the white matter in MS are sharply delineated, while the glial scar in ADEM is smooth. Axons are better preserved in ADEM lesions. | Being an acute monophasic illness, EAE is far more similar to ADEM than MS.
See also
Optic neuritis
Transverse myelitis
Victoria Arlen
References
External links
Acute disseminated encephalomyelitis at NIHs Office of Rare Diseases
Acute Disseminated Encephalomyelitis Information Page at NINDS
Information for parents about Acute disseminated encephalomyelitis | 11
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These criteria are designed to differentiate the disorder from ALS (purely motor but with UMN signs), the Lewis-Sumner Syndrome variant of Chronic inflammatory demyelinating polyneuropathy (CIDP) (similar to MMN but usually with significant sensory loss), and "vasculitis" (a type of multiple mononeuropathy syndrome caused by inflammatory damage to the blood vessels in nerves that also causes sensory and motor symptoms).A neurologist is usually needed to determine the diagnosis, which is based on the history and physical examination along with the electrodiagnostic study, which includes nerve conduction studies (NCS) and needle electromyography (EMG). The NCS usually demonstrate conduction block. This can be done by showing that the nerve signal cannot conduct past a "lesion" at some point along the nerve. For example, if the nerve is blocked in the forearm, an electrical impulse can easily get from the wrist to the hand if the stimulus is placed at the wrist. However, the signal will be blocked from reaching the hand if the stimulus is applied at the elbow. In MMN, sensory conduction along the same path should be normal. The EMG portion of the test looks for signals in the way muscles fire. In MMN it will most likely reveal abnormalities suggesting that some percentage of the motor axons has been damaged. Laboratory testing for GM1 antibodies is frequently done, and can be very helpful if they are abnormal. However, since only a third of patients with MMN have these antibodies, a negative test does not rule out the disorder. | Spinal fluid examination is not usually helpful. Treatment
Multifocal motor neuropathy is normally treated by receiving intravenous immunoglobulin (IVIG), which can in many cases be highly effective, or immunosuppressive therapy with cyclophosphamide or rituximab. Steroid treatment (prednisone) and plasmapheresis are no longer considered to be useful treatments(not usually some pt highly recommended); prednisone can exacerbate symptoms. IVIg is the primary treatment, with about 80% of patients responding, usually requiring regular infusions at intervals of 1 week to several months. Other treatments are considered in case of lack of response to IVIg, or sometimes because of the high cost of immunoglobulin. Subcutaneous immunoglobulin is under study as a less invasive, more-convenient alternative to IV delivery. References
External links
Overview of MMN at National Institute of Neurological Disorders and Stroke | 11
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Regions most at risk for great loss of life include those where earthquakes are relatively rare but powerful, and poor regions with lax, unenforced, or nonexistent seismic building codes. Prediction
Earthquake prediction is a branch of the science of seismology concerned with the specification of the time, location, and magnitude of future earthquakes within stated limits. Many methods have been developed for predicting the time and place in which earthquakes will occur. Despite considerable research efforts by seismologists, scientifically reproducible predictions cannot yet be made to a specific day or month. Forecasting
While forecasting is usually considered to be a type of prediction, earthquake forecasting is often differentiated from earthquake prediction. Earthquake forecasting is concerned with the probabilistic assessment of general earthquake hazard, including the frequency and magnitude of damaging earthquakes in a given area over years or decades. For well-understood faults the probability that a segment may rupture during the next few decades can be estimated.Earthquake warning systems have been developed that can provide regional notification of an earthquake in progress, but before the ground surface has begun to move, potentially allowing people within the systems range to seek shelter before the earthquakes impact is felt. Preparedness
The objective of earthquake engineering is to foresee the impact of earthquakes on buildings and other structures and to design such structures to minimize the risk of damage. Existing structures can be modified by seismic retrofitting to improve their resistance to earthquakes. Earthquake insurance can provide building owners with financial protection against losses resulting from earthquakes. | A particularly dangerous form of slow earthquake is the tsunami earthquake, observed where the relatively low felt intensities, caused by the slow propagation speed of some great earthquakes, fail to alert the population of the neighboring coast, as in the 1896 Sanriku earthquake. Co-seismic overpressuring and effect of pore pressure
During an earthquake, high temperatures can develop at the fault plane so increasing pore pressure consequently to vaporization of the ground water already contained within rock. In the coseismic phase, such increase can significantly affect slip evolution and speed and, furthermore, in the post-seismic phase it can control the Aftershock sequence because, after the main event, pore pressure increase slowly propagates into the surrounding fracture network. From the point of view of the Mohr-Coulomb strength theory, an increase in fluid pressure reduces the normal stress acting on the fault plane that holds it in place, and fluids can exert a lubricating effect. As thermal overpressurization may provide positive feedback between slip and strength fall at the fault plane, a common opinion is that it may enhance the faulting process instability. After the mainshock, the pressure gradient between the fault plane and the neighboring rock causes a fluid flow which increases pore pressure in the surrounding fracture networks; such increase may trigger new faulting processes by reactivating adjacent faults, giving rise to aftershocks. Analogously, artificial pore pressure increase, by fluid injection in Earths crust, may induce seismicity. Tidal forces
Tides may induce some seismicity. | 11
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Iron released from the heme generates reactive oxygen species, damaging the kidney cells. In addition to the myoglobinuria, two other mechanisms contribute to kidney impairment: low blood pressure leads to constriction of the blood vessels and therefore a relative lack of blood flow to the kidney, and finally uric acid may form crystals in the tubules of the kidneys, causing obstruction. Together, these processes lead to acute tubular necrosis, the destruction of the cells of tubules. Glomerular filtration rate falls and the kidney is unable to perform its normal excretory functions. This causes disruption of electrolyte regulation, leading to a further rise in potassium levels, and interferes with vitamin D processing, further worsening the low calcium levels. Diagnosis
A diagnosis of rhabdomyolysis may be suspected in anyone who has sustained trauma, crush injury or prolonged immobilization, but it may also be identified at a later stage due to deteriorating kidney function (abnormally raised or increasing creatinine and urea levels, falling urine output) or reddish-brown discoloration of the urine. General investigations
The most reliable test in the diagnosis of rhabdomyolysis is the level of creatine kinase (CK) in the blood. This enzyme is released by damaged muscle, and levels above 1000 U/L (5 times the upper limit of normal (ULN)) indicate rhabdomyolysis. More than 5,000 U/L indicates severe disease but depending on the extent of the rhabdomyolysis, concentrations up to 100,000 U/l are not unusual. CK concentrations rise steadily for 12 hours after the original muscle injury, remain elevated for 1–3 days and then fall gradually. | Peritoneal dialysis may be difficult to administer in someone with severe abdominal injury, and it may be less effective than the other modalities. Other complications
Compartment syndrome is treated with surgery to relieve the pressure inside the muscle compartment and reduce the risk of compression on blood vessels and nerves in that area. Fasciotomy is the incision of the affected compartment. Often, multiple incisions are made and left open until the swelling has reduced. At that point, the incisions are closed, often requiring debridement (removal of non-viable tissue) and skin grafting in the process. The need for fasciotomy may be decreased if mannitol is used, as it can relieve muscle swelling directly.Disseminated intravascular coagulation generally resolves when the underlying causes are treated, but supportive measures are often required. For instance, if the platelet count drops significantly and there is resultant bleeding, platelets may be administered. Prognosis
The prognosis depends on the underlying cause and whether any complications occur. Rhabdomyolysis complicated by acute kidney impairment in patients with traumatic injury may have a mortality rate of 20%. Admission to the intensive care unit is associated with a mortality of 22% in the absence of acute kidney injury, and 59% if kidney impairment occurs. Most people who have sustained kidney impairment due to rhabdomyolysis fully recover their kidney function. Epidemiology
The exact number of cases of rhabdomyolysis is difficult to establish because different definitions have been used. In 1995, hospitals in the U.S. reported 26,000 cases of rhabdomyolysis. | 11
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In a subset of patients with the tt genotype of the TaqI vitamin D receptor and who are vitamin D deficient, vitamin D supplementation appears to hasten sputum culture conversion. There are no studies of vitamin D using the gold standard outcome of relapse, so the true benefit of vitamin D is not at present known.It was noted as early as the mid-19th century that cod liver oil (which is rich in vitamin D) improved patients with tuberculosis, and the mechanism for this is probably an enhancement of immune responses to tuberculosis.The addition of vitamin D appears to enhance the ability of monocytes and macrophages to kill M. tuberculosis in vitro as well as ameliorating potentially harmful effects of the human immune system. Another reason Vitamin D can be used as a treatment for mycobacterial infections like tuberculosis is because of pro-anti-inflammatory cytokines that are influenced by vitamin D. Vitamin D has a post-anti-inflammatory effect on tuberculosis. Other
arginine has some clinical evidence as an adjuvant. Mycobacterium vaccae has been completed in Phase III trials by Anhui Zhifei Longcom Biologic Pharmacy Co., Ltd., injectable Vaccae(TM) and Immunitor LLC., oral tablet Tubivac (V7). Latent tuberculosis
The treatment of latent tuberculosis infection (LTBI) is essential to controlling and eliminating TB by reducing the risk that TB infection will progress to disease. | Citizens attending religious sermons were able to distribute information about tuberculosis and inform their communities on where to seek treatment and how to adhere to treatment protocols The DOTS-Plus strategy, designed to deliver from within familiar local institutions, was successful at conveying information about tuberculosis prevention and treatment. India
In 1906, India opened its first air sanatorium for treatment and isolation of TB patients.However, the World Health Organization reviewed the national program in India which lacked funding and treatment regimens that could report accurate tuberculosis case management. By 1945, there were successful immunization screenings due to campaigns that helped spread messages about the prevention of disease. This was also around the same time that the World Health Organization declared tuberculosis to be a global emergency and recommended countries adopt the DOTS strategy. Bangladesh, Cambodia, Thailand
In Bangladesh, Cambodia, and Indonesia, there is a diagnostic treatment for latent tuberculosis in children below 5 years of age. The IGRA approach (Interferon Gamma Release Assay) is used in these countries. IGRA testing and diagnosis are whole blood cell tests where fresh blood samples are mixed with antigens and controls. A person infected with tuberculosis will have interferon-gammas in the blood stream when mixed with the antigen. It is a highly accurate but expensive test and is technologically complex for immuno-compromised patients. These developing countries were unable to get rid of tuberculosis effectively because the national health policies did not cover screening and testing for tuberculosis. There were also no programs in place to educate citizens and provide training for healthcare workers. | 11
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Cutibacterium acnes almost exclusively causes endocarditis on prosthetic heart valves. Signs and symptoms
Fever occurs in 97% of people; malaise and endurance fatigue in 90% of people. A new or changing heart murmur, weight loss, and coughing occurs in 35% of people. Vascular phenomena: septic embolism (a piece of infected debris or tissue breaking off and traveling through the bloodstream to a distant site) (causing thromboembolic problems such as a stroke or gangrene of the fingers), Janeway lesions (painless hemorrhagic cutaneous lesions on the palms and soles), bleeding in the brain, conjunctival hemorrhage, splinter hemorrhages, kidney infarcts, and splenic infarcts. Infective endocarditis can also lead to the formation of mycotic aneurysms. Immunologic phenomena: glomerulonephritis which allows for blood and albumin to enter the urine, Oslers nodes ("ephemeral spots of a painful nodular erythema, chiefly in the skin of the hands and feet"), Roths spots on the retina, positive serum rheumatoid factor
Other signs may include night sweats, rigors, anemia, spleen enlargement
Cause
Many microorganisms can cause infective endocarditis. These are generally isolated by blood culture, where the patients blood is drawn and any growth is noted and identified. The term bacterial endocarditis (BE) commonly is used, reflecting the fact that most cases of IE are due to bacteria; however, infective endocarditis (IE) has become the preferred term. Bacterial
Staphylococcus aureus is the leading cause of infective endocarditis in most parts of the world and is responsible for about 31% of cases. Staphylococcus aureus is the most common cause of endocarditis in people who use intravenous drugs. | allergy and increased bacterial resistance) of taking antibiotics that may outweigh the benefits.Antibiotics were historically commonly recommended to prevent IE in those with heart problems undergoing dental procedures (known as dental antibiotic prophylaxis). There is, however, insufficient evidence to support whether antibiotics are effective or ineffective at preventing IE when given prior to a dental procedures in people at high risk. They are less commonly recommended for this procedure.In some countries e.g. the US, high risk patients may be given prophylactic antibiotics such as penicillin or clindamycin for penicillin-allergic people prior to dental procedures. Prophylactics should be bactericidal rather than bacteriostatic. Such measures are not taken in certain countries e.g. Scotland due to the fear of antibiotic resistance. Because bacteria are the most common cause of infective endocarditis, antibiotics such as penicillin and amoxicillin (for beta lactamase-producing bacteria) are used in prophylaxis. Treatment
High-dose antibiotics are the cornerstone of treatment for infective endocarditis. These antibiotics are administered by the intravenous (IV) route to maximize diffusion of antibiotic molecules into vegetation(s) from the blood filling the chambers of the heart. This is necessary because neither the heart valves nor the vegetations adhering to them are supplied by blood vessels. Antibiotics are typically continued for two to six weeks depending on the characteristics of the infection and the causative microorganisms. | 11
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Reoperation (return to the operating room) refers to a return to the operating theater after an initial surgery is performed to re-address an aspect of patient care best treated surgically. Reasons for reoperation include persistent bleeding after surgery, development of or persistence of infection. Description of surgical procedure
Location
Inpatient surgery is performed in a hospital, and the person undergoing surgery stays at least one night in the hospital after the surgery. Outpatient surgery occurs in a hospital outpatient department or freestanding ambulatory surgery center, and the person who had surgery is discharged the same working day. Office surgery occurs in a physicians office, and the person is discharged the same working day.At a hospital, modern surgery is often performed in an operating theater using surgical instruments, an operating table, and other equipment. Among United States hospitalizations for non-maternal and non-neonatal conditions in 2012, more than one-fourth of stays and half of hospital costs involved stays that included operating room (OR) procedures. The environment and procedures used in surgery are governed by the principles of aseptic technique: the strict separation of "sterile" (free of microorganisms) things from "unsterile" or "contaminated" things. All surgical instruments must be sterilized, and an instrument must be replaced or re-sterilized if it becomes contaminated (i.e. handled in an unsterile manner, or allowed to touch an unsterile surface). | The patients history might also exhibit kidney problems, such as proximal nephron dysfunction. There may also be endocrine conditions, such as diabetes or hypoparathyroidism. The patient might have also had a gastrointestinal condition which could have been due to liver disease, as well as episodes of nausea or vomiting. Multiple lipomas in the skin, sideroblastic anemia and pancytopenia in the metabolic system, or short stature might all be examples of patients with possible symptoms of MERRF disease. Treatment
Like many mitochondrial diseases, there is no cure for MERRF, no matter the means for diagnosis of the disease. The treatment is primarily symptomatic. High doses of coenzyme Q10, B complex vitamins, and L-Carnitine are used for the altered metabolic processing that results in the disease. There is very little success with these treatments as therapies in hopes of improving mitochondrial function. The treatment only alleviates symptoms, and these do not prevent the disease from progressing. Patients with concomitant disease, such as diabetes, deafness, or cardiac disease, are treated in combination to manage symptoms. Research
The Journal of Child Neurology published a paper that discusses possible new methods to test for MERRF and other mitochondrial diseases through a simple swabbing technique. This is a less invasive technique which allows for an analysis of buccal mitochondrial DNA, and showed significant amounts of the common 5 kb and 7.4 kb mitochondrial DNA deletions, which are also detectable in blood. | 0-1
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Treatment via hydration and over-the-counter hydration solutions can be started without or before confirmation by laboratory analysis, especially where cholera is a common problem.Stool and swab samples collected in the acute stage of the disease, before antibiotics have been administered, are the most useful specimens for laboratory diagnosis. If an epidemic of cholera is suspected, the most common causative agent is V. cholerae O1. If V. cholerae serogroup O1 is not isolated, the laboratory should test for V. cholerae O139. However, if neither of these organisms is isolated, it is necessary to send stool specimens to a reference laboratory.Infection with V. cholerae O139 should be reported and handled in the same manner as that caused by V. cholerae O1. The associated diarrheal illness should be referred to as cholera and must be reported in the United States. Prevention
The World Health Organization (WHO) recommends focusing on prevention, preparedness, and response to combat the spread of cholera. They also stress the importance of an effective surveillance system. Governments can play a role in all of these areas. Water, sanitation and hygiene
Although cholera may be life-threatening, prevention of the disease is normally straightforward if proper sanitation practices are followed. In developed countries, due to their nearly universal advanced water treatment and sanitation practices, cholera is rare. For example, the last major outbreak of cholera in the United States occurred in 1910–1911. Cholera is mainly a risk in developing countries in those areas where access to WASH (water, sanitation and hygiene) infrastructure is still inadequate. | If cefuroxime axetil is given with food, absorption values can increase by 52% compared to fasting patients.Distribution: It has been reported that after cefuroxime axetil administration, it can be found in tonsil tissue, sinus tissue, bronchial tissue and middle ear effusion.Elimination: After cefuroxime production, the body is unable to metabolize the drug, and is eliminated unchanged in the urine. History
It was discovered by Glaxo (now GlaxoSmithKline) and introduced in 1987. It was approved by FDA on December 28, 1987. It is available by GSK as Ceftin in US and Ceftum in India. See also
Cefuroxime
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With that information the diagnosis of BS was not only determined by phenotype but now by genotype.Early onset sarcoidosis is BS without a family history, BS has been diagnosed in patients who have not only the classic triad but granuloma in multiple organs. See also
List of cutaneous conditions
References
Further reading
Wouters CH, Maes A, Foley KP, Bertin J, and Rose CD: Blau Syndrome, the prototypic auto-inflammatory granulomatous disease. Pediatric Rheumatology 2014;12:33. PMID 25136265. PMC 4136643. doi:10.1186/1546-0096-12-33. Blau EB : Familial Granulomatous Arthritis, Iritis, and Rash. The Journal of Pediatrics 1985; 107: 689-693. PMID 4056967. doi:10.1016/s0022-3476(85)80394-2. Jabs DA, Houk JL, Bias WB, and Arnett FC: Familial Granulomatous Synovitis, Uveitis, and Cranial Neuropathies. The American Journal of Medicine 1985; 78: 801–804. PMID 3993660. doi:10.1016/0002-9343(85)90286-4. Malleson P, Schaller JG, Dega F, Cassidy SB, and Pagon RA : Familial Arthritis and Camplodactyly. Arthritis and Rheumatism 1981; 24: 1199–1204. PMID 7306244. doi:10.1002/art.1780240915. Rotenstein D, Gibbas DL, Majmudar B, and Chastain EA: Familial Granulomatous Arteritis with Polyarthritis of Juvenile Onset. The New England Journal of Medicine 1982; 306: 85–90. PMID 7053492. doi:10.1056/NEJM198201143060208. Pastores GM, Michels VV, Stickler GB, Su WP, Nelson AM, and Bovenmyer DA: Autosomal dominant granulomatous arthritis, uveitis, skin rash, and synovial cysts. The Journal of Pediatrics 1990; 117: 403–408. PMID 2391595. doi:10.1016/s0022-3476(05)81080-7. Tromp G, Kuivaniemi H, Raphael S, et al. : Genetic Linkage of Familial Granulomatous Inflammatory Arthritis, Skin Rash, and Uveitis to Chromosome 16. The American Journal of Human Genetics 1996; 59: 1097-1107. PMID 8900239. PMC 1914842. | Recombinant factor VIIa also known as eptacog alfa (INN), and sold under the brand name NovoSeven among others, is a form of blood factor VII that has been manufactured via recombinant technology. It is administered intravenously (IV). Medical uses
NovoSeven is approved for use in the United States and is indicated for the treatment of bleeding episodes and for the prevention of bleeding in surgical interventions or invasive procedures in patients with acquired hemophilia.NovoSeven RT is approved in the United States and is indicated for the treatment of bleeding episodes and peri-operative management in adults and children with hemophilia A or B with inhibitors, congenital Factor VII (FVII) deficiency, and Glanzmanns thrombasthenia with refractoriness to platelet transfusions, with or without antibodies to platelets and for the treatment of bleeding episodes and peri-operative management in adults with acquired hemophilia.Sevenfact [coagulation factor VIIa (recombinant)-jncw] is approved for use in the United States and is indicated for the treatment and control of bleeding episodes occurring in adults and adolescents twelve years of age and older with hemophilia A or B with inhibitors (neutralizing antibodies).As of 2012, recombinant factor VIIa is not supported by the evidence for treating most cases of major bleeding. There is a significant risk of arterial thrombosis with its use and thus, other than in those with factor VII deficiency, it should only be given in clinical trials. | 0-1
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No injectable preparation of quinine is licensed in the US; quinidine is used instead. Beverages
Quinine is a flavor component of tonic water and bitter lemon drink mixers. On the soda gun behind many bars, tonic water is designated by the letter "Q" representing quinine.Tonic water was initially marketed as a means of delivering quinine to consumers in order to offer anti-malarial protection. According to tradition, because of the bitter taste of anti-malarial quinine tonic, British colonials in India mixed it with gin to make it more palatable, thus creating the gin and tonic cocktail, which is still popular today. While it is possible to drink enough tonic water to temporarily achieve quinine levels that offer anti-malarial protection, this is not a sustainable long-term means of protection.In France, quinine is an ingredient of an apéritif known as quinquina, or "Cap Corse," and the wine-based apéritif Dubonnet. In Spain, quinine (also known as "Peruvian bark" for its origin from the native cinchona tree) is sometimes blended into sweet Malaga wine, which is then called "Malaga Quina". In Italy, the traditional flavoured wine Barolo Chinato is infused with quinine and local herbs, and is served as a digestif. In Scotland, the company A.G. Barr uses quinine as an ingredient in the carbonated and caffeinated beverage Irn-Bru. In Uruguay and Argentina, quinine is an ingredient of a PepsiCo tonic water named Paso de los Toros. In Denmark, it is used as an ingredient in the carbonated sports drink Faxe Kondi made by Royal Unibrew. | This is especially useful in cases where more than two lesions may be responsible for the clinical symptoms and signs, such as in patients with two or more cervical disc hernias
Follow-up the progression of myelopathy in time, for example before and after cervical spine surgeryTMS can also help in the differential diagnosis of different causes of pyramidal tract damage. Treatment
The treatment and prognosis of myelopathy depends on the underlying cause: myelopathy caused by infection requires medical treatment with pathogen specific antibiotics. Similarly, specific treatments exist for multiple sclerosis, which may also present with myelopathy. As outlined above, the most common form of myelopathy is secondary to degeneration of the cervical spine. Newer findings have challenged the existing controversy with respect to surgery for cervical spondylotic myelopathy by demonstrating that patients benefit from surgery. See also
Surfers myelopathy
References
== External links == | 0-1
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Urticarial vasculitis (also known as "chronic urticaria as a manifestation of venulitis", "hypocomplementemic urticarial vasculitis syndrome", "hypocomplementemic vasculitis" and "unusual lupus-like syndrome") is a skin condition characterized by fixed urticarial lesions that appear histologically as a vasculitis. : 834
Mechanism
Antibodies are usually raised against foreign proteins, such as those made by a replicating virus or invading bacterium. Virus or bacteria with antibodies opsonized or "stuck" to them highlight them to other cells of the immune system for clearance. Antibodies against self proteins are known as autoantibodies, and are not found in healthy individuals. These autoantibodies can be used to detect certain diseases. C1q
C1q is an integral component within the complement pathway – a complicated cascade of protein interactions, culminating in an immune response against a broad variety of pathogens. The anti-C1q antibodies found in patients with hypocomplementemic urticarial vasculitis activate C1q, which instigates activation of the entire complement pathway. Consequently, levels of all complement proteins become low. Impaired classical complement pathway
The complement pathway is composed of several subset pathways: the lectin/mannose pathway, alternative pathway and the classical pathway. | All pathways culminate in the production of a C3 convertase, which catalyses C3 into its constitutive parts (better detailed here – classical complement pathway).In brief, the crucial role of C1q in the pathway is its importance as the first protein to start the complement cascade (which ends in the destruction of the invading bacteria or virus), and its ability to link the two important arms of the immune system – the innate immune system: a broad defence system; and the adaptive immune system: the strong immune response capable of remembering previous infections, allowing fast response against recurrent infections, meaning that people with a normal immune system dont continually catch the same cold or same strain of flu repeatedly.Case studies of individuals with HUV have also highlighted other potential complicating factors which it seems the anti-C1q antibodies play a role in. This can mean in some cases the deposition of large immune complexes in the kidney which cannot be cleared by the usual cells of the immune system (e.g. macrophages which are unable to bind the Fc portion of the C1q antibody), leading to further complications. This seems to be rare, but can occur when a pre-existing renal condition is apparent. Also, there has been some speculation as to an additional autoantibody against an inhibitor protein (in the complement pathway) named C1-inhibitor. The inhibition of C1-inhibitor leads to over-activation of the complement pathway and one protein that builds up controls angioedema (vessel – swelling), resulting in excess water building up under the skin (the weal appearance). | 11
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Tolosa–Hunt syndrome is a rare disorder characterized by severe and unilateral headaches with orbital pain, along with weakness and paralysis (ophthalmoplegia) of certain eye muscles (extraocular palsies).In 2004, the International Headache Society provided a definition of the diagnostic criteria which included granuloma. Signs and symptoms
Symptoms are usually limited to one side of the head, and in most cases the individual affected will experience intense, sharp pain and paralysis of muscles around the eye. Symptoms may subside without medical intervention, yet recur without a noticeable pattern.In addition, affected individuals may experience paralysis of various facial nerves and drooping of the upper eyelid (ptosis). Other signs include double vision, fever, chronic fatigue, vertigo or arthralgia. Occasionally the patient may present with a feeling of protrusion of one or both eyeballs (exophthalmos). Causes
The cause of Tolosa–Hunt syndrome is not known, but the disorder is thought to be, and often assumed to be, associated with inflammation of the areas behind the eyes (cavernous sinus and superior orbital fissure). Diagnosis
Tolosa–Hunt syndrome is usually diagnosed via exclusion, and as such a vast amount of laboratory tests are required to rule out other causes of the patients symptoms. These tests include a complete blood count, thyroid function tests and serum protein electrophoresis. | The absence of secondary causes of severe hypertriglyceridemia (like e.g. diabetes, alcohol, estrogen-, glucocorticoid-, antidepressant- or isotretinoin-therapy, certain antihypertensive agents, and paraproteinemic disorders) increases the possibility of LPL deficiency. In this instance besides LPL also other loss-of-function mutations in genes that regulate catabolism of triglyceride-rich lipoproteins (like e.g. ApoC2, ApoA5, LMF-1, GPIHBP-1 and GPD1) should also be consideredThe diagnosis of familial lipoprotein lipase deficiency is finally confirmed by detection of either homozygous or compound heterozygous pathogenic gene variants in LPL with either low or absent lipoprotein lipase enzyme activity.Lipid measurements
· Milky, lipemic plasma revealing severe hyperchylomicronemia;· Severely elevated fasting plasma triglycerides (>2000 mg/dL);LPL enzyme
· Low or absent LPL activity in post-heparin plasma;· LPL mass level reduced or absent in post-heparin plasma;Molecular genetic testing
The LPL gene is located on the short (p) arm of chromosome 8 at position 22. More than 220 mutations in the LPL gene have been found to cause familial lipoprotein lipase deficiency so far. Treatment
Treatment of LPLD has two different objectives: immediate prevention of pancreatitis attacks and long-term reduction of cardiovascular disease risk. Treatment is mainly based on medical nutrition therapy to maintain plasma triglyceride concentration below 11,3 mmol/L (1000 mg/dL). Maintenance of triglyceride levels below 22,6 mmol/L (2000 mg/dL) prevents in general from recurrent abdominal pain. | 0-1
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Eosinophilic cystitis is a rare condition where eosinophiles are present in the bladder wall. Signs and symptoms are similar to a bladder infection. Its cause is not entirely clear; however, may be linked to food allergies, infections, and medications among others. Management
Treatment involves avoiding the trigger if that can be determined. Prognosis
Long term outcomes in children are generally good. == References == | It has been hypothesized that the portion of the brain responsible for processing stimulation from amputated limbs, being deprived of input, expands into the surrounding brain, (Phantoms in the Brain: V.S. Ramachandran and Sandra Blakeslee) such that an individual who has had an arm amputated will experience unexplained pressure or movement on his face or head. In many cases, the phantom limb aids in adaptation to a prosthesis, as it permits the person to experience proprioception of the prosthetic limb. To support improved resistance or usability, comfort or healing, some type of stump socks may be worn instead of or as part of wearing a prosthesis.Another side effect can be heterotopic ossification, especially when a bone injury is combined with a head injury. The brain signals the bone to grow instead of scar tissue to form, and nodules and other growth can interfere with prosthetics and sometimes require further operations. This type of injury has been especially common among soldiers wounded by improvised explosive devices in the Iraq War.Due to technological advances in prosthetics, many amputees live active lives with little restriction. Organizations such as the Challenged Athletes Foundation have been developed to give amputees the opportunity to be involved in athletics and adaptive sports such as amputee soccer.Nearly half of the individuals who have an amputation due to vascular disease will die within 5 years, usually secondary to the extensive co-morbidities rather than due to direct consequences of amputation. | 0-1
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Exercise
Exercise-induced arterial hypoxemia occurs during exercise when a trained individual exhibits an arterial oxygen saturation below 93%. It occurs in fit, healthy individuals of varying ages and genders. Adaptations due to training include an increased cardiac output from cardiac hypertrophy, improved venous return, and metabolic vasodilation of muscles, and an increased VO2 max. There must be a corresponding increase in VCO2 thus a necessity to clear the carbon dioxide to prevent a metabolic acidosis. Hypoxemia occurs in these individuals due to increased pulmonary blood flow causing:
Reduced capillary transit time due to an increased blood flow within the pulmonary capillary. Capillary transit time (tc), at rest is around 0.8s, allowing plenty of time for the diffusion of oxygen into the circulation and the diffusion of CO2 out of the circulation. After training, the capillary volume is still the same however cardiac output is increased, resulting in a decreased capillary transit time, reducing to around 0.16s in trained individuals at maximal work rates. This does not give sufficient time for gas diffusion and results in a hypoxemia. Intrapulmonary arteriovenous shunts are dormant capillaries within the lungs that become recruited when venous pressures become too high. They are normally located within deadspace area where gas diffusion does not occur, thus the blood passing through does not become oxygenated resulting in a hypoxemia. | Field may refer to:
Expanses of open ground
Field (agriculture), an area of land used for agricultural purposes
Airfield, an aerodrome that lacks the infrastructure of an airport
Battlefield
Lawn, an area of mowed grass
Meadow, a grassland that is either natural or allowed to grow unmowed and ungrazed
Playing field, used for sports or games
Arts and media
In decorative art, the main area of a decorated zone, often contained within a border, often the background for motifs
Field (heraldry), the background of a shield
In flag terminology, the background of a flag
FIELD (magazine), a literary magazine published by Oberlin College in Oberlin, Ohio
Field (sculpture), by Anthony Gormley
Organizations
Field department, the division of a political campaign tasked with organizing local volunteers and directly contacting voters
Field Enterprises, a defunct private holding company
Field Communications, a division of Field Enterprises
Field Museum of Natural History, in Chicago
People
Field (surname)
Field Cate (born 1997), American child actor
Places
Field, British Columbia, Canada
Field, Kentucky, United States
Field, Minneapolis, Minnesota, United States
Field, Ontario, Canada
Field, Staffordshire, England, United Kingdom
Field, South Australia
Field Hill, British Columbia, Canada
Field Island, Nunavut, Canada
Mount Field (disambiguation), mountains in Canada, the United States, Australia and Antarctica
Science, technology, and mathematics
Computing
Field (computer science), a smaller piece of data from a larger collection (e.g., database fields)
Field-programmability, an electronic devices capability of being reprogrammed with new logic
Geology
Field (mineral deposit), a mineral deposit containing valuable resources in a cost-competitive concentration
Polje or karst field, a characteristic landform in karst topography
Mathematics
Field (mathematics), type of algebraic structure
Number field, specific type of the above algebraic structure
Scalar field, assignment of a scalar to each point in a mathematical space
Tensor field, assignment of a tensor to each point in a mathematical space
Vector field, assignment of a vector to each point in a mathematical space
Field of sets, a mathematical structure of sets in an abstract space
Field of a binary relation, union of its domain and its range
Optics
Field of view, the area of a view imaged by a lens
Visual field, the part of the field of view which can be perceived by the eyes retina
Depth of field, the distance from before to beyond the subject that appears to be in focus (and likewise, field, in the context of depth, is the portion of a scene for which objects within its range are or would be in focus)
Physics
Field (physics), a mathematical construct for analysis of remote effects
Electric field, term in physics to describe the energy that surrounds electrically charged particles
Magnetic field, force produced by moving electric charges
Electromagnetic field, combination of an electric field and magnetic field
Gravitational field, a representation of the combined effects of remote masses on a test particle at each point
Sociology
Field (Bourdieu), a sociological term coined by Pierre Bourdieu to describe the system of objective relations constituted by various species of capital
Sexual field, the systems of objective relations within collective sexual life
Other uses in science and technology
Field (geography), a spatially dependent variable
Field (video), one half of a frame in an interlaced display
Field coil, of an electric motor or generator
Field experiment
Field magnet, a magnet used to produce a magnetic field
Field research or fieldwork, the collection of information outside a laboratory, library or workplace setting
Field of heliostats, an assembly of heliostats acting together
Sports
Pitch (sports field)
Other uses
Field of study, a subdivision of an academic discipline
Field of use, permissible operation by the licensee of a patent
Track and field, a group of sports
See also
The Field (disambiguation)
Fields (disambiguation)
The Fields (disambiguation)
Fielding (disambiguation)
Feeld, a location-based social discovery service application for iOS and Android
Feild, surname
All pages with titles beginning with Field
All pages with titles containing Field | 0-1
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If the complication of multi-organ failure ensues, signs and symptoms of those failing organs will appear, such as abdominal pain, jaundice, shortness of breath, and diminished urine output. Onset
The seizures of eclampsia typically present during pregnancy and prior to delivery (the antepartum period), but may also occur during labor and delivery (the intrapartum period) or after the baby has been delivered (the postpartum period). If postpartum seizures develop, it is most likely to occur within the first 48 hours after delivery. However, late postpartum seizures of eclampsia may occur as late as 4 weeks after delivery. Characteristics
Eclamptic seizure is typically described as a tonic–clonic seizure which may cause an abrupt loss of consciousness at onset. This is often associated with a shriek or scream followed by stiffness of the muscles of the arms, legs, back and chest. During the tonic phase, the mother may begin to appear cyanotic. This presentation lasts for about a minute, after which the muscles begin in jerk and twitch for an additional one to two minutes. Other signs include tongue biting, frothy and bloody sputum coming out of the mouth. Complications
There are risks to both the mother and the fetus when eclampsia occurs. The fetus may grow more slowly than normal within the womb (uterus) of a woman with eclampsia, which is termed intrauterine growth restriction and may result in the child appearing small for gestational age or being born with low birth weight. Eclampsia may also cause problems with the placenta. | Following intramuscular administration the onset of action is about one hour and lasts for three to four hours. Magnesium is excreted solely by the kidneys at a rate proportional to the plasma concentration (concentration in the blood) and glomerular filtration (rate at which the blood is filtered through the kidneys). Magnesium sulfate is associated with several minor side effects; serious side effects are uncommon, occurring at elevated magnesium serum concentrations greater than 7.0 mEq/L. Serious toxicity can be counteracted with calcium gluconate.Even with therapeutic serum magnesium concentrations, recurrent convulsions may occur, and additional magnesium may be needed, but with close monitoring for respiratory, cardiac, and neurological depression. If magnesium administration with resultant high serum concentrations fails to control convulsions, the addition of other intravenous anticonvulsants may be used and intubation and mechanical ventilation may be initiated. It is important to avoid magnesium toxicity, including thoracic muscle paralysis, which could cause respiratory failure and death. Magnesium sulfate results in better outcomes than diazepam, phenytoin or a combination of chlorpromazine, promethazine, and pethidine. Blood pressure management
Blood pressure control is used to prevent stroke, which accounts for 15 to 20 percent of deaths in women with eclampsia. The agents of choice for blood pressure control during eclampsia are hydralazine or labetalol. This is because of their effectiveness, lack of negative effects on the fetus, and mechanism of action. Blood pressure management is indicated with a diastolic blood pressure above 105–110 mm Hg. | 11
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It should be understood, however, that the greater affinity bromocriptine and many similar antiparkinsons drugs have for the D2S receptor form (considered to be mostly present at inhibitory D2 autoreceptor locatations) relative to the D2L form, sufficiently low partial agonist activity (ie where a molecule binding to a receptor induces limited effects while preventing a stronger ligand like dopamine from binding), and, possibly, the functional selectivity of a particular drug may generate antidopaminergic effects that are more similar than oppositional in nature to antipsychotics. Pulmonary fibrosis has been reported when bromocriptine was used in high doses for the treatment of Parkinsons disease.Use to suppress milk production after childbirth was reviewed in 2014 and it was concluded that in this context a causal association with serious cardiovascular, neurological or psychiatric events could not be excluded with an overall incidence estimated to range between 0.005% and 0.04%. Additional safety precautions and stricter prescribing rules were suggested based on the data. It is a bile salt export pump inhibitor.After long-term use of dopamine agonists, a withdrawal syndrome may occur during dose reduction or discontinuation with the following possible side effects: anxiety, panic attacks, dysphoria, depression, agitation, irritability, suicidal ideation, fatigue, orthostatic hypotension, nausea, vomiting, diaphoresis, generalized pain, and drug cravings. For some individuals, these withdrawal symptoms are short-lived and they make a full recovery, for others a protracted withdrawal syndrome may occur with withdrawal symptoms persisting for months or years. Pharmacology
Pharmacodynamics
Bromocriptine is a partial agonist of the dopamine D2 receptor. | Roths spots, also known as Litten spots or the Litten sign, are non-specific red spots with white or pale centres, seen on the retina and although traditionally associated with infective endocarditis, can occur in a number of other conditions including hypertension, diabetes, collagen vascular disease, extreme hypoxia, leukemia and HIV.Red and white retinal spots were first observed in 1872 by Swiss physician Moritz Roth, and named "Roth spots" six years later by Moritz Litten. They are typically observed via fundoscopy (using an ophthalmoscope to view inside the eye) or slit lamp exam.The original retinal spots identified in 1872 were attributed to nerve-fibres that had burst. Present-day analysis shows that they can be composed of coagulated fibrin including platelets, focal ischaemia, inflammatory infiltrate, infectious organisms, or neoplastic cells. Cause
Roths spots occur in conditions that predispose to endothelial damage of retinal capillaries, that is when there is dysfunction and disruption of the endothelium of retinal capillaries. Looking through the microscope reveals lesions with white centers made mainly of fibrin, depicting a fibrin-platelet plug at the site of vessel damage. Associated conditions
Conditions associated with Roths spots include:
Infective endocarditis
Anaemia/thrombocytopenia
Collagen vascular disease
Leukemia
Hypertensive retinopathy
Diabetic retinopathy
Pre-eclampsia
Human Immunodeficiency Virus (HIV)
Extreme hypoxia
Shaken-baby syndromeand also:
Candida albicans infection
vascular diseases
kala azar
Prevalence
Roths spots occur in only 5% of people with infective endocarditis. Litten, however reported a figure of 80%. See also
Oslers nodes
Janeway lesion
Splinter haemorrhage
References
External links
Image from the New England Journal of Medicine: Endocarditis
Image from the New England Journal of Medicine: CML | 0-1
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This is a changing clinical state, with transient delusions, fragments of other syndromes, extreme fear or ecstasy, perplexity, confusion, and motility disturbances. In the past, some experts regarded this as pathognomonic (specific) for puerperal psychosis, but this syndrome is found in other settings, not just the reproductive process, and in men. These psychoses are placed in the World Health Organizations ICD-10 under the rubric of acute and transient psychotic disorders. In general psychiatry, manic and cycloid syndromes are regarded as distinct, but, studied long-term among childbearing women, the bipolar and cycloid variants are intermingled in a bewildering variety of combinations, and, in this context, it seems best to regard them as members of the same bipolar/cycloid group. Together, the manic and cycloid variants make up about two thirds of childbearing psychoses. Diagnosis
Postpartum bipolar disorders must be distinguished from a long list of organic psychoses that can present in the puerperium, and from other non-organic psychoses; both of these groups are described below. It is also necessary to distinguish them from other psychiatric disorders associated with childbirth, such as anxiety disorders, depression, post-traumatic stress disorder, complaining disorders and bonding disorders (emotional rejection of the infant), which occasionally cause diagnostic difficulties. Clinical assessment requires obtaining the history from the mother herself and, because she is often severely ill, lacking in insight and unable to give a clear account of events, from at least one close relative. A social work report and, in mothers admitted to hospital, nursing observations are information sources of great value. | Gangliosidosis contains different types of lipid storage disorders caused by the accumulation of lipids known as gangliosides. There are two distinct genetic causes of the disease. Both are autosomal recessive and affect males and females equally. Types
GM1 gangliosidoses - GM1
GM2 gangliosidoses - GM2
See also
Sphingolipidoses#Overview
References
== External links == | 0-1
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Arteritic anterior ischemic optic neuropathy (AAION or arteritic AION) is the cause of vision loss that occurs in temporal arteritis (aka giant-cell arteritis). Temporal arteritis is an inflammatory disease of medium-sized blood vessels that happens especially with advancing age. AAION occurs in about 15-20 percent of patients with temporal arteritis. Damage to the blood vessels supplying the optic nerves leads to insufficient blood supply (ischemia) to the nerve and subsequent optic nerve fiber death. Most cases of AAION result in nearly complete vision loss first to one eye. If the temporal arteritis is left untreated, the fellow eye will likely suffer vision loss as well within 1–2 weeks. Arteritic AION falls under the general category of anterior ischemic optic neuropathy, which also includes non-arteritic AION. AION is considered an eye emergency, immediate treatment is essential to rescue remaining vision. An exhaustive review article published in March 2009 described the latest information on arteritic and non-arteritic ischemic optic neuropathy, both anterior (A-AION and NA-AION) and posterior (A-PION, NA-PION, and surgical). Symptoms
There are several constitutional symptoms of temporal arteritis that may aid in diagnosis of AAION such as jaw claudication (spasms of the jaw muscle), scalp tenderness, unintentional weight loss, fatigue, myalgias and loss of appetite. However, many cases are asymptomatic. There are also elevations in three blood tests that help identify AAION: erythrocyte sedimentation rate (ESR), C reactive protein (CRP) and platelet count (thrombocytosis). A relate rheumatic disease called polymyalgia rheumatica has a 15 percent incidence of giant cell arteritis. | Coronary artery disease (CAD), also called coronary heart disease (CHD), ischemic heart disease (IHD), myocardial ischemia, or simply heart disease, involves the reduction of blood flow to the heart muscle due to build-up of atherosclerotic plaque in the arteries of the heart. It is the most common of the cardiovascular diseases. Types include stable angina, unstable angina, myocardial infarction, and sudden cardiac death. A common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw. Occasionally it may feel like heartburn. Usually symptoms occur with exercise or emotional stress, last less than a few minutes, and improve with rest. Shortness of breath may also occur and sometimes no symptoms are present. In many cases, the first sign is a heart attack. Other complications include heart failure or an abnormal heartbeat.Risk factors include high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, depression, and excessive alcohol consumption. A number of tests may help with diagnoses including: electrocardiogram, cardiac stress testing, coronary computed tomographic angiography, and coronary angiogram, among others.Ways to reduce CAD risk include eating a healthy diet, regularly exercising, maintaining a healthy weight, and not smoking. Medications for diabetes, high cholesterol, or high blood pressure are sometimes used. There is limited evidence for screening people who are at low risk and do not have symptoms. Treatment involves the same measures as prevention. Additional medications such as antiplatelets (including aspirin), beta blockers, or nitroglycerin may be recommended. | 0-1
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Ductile
In ductile fracture, extensive plastic deformation (necking) takes place before fracture. The terms "rupture" and "ductile rupture" describe the ultimate failure of ductile materials loaded in tension. The extensive plasticity causes the crack to propagate slowly due to the absorption of a large amount of energy before fracture. Because ductile rupture involves a high degree of plastic deformation, the fracture behavior of a propagating crack as modelled above changes fundamentally. Some of the energy from stress concentrations at the crack tips is dissipated by plastic deformation ahead of the crack as it propagates. The basic steps in ductile fracture are void formation, void coalescence (also known as crack formation), crack propagation, and failure, often resulting in a cup-and-cone shaped failure surface. Voids typically coalesce around precipitates, secondary phases, inclusions, and at grain boundaries in the material. Ductile fracture is typically transgranular and deformation due to dislocation slip can cause the shear lip characteristic of cup and cone fracture. Characteristics
The manner in which a crack propagates through a material gives insight into the mode of fracture. With ductile fracture a crack moves slowly and is accompanied by a large amount of plastic deformation around the crack tip. A ductile crack will usually not propagate unless an increased stress is applied and generally cease propagating when loading is removed. In a ductile material, a crack may progress to a section of the material where stresses are slightly lower and stop due to the blunting effect of plastic deformations at the crack tip. | Choline is an essential nutrient for humans and many other animals. Choline occurs as a cation that forms various salts (X− in the depicted formula is an undefined counteranion). To maintain health, it must be obtained from the diet as choline or as choline phospholipids, like phosphatidylcholine. Humans, as well as most other animal species, do make choline de novo; however, production is generally insufficient. Choline is often not classified as a vitamin, but as a nutrient with an amino acid–like metabolism. In most animals, choline phospholipids are necessary components in cell membranes, in the membranes of cell organelles, and in very low-density lipoproteins. Choline is required to produce acetylcholine – a neurotransmitter – and S-adenosylmethionine (SAM), a universal methyl donor. Upon methylation SAM is transformed into homocysteine. Symptomatic choline deficiency – rare in humans – causes nonalcoholic fatty liver disease and muscle damage. Excessive consumption of choline (greater than 7.5 g/day) can cause low blood pressure, sweating, diarrhea and fish-like body odor due to trimethylamine, which forms in its metabolism. Rich dietary sources of choline and choline phospholipids include organ meats and egg yolks, dairy products, peanuts, certain beans, nuts, seeds and vegetables with pasta and rice also contributing to choline intake in the American diet. Chemistry
The cholines are a family of water-soluble quaternary ammonium compounds. Choline is the parent compound of the cholines class, consisting of ethanolamine having three methyl substituents attached to the amino function. Choline hydroxide is known as choline base. | 0-1
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British desires to secure control of West African gold deposits played a role in the Anglo-Ashanti wars of the late 19th century, which saw the Ashanti Empire annexed by Britain.Gold played a role in western culture, as a cause for desire and of corruption, as told in childrens fables such as Rumpelstiltskin—where Rumpelstiltskin turns hay into gold for the peasants daughter in return for her child when she becomes a princess—and the stealing of the hen that lays golden eggs in Jack and the Beanstalk. The top prize at the Olympic Games and many other sports competitions is the gold medal. 75% of the presently accounted for gold has been extracted since 1910, two-thirds since 1950. One main goal of the alchemists was to produce gold from other substances, such as lead — presumably by the interaction with a mythical substance called the philosophers stone. Trying to produce gold led the alchemists to systematically find out what can be done with substances, and this laid the foundation for todays chemistry, which can produce gold (albeit uneconomically) by using nuclear transmutation. Their symbol for gold was the circle with a point at its center (☉), which was also the astrological symbol and the ancient Chinese character for the Sun. The Dome of the Rock is covered with an ultra-thin golden glassier. The Sikh Golden temple, the Harmandir Sahib, is a building covered with gold. Similarly the Wat Phra Kaew emerald Buddhist temple (wat) in Thailand has ornamental gold-leafed statues and roofs. | Serological assays are the best means of diagnosing this disease, with the indirect microimmunofluorescence assay (IFA) being considered the best tool. However, underlying illnesses, such as rheumatologic and other immune-mediated disorders, can lead to false positives. To combat these limitations, a PCR test may also be used; this test looks for rickettsial DNA. It can sensitively detect the target DNA in a sample taken from an eschar or blood during the first few days of infection. Prevention
There is no vaccine available for this disease, so to prevent infection, the US CDC recommends taking personal safety measures when venturing out into areas known to harbour ticks. Before going into these areas, the following preparations should be followed:
Wear protective clothing that will cover your arms and legs, with closed-toed shoes. Wearing long socks that you can tuck your pants into will provide an extra layer of safety, especially if you are walking in areas with tall grass for an extended period of time. Use strong insect repellent such as DEET on your body and Permethrin on your clothes
If you are taking a pet with you, they should also be updated on all preventative medications, and a veterinarian should be consulted for any extra precautions.After you return from these areas, the following precautions should be taken to prevent ticks from entering your home:
Check clothes and gear used for any ticks. Dry clothes should be put into a dryer on high heat for 10 minutes to effectively kill any small ticks that may not be visible to the naked eye. | 0-1
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Inclusion-cell (I-cell) disease, also referred to as mucolipidosis II (ML II), is part of the lysosomal storage disease family and results from a defective phosphotransferase (an enzyme of the Golgi apparatus). This enzyme transfers phosphate to mannose residues on specific proteins. Mannose-6-phosphate serves as a marker for proteins to be targeted to lysosomes within the cell. Without this marker, proteins are instead secreted outside the cell, which is the default pathway for proteins moving through the Golgi apparatus. Lysosomes cannot function without these proteins, which function as catabolic enzymes for the normal breakdown of substances (e.g. oligosaccharides, lipids, and glycosaminoglycans) in various tissues throughout the body (i.e. fibroblasts). As a result, a buildup of these substances occurs within lysosomes because they cannot be degraded, resulting in the characteristic I-cells, or "inclusion cells" seen microscopically. In addition, the defective lysosomal enzymes normally found only within lysosomes are instead found in high concentrations in the blood, but they remain inactive at blood pH (around 7.4) because they require the low lysosomal pH 5 to function. Signs and symptoms
Mucolipidosis II (ML II) is a particularly severe form of ML that has a significant resemblance to another mucopolysaccharidosis called Hurler syndrome. Generally only
laboratory testing can distinguish the two as the presentation is so similar, with high plasma concentrations of lysosomal enzymes, often fatal in childhood. Typically, by the age of 6 months, failure to thrive and developmental delays are obvious signs of this disorder. | The Yash Gandhi Foundation is a US non-profit organization which funds research for I-Cell disease
References
External links
mucolipidoses at NINDS — article derived from detail sheet available here
I cell disease at NIHs Office of Rare Diseases
GeneReview/NIH/UW entry on Mucolipidosis II | 11
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Visits to retail outlets selling these products reveal that some manufacturers have since reformulated their products to abide by the regulations, through the use of the legal cyclohexyl nitrite as the primary ingredient in their products, which are sold as video head cleaners, polish removers, or room odorants. Nitrous oxide
In the United States, possession of nitrous oxide is legal under federal law and is not subject to DEA purview. It is, however, regulated by the Food and Drug Administration under the Food Drug and Cosmetics Act; prosecution is possible under its "misbranding" clauses, prohibiting the sale or distribution of nitrous oxide for the purpose of human consumption as a recreational drug. Many states have laws regulating the possession, sale, and distribution of nitrous oxide. Such laws usually ban distribution to minors or limit the amount of nitrous oxide that may be sold without a special license. For example, in the state of California, possession for recreational use is prohibited and qualifies as a misdemeanor. In New Zealand, the Ministry of Health has warned that nitrous oxide is a prescription medicine, and its sale or possession without a prescription is an offense under the Medicines Act. This statement would seemingly prohibit all non-medicinal uses of the chemical, though it is implied that only recreational use will be legally targeted. In India, for general anesthesia purposes, nitrous oxide is available as Nitrous Oxide IP. Indias gas cylinder rules (1985) permit the transfer of gas from one cylinder to another for breathing purposes. | A small number of recreational inhalant drugs are pharmaceutical products that are used illicitly. Product category
Another way to categorize inhalants is by their product category. There are three main product categories: solvents; gases; and medical drugs which are used illicitly. Solvents
A wide range of volatile solvents intended for household or industrial use are inhaled as recreational drugs. This includes petroleum products (gasoline and kerosene), toluene (used in paint thinner, permanent markers, contact cement and model glue), and acetone (used in nail polish remover). These solvents vaporize at room temperature. Ethanol (the alcohol which is normally drunk) is sometimes inhaled, but this cannot be done at room temperature. The ethanol must be converted from liquid into gaseous state (vapor) or aerosol (mist), in some cases using a nebulizer, a machine that agitates the liquid into an aerosol. The sale of nebulizers for inhaling ethanol was banned in some US states due to safety concerns. Gases
A number of gases intended for household or industrial use are inhaled as recreational drugs. This includes chlorofluorocarbons used in aerosols and propellants (e.g., aerosol hair spray, aerosol deodorant). A gas used as a propellant in whipped cream aerosol containers, nitrous oxide, is used as a recreational drug. Pressurized canisters of propane and butane gas, both of which are intended for use as fuels, are used as inhalants. | 11
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Minor criteria
Arthralgia: Polyarthralgia in low-risk populations and monoarthralgia in others. However, joint manifestations cannot be considered in both major and minor categories in the same patient. Fever: ≥ 38.5 °C (101.3 °F) in low-incidence populations and ≥ 38 °C (100.4 °F) in high-risk populations. Raised erythrocyte sedimentation rate (≥60 mm in the first hour in lox-risk populations and ≥30 mm/h in others) or C reactive protein (>3.0 mg/dL). ECG showing a prolonged PR interval after accounting for age variability (Cannot be included if carditis is present as a major symptom)
Prevention
Rheumatic fever can be prevented by effectively and promptly treating strep throat with antibiotics.In those who have previously had rheumatic fever, antibiotics in a preventative manner are occasionally recommended. As of 2017 the evidence to support long term antibiotics in those with underlying disease is poor.The American Heart Association suggests that dental health be maintained, and that people with a history of bacterial endocarditis, a heart transplant, artificial heart valves, or "some types of congenital heart defects" may wish to consider long-term antibiotic prophylaxis. Treatment
The management of rheumatic fever is directed toward the reduction of inflammation with anti-inflammatory medications such as aspirin or corticosteroids. Individuals with positive cultures for strep throat should also be treated with antibiotics.Aspirin is the drug of choice and should be given at high doses.One should watch for side effects like gastritis and salicylate poisoning. In children and teenagers, the use of aspirin and aspirin-containing products can be associated with Reyes syndrome, a serious and potentially deadly condition. | The pathogenesis of RHD is complex and not fully understood, but it is known to involve molecular mimicry and genetic predisposition that lead to autoimmune reactions.Molecular mimicry occurs when epitopes are shared between host antigens and Streptococcus antigens. This causes an autoimmune reaction against native tissues in the heart that are incorrectly recognized as "foreign" due to the cross-reactivity of antibodies generated as a result of epitope sharing. The valvular endothelium is a prominent site of lymphocyte-induced damage. CD4+ T cells are the major effectors of heart tissue autoimmune reactions in RHD. Normally, T cell activation is triggered by the presentation of bacterial antigens. In RHD, molecular mimicry results in incorrect T cell activation, and these T lymphocytes can go on to activate B cells, which will begin to produce self-antigen-specific antibodies. This leads to an immune response attack mounted against tissues in the heart that have been misidentified as pathogens. Rheumatic valves display increased expression of VCAM-1, a protein that mediates the adhesion of lymphocytes. Self-antigen-specific antibodies generated via molecular mimicry between human proteins and streptococcal antigens up-regulate VCAM-1 after binding to the valvular endothelium. This leads to the inflammation and valve scarring observed in rheumatic valvulitis, mainly due to CD4+ T cell infiltration.While the mechanisms of genetic predisposition remain unclear, a few genetic factors have been found to increase susceptibility to autoimmune reactions in RHD. The dominant contributors are a component of MHC class II molecules, found on lymphocytes and antigen-presenting cells, specifically the DR and DQ alleles on human chromosome 6. | 11
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Eighteen months after the CRADA, BMS filed a new drug application (NDA), which was given FDA approval at the very end of 1992. Although there was no patent on the compound, the provisions of the Waxman-Hatch Act gave Bristol-Myers Squibb five years exclusive marketing rights. In 1990, BMS applied to trademark the name taxol as Taxol(R). This was controversially approved in 1992. At the same time, paclitaxel replaced taxol as the generic (INN) name of the compound. Critics, including the journal Nature, argued the name taxol had been used for more than two decades and in more than 600 scientific articles and suggested the trademark should not have been awarded and the BMS should renounce its rights to it. BMS argued changing the name would cause confusion among oncologists and possibly endanger the health of patients. BMS has continued to defend its rights to the name in the courts. BMS has also been criticized for misrepresentation by Goodman and Walsh, who quote from a company report saying "It was not until 1971 that ... testing ... enabled the isolation of paclitaxel, initially described as compound 17". This quote is, strictly speaking, accurate: the objection seems to be that this misleadingly neglects to explain that it was the scientist doing the isolation who named the compound taxol and it was not referred to in any other way for more than twenty years. Annual sales peaked in 2000, reaching US$1.6 billion; paclitaxel is now available in generic form. | Mutations were mainly found in exons 12-22 of the intracellular TKD, including 10 missense mutations that have a single nucleotide deletion and a single codon deletion that consists of a triplet of nucleotides that have been removed causing a whole amino acid to not be coded. Additionally, three splice site mutations were identified that caused an in-frame deletion of an exon, an expressed nucleotide sequence, leading to the removal of more than 40 amino acids in the TKD.This determination has based upon genetic studies of 14 HDLS families confirming mutations in this gene. The CSF1 receptor protein primarily functions in regulation, survival, proliferation, and differentiation of microglial cells. The mechanism of microglial dysfunction due to mutations in CSF1R to the myelin loss and axonal spheroid formation remains unknown. Further research is needed to better understand disease pathogenesis. Pathology
In HDLS, there is enlargement of the lateral ventricles and marked thinning or weakening of cerebral white matter. The loss of white matter is caused by myelin loss. These changes are associated with diffuse gliosis, moderate loss of axons and many axonal spheroids.Activated or ameboid microglia and macrophages that contain myelin debris, lipid droplets and brown autofluorescent pigment granules are found in the areas with demyelination and axonal spheroids. In severely degenerated areas there are many large, reactive astrocytes filled with glial fibrils.In autopsy cases, it has been shown that white matter abnormalities are relatively confined to the cerebrum while avoiding the cerebellum and many of the major fiber tracts of the nervous system. | 0-1
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Signs and Symptoms
Comma sign: Comma shaped vessels in the bulbar conjunctiva is due to vascular occlusion of conjunctival vessels. Vitreoretinal traction or retinal detachment cause flashes, floaters or dark shadows. Sudden loss of vision may occur due to retinal artery occlusion, vitreous hemorrhage or retinal detachment. Intravascular occlusions may be seen in optic disc vessels. Cause
Normal adult hemoglobin A molecule comprises two α and two β globin chains associated with a heme ring. Mutation at the 6th position of the beta chain is the cause of sickle cell disease. Due to sickle cell disease, vascular occlusion may occur in the conjunctiva, iris, retina, or choroid. Retinal changes occur due to blockage of retinal blood vessels by abnormal RBCs. Diagnosis
Diagnostic Techniques
Diagnosis is conducted in a multidisciplinary manner. The diagnosis of sickle cell disease can be confirmed by cation high performance liquid chromatography, haemoglobin electrophoresis in adolescents and adults and molecular genetic diagnosis in prenatal and neonatal populations. Anterior segment signs including the conjunctival sign and iris atrophy are ocular manifestations that are strongly indicative of sickle cell disease. Early stages of sickle cell retinopathy are asymptomatic. However, retinal changes that are diagnostic of sickle cell retinopathy can be visualized using fundoscopic examinations, retinography, fluorescein angiography and coherence tomography. Ultra Widefield Fluorescein Angiography is the gold standard for diagnosis of proliferative sickle cell retinopathy. It is an invasive method that assesses both anterior and posterior segment structures. Spectral Domain Optical Coherence Tomography and Coherence Tomography Angiography are non invasive methods of diagnosing proliferative retinopathy. | Sickle cell retinopathy can be defined as retinal changes due to blood vessel damage in the eye of a person with a background of sickle cell disease. It can likely progress to loss of vision in late stages due to vitreous hemorrhage or retinal detachment. Sickle cell disease is a structural red blood cell disorder leading to consequences in multiple systems. It is characterized by chronic red blood cell destruction, vascular injury, and tissue ischemia causing damage to the brain, eyes, heart, lungs, kidneys, spleen, and musculoskeletal system.People affected by sickle cell disease are commonly of African or Asian descent. Emigration patterns towards the Western Hemisphere have led to increased numbers of persons affected by sickle cell disease in regions where it was previously uncommon. Knowledge and understanding of sickle cell disease and its management are now increasingly relevant in areas such as the European Union. At a young age, a great proportion of people living with sickle cell disease can develop retinal changes. Sickle cell disease consists of several subtypes; however, the Haemoglobin type C (HbSC) subtype carries the gravest prognosis for sickle cell retinopathy and vision changes.Regular retinal examinations can aid in early detection and treatment, thus reducing the impact of the condition and the risk of vision loss. Development and progression of sickle cell retinopathy can be favorably modified through management of the underling sickle cell disease. Treatment of the general disease can ameliorate its systemic effects. Classification
Sickle cell retinopathy can be classified based on retinal changes into non-proliferative and proliferative subtypes. | 11
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Omorashi: The act of holding ones own urine until the need to urinate is urgent, making another hold in their urine, or watching another person with an urgent need to urinate. This fetish sometimes originates from childhood memories of needing, or of seeing another needing, to urinate. Arousal may be triggered by seeing the body movements or facial expressions of that person. It can also be heightened by the person saying that they have to urinate. The arousal from being desperate comes from the sensation of having a full bladder. Voyeurism: Seeing another urinate without the persons knowledge either through video taping by a hidden camera, or by lurking in locations where people are urinating or are likely to have an urge to urinate. Frequency
Jennifer Eve Rehor of San Francisco State University points out that such data as exists on what she calls "unconventional" or "kink" sexual behavior is generally problematic because of the way that it has been collected, through criminal and clinical case studies. Behavior that appears neither in criminal trials nor in clinical studies (for example, because the individuals concerned do not commonly seek professional help) is therefore under-reported. Rehor therefore surveyed 1,764 female participants in "kink" behavior (mostly association with BDSM) in 2010–11, receiving 1,580 valid responses. What Rehor calls "urine play" is relatively infrequent, with only 36.52% of her sample reporting having done it or having had it done to them. | The University of Maryland Medical Center defines pathological gambling as "being unable to resist impulses to gamble, which can lead to severe personal or social consequences".Most other definitions of problem gambling can usually be simplified to any gambling that causes harm to the gambler or someone else in any way; however, these definitions are usually coupled with descriptions of the type of harm or the use of diagnostic criteria. The DSM-V has since reclassified pathological gambling as "gambling disorder" and has listed the disorder under substance-related and addictive disorders rather than impulse-control disorders. This is due to the symptomatology of the disorder resembling an addiction not dissimilar to that of a substance use disorder. | 0-1
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Indeed, homoploid speciation (hybrid speciation without a change in chromosome number) has been evidenced for some fungal species (such as the basidiomycota Microbotryum violaceum). As for plants and animals, fungal hybrids and polyploids display structural and functional modifications compared to their progenitors and diploid counterparts. In particular, the structural and functional outcomes of polyploid Saccharomyces genomes strikingly reflect the evolutionary fate of plant polyploid ones. Large chromosomal rearrangements leading to chimeric chromosomes have been described, as well as more punctual genetic modifications such as gene loss. The homoealleles of the allotetraploid yeast S. pastorianus show unequal contribution to the transcriptome. Phenotypic diversification is also observed following polyploidization and/or hybridization in fungi, producing the fuel for natural selection and subsequent adaptation and speciation. Chromalveolata
Other eukaryotic taxa have experienced one or more polyploidization events during their evolutionary history (see Albertin and Marullo, 2012 for review). The oomycetes, which are non-true fungi members, contain several examples of paleopolyploid and polyploid species, such as within the genus Phytophthora. Some species of brown algae (Fucales, Laminariales and diatoms) contain apparent polyploid genomes. In the Alveolata group, the remarkable species Paramecium tetraurelia underwent three successive rounds of whole-genome duplication and established itself as a major model for paleopolyploid studies. Bacteria
Each Deinococcus radiodurans bacterium contains 4-8 copies of its chromosome. Exposure of D. radiodurans to X-ray irradiation or desiccation can shatter its genomes into hundred of short random fragments. Nevertheless, D. radiodurans is highly resistant to such exposures. | The letter x is used to represent the number of chromosomes in a single set:
haploid (one set; 1x)
diploid (two sets; 2x)
triploid (three sets; 3x), for example sterile saffron crocus, or seedless watermelons, also common in the phylum Tardigrada
tetraploid (four sets; 4x), for example Salmonidae fish, the cotton Gossypium hirsutum
pentaploid (five sets; 5x), for example Kenai Birch (Betula kenaica)
hexaploid (six sets; 6x), for example some species of wheat, kiwifruit
heptaploid or septaploid (seven sets; 7x)
octaploid or octoploid, (eight sets; 8x), for example Acipenser (genus of sturgeon fish), dahlias
decaploid (ten sets; 10x), for example certain strawberries
dodecaploid or duodecaploid (twelve sets; 12x), for example the plants Celosia argentea and Spartina anglica or the amphibian Xenopus ruwenzoriensis. Classification
Autopolyploidy
Autopolyploids are polyploids with multiple chromosome sets derived from a single taxon. Two examples of natural autopolyploids are the piggyback plant, Tolmiea menzisii and the white sturgeon, Acipenser transmontanum. Most instances of autopolyploidy result from the fusion of unreduced (2n) gametes, which results in either triploid (n + 2n = 3n) or tetraploid (2n + 2n = 4n) offspring. Triploid offspring are typically sterile (as in the phenomenon of triploid block), but in some cases they may produce high proportions of unreduced gametes and thus aid the formation of tetraploids. This pathway to tetraploidy is referred to as the triploid bridge. Triploids may also persist through asexual reproduction. In fact, stable autotriploidy in plants is often associated with apomictic mating systems. In agricultural systems, autotriploidy can result in seedlessness, as in watermelons and bananas. | 11
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Such allegations may arise because of incomplete amnesia, disinhibition, and impaired ability to process cues. Because of its relatively long duration of residual effects (sedation, ataxia, hypotension, and amnesia), lorazepam premedication is best suited for hospital inpatient use. People should not be discharged from the hospital within 24 hours of receiving lorazepam premedication unless accompanied by a caregiver. They should also not drive, operate machinery, or use alcohol within this period. Drug and alcohol dependence – The risk of abuse of lorazepam is increased in dependent people. Comorbid psychiatric disorders also increase the risk of dependence and paradoxical adverse effects. Tolerance and dependence
Dependence typified by a withdrawal syndrome occurs in about one-third of individuals who are treated for longer than four weeks with a benzodiazepine. Higher doses and longer periods of use increase the risk of developing a benzodiazepine dependence. Potent benzodiazepines with a relatively short half life, such as lorazepam, alprazolam, and triazolam, have the highest risk of causing a dependence. Tolerance to benzodiazepine effects develops with regular use. This is desirable with amnesic and sedative effects but undesirable with anxiolytic, hypnotic, and anticonvulsant effects. People initially experience drastic relief from anxiety and sleeplessness, but symptoms gradually return, relatively soon in the case of insomnia, but more slowly in the case of anxiety symptoms. | Global developmental delay is an umbrella term used when children are significantly delayed in their cognitive and physical development. It can be diagnosed when a child is delayed in one or more milestones, categorised into motor skills, speech, cognitive skills, and social and emotional development. There is usually a specific condition which causes this delay, such as Fragile X syndrome or other chromosomal abnormalities. However, it is sometimes difficult to identify this underlying condition.Other terms associated with this condition are failure to thrive (which focuses on lack of weight gain and physical development), intellectual disability (which focuses on intellectual deficits and the changes they cause to development) and developmental disability (which can refer to both intellectual and physical disability altering development). Causes
Developmental delay can be caused by learning disabilities, in which case the delay can usually be overcome with time and support - such as with physiotherapists, occupational therapists,vision therapist and speech and language therapists. Other causes which may cause a permanent delay in development include genetic disorders such as Down syndrome and Fragile X, childhood infections such as meningitis or encephalitis, and metabolic disorders such as hypothyroidism. Metabolic disorders are more likely to cause delayed development in older children, as many congenital metabolic problems which are easily managed are screened for in the neonatal period. Child born prematurely (born before 37 weeks). The use of toxic substances in pregnancy, particularly alcohol, can lead to developmental delay if they affect the neurological development of the fetus, such as in fetal alcohol syndrome. | 0-1
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Early identification
It is recommended that patients with a history of acute porphyria, and even genetic carriers, wear an alert bracelet or other identification at all times. This is in case they develop severe symptoms, or in case of accidents where there is a potential for drug exposure, and as a result they are unable to explain their condition to healthcare professionals. Some drugs are absolutely contraindicated for patients with any form of porphyria. Neurologic and psychiatric disorders
Patients who experience frequent attacks can develop chronic neuropathic pain in extremities as well as chronic pain in the abdomen. Intestinal pseudo-obstruction, ileus, intussusception, hypoganglionosis, and encopresis in children have been associated with porphyrias. This is thought to be due to axonal nerve deterioration in affected areas of the nervous system and vagal nerve dysfunction. Pain treatment with long-acting opioids, such as morphine, is often indicated, and, in cases where seizure or neuropathy is present, gabapentin is known to improve outcome.Seizures often accompany this disease. Most seizure medications exacerbate this condition. Treatment can be problematic: barbiturates especially must be avoided. Some benzodiazepines are safe and, when used in conjunction with newer anti-seizure medications such as gabapentin, offer a possible regimen for seizure control. Gabapentin has the additional feature of aiding in the treatment of some kinds of neuropathic pain. Magnesium sulfate and bromides have also been used in porphyria seizures; however, development of status epilepticus in porphyria may not respond to magnesium alone. | Alpha-thalassemia can be mistaken for iron-deficiency anaemia on a full blood count or blood film, as both conditions have a microcytic anaemia. Serum iron and serum ferritin can be used to exclude iron-deficiency anaemia. Types
Two genetic loci exist for α globin, thus four alleles are in diploid cells. Two alleles are maternal and two alleles are paternal in origin. The severity of the α-thalassemias is correlated with the number of affected α-globin alleles: the greater, the more severe will be the manifestations of the disease. When noting the genotype, an "α" indicates a functional alpha chain, and - a pathological one. Laboratory diagnosis
The ability to measure hemoglobin Barts makes it useful in newborn screening tests. If hemoglobin Barts is detected on a newborn screen, the patient is usually referred for further evaluation since detection of hemoglobin Barts can indicate either one alpha globin gene deletion, making the baby a silent alpha thalassemia carrier, two alpha globin gene deletions (alpha thalassemia), or hemoglobin H disease (three alpha globin gene deletions).Deletion of four alpha globin genes was previously felt to be incompatible with life, but there are currently 69 patients who have survived past infancy. All such children too show high level of hemoglobin Barts on newborn screen along with other variants.Post-newborn ages, initial laboratory diagnosis should include a complete blood count and red blood cell indices. As well, a peripheral blood smear should be carefully reviewed. | 0-1
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Ritalin SR), and 8–12 hours for extended release (i.e. Concerta). The half-life of methylphenidate is 2–3 hours, depending on the individual. The peak plasma time is achieved at about 2 hours. Methylphenidate has a low plasma protein binding of 10-33% and a volume of distribution of 2.65 L/kg.Dextromethylphenidate is much more bioavailable than levomethylphenidate when administered orally, and is primarily responsible for the psychoactivity of racemic methylphenidate.The oral bioavailability and speed of absorption for immediate-release methylphenidate is increased when administered with a meal. The effects of a high fat meal on the observed Cmax differ between some extended release formulations, with combined IR/ER and OROS formulations showing reduced Cmax levels while liquid-based extended release formulations showed increased Cmax levels when administered with a high fat meal, according to some researchers. A 2003 study, however, showed no difference between a high fat meal administration and a fasting administration of oral methylphenidate.Methylphenidate is metabolized into ritalinic acid by CES1A1, enzymes in the liver. Dextromethylphenidate is selectively metabolized at a slower rate than levomethylphenidate. 97% of the metabolised drug is excreted in the urine, and between 1 and 3% is excreted in the faeces. A small amount, less than 1%, of the drug is excreted in the urine in its unchanged form. Chemistry
Four isomers of methylphenidate are possible, since the molecule has two chiral centers. One pair of threo isomers and one pair of erythro are distinguished, from which primarily d-threo-methylphenidate exhibits the pharmacologically desired effects. | Genetic mutations in mitochondrial DNA, vitamin depletion, alcohol and tobacco abuse, and use of certain drugs can cause derangements in efficient transport of mitochondria, which can cause a primary or secondary optic neuropathy. Nutritional optic neuropathies
A nutritional optic neuropathy may be present in a patient with obvious evidence of under-nutrition (weight loss and wasting). Months of depletion are usually necessary to deplete body stores of most nutrients. Undernourished patients often have many vitamin and nutrient deficiencies and have low serum protein levels. However, the optic neuropathy associated with pernicious anemia and vitamin B12 deficiency can even be seen in well-nourished individuals. Gastric bypass surgery may also cause a vitamin B12 deficiency from poor absorption. Patients who have nutritional optic neuropathy may notice that colors are not as vivid or bright as before and that the color red is washed out. This normally occurs in both eyes at the same time and is not associated with any eye pain. They might initially notice a blur or fog, followed by a drop in vision. While vision loss may be rapid, progression to blindness is unusual. These patients tend to have blind spots in the center of their vision with preserved peripheral vision. In most cases, the pupils continue to respond normally to light. Toxic optic neuropathies
The most recognized cause of toxic optic neuropathy is methanol poisoning. This can be a life-threatening event that normally accidentally occurs when the person mistook or substituted, methanol for ethyl alcohol. | 0-1
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It is proposed that repetitive use of the arm can affect the biomechanics of the upper limb or cause damage to tissues. It is proposed that postural and spinal assessment along with ergonomic assessments should be considered, based on observation that addressing these factors has been found to improve comfort in some studies although experimental data are lacking and the perceived benefits may not be specific to those interventions. A 2010 survey by NIOSH showed that 2/3 of the 5 million carpal tunnel diagnosed in the US that year were related to work. Women are more likely to be diagnosed with work-related carpal tunnel syndrome than men. Associated conditions
A variety of patient factors can lead to CTS, including heredity, size of the carpal tunnel, associated local and systematic diseases, and certain habits. Non-traumatic causes generally happen over a period of time, and are not triggered by one certain event. Many of these factors are manifestations of physiologic aging. Diagnosis
There is no consensus reference standard for the diagnosis of carpal tunnel syndrome. A combination of characteristic symptoms (how it feels) and signs (what the clinician finds on exam) are associated with a high probability of IMNCT without electrophysiological testing. Electrodiagnostic testing (electromyography and nerve conduction velocity) can objectively measure and verify median neuropathy.Ultrasound can image and measure the cross sectional diameter of the median nerve, which has some correlation with idiopathic median neuropathy at the carpal tunnel (IMNCT). The role of ultrasound in diagnosis--just as for electrodiagnostic testing--is a matter of debate. | They experience neurological problems including weak muscle tone (hypotonia), abnormal movements, seizures, and coma. Infants with this form of the condition usually survive for less than 3 months after birth. Type C
This type is characterised by its late onset and is associated with isolated mild intellectual delay. Treatment
Pyruvate carboxylase deficiency treatment typically consists of providing the body with alternate sources of energy (anaplerotic therapy). This may include a diet rich in proteins and carbohydrates but not lipids. Acutely, triheptanoin may be administered as a source of acetyl-CoA. Epidemiology
Pyruvate carboxylase deficiency is very rare, and is estimated to affect around 1 in 250,000 people. References
External links
GeneReview/NCBI/NIH/UW entry on Pyruvate Carboxylase Deficiency
Pyruvate carboxylase deficiency at NLM Genetics Home Reference This article incorporates text from this source, which is in the public domain. | 0-1
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Enoxaparin sodium, sold under the brand name Lovenox among others, is an anticoagulant medication (blood thinner). It is used to treat and prevent deep vein thrombosis (DVT) and pulmonary embolism (PE) including during pregnancy and following certain types of surgery. It is also used in those with acute coronary syndrome (ACS) and heart attacks. It is given by injection just under the skin or into a vein. It is also used during hemodialysis.Common side effects include bleeding, fever, and swelling of the legs. Bleeding may be serious especially in those who are undergoing a spinal tap. Use during pregnancy appears to be safe for the baby. Enoxaparin is in the low molecular weight heparin family of medications.Enoxaparin was first made in 1981 and approved for medical use in 1993. It is on the World Health Organizations List of Essential Medicines. Enoxaparin is sold under several brand names and is available as a generic medication. Enoxaparin is made from heparin. In 2017, it was the 299th most commonly prescribed medication in the United States, with more than one million prescriptions. Medical uses
Treatment of unstable angina (UA) and non-Q-wave myocardial infarction (NQMI), administered concurrently with aspirin
DVT and pulmonary embolism prophylaxis in bed-ridden patients
DVT prophylaxis in knee replacement surgery
DVT prophylaxis in hip replacement surgery
DVT prophylaxis in abdominal surgery
Treatment of DVT with or without pulmonary embolism
Treatment of DVT inpatient, with ST-segment elevation myocardial infarction (STEMI)
Bridging treatment for those with INR below therapeutic range
Monitoring
Enoxaparin has predictable absorption, bioavailability, and distribution therefore monitoring is not typically done. | Hyperventilation is irregular breathing that occurs when the rate or tidal volume of breathing eliminates more carbon dioxide than the body can produce. This leads to hypocapnia, a reduced concentration of carbon dioxide dissolved in the blood. The body normally attempts to compensate for this homeostatically, but if this fails or is overridden, the blood pH will rise, leading to respiratory alkalosis. The symptoms of respiratory alkalosis include: dizziness, tingling in the lips, hands or feet, headache, weakness, fainting, and seizures. In extreme cases it may cause carpopedal spasms, a flapping and contraction of the hands and feet.Factors that may induce or sustain hyperventilation include: physiological stress, anxiety or panic disorder, high altitude, head injury, stroke, respiratory disorders such as asthma, pneumonia, or hyperventilation syndrome, cardiovascular problems such as pulmonary embolisms, anemia, an incorrectly calibrated medical respirator, and adverse reactions to certain drugs. Hyperventilation can also be induced intentionally to achieve an altered state of consciousness such as in the choking game, during breathwork, or in an attempt to extend a breath-hold dive. See also
List of terms of lung size and activity
Control of respiration
Choking game a game which may involve hyperventilation in order to induce temporary syncope and euphoria
Respiratory alkalosis
Kussmaul breathing
Shallow water blackout, the role of hyperventilation in some drowning incidents
References
== External links == | 0-1
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These "short circuits in the wiring" sometimes run in families or result from a difficult birth, just like any learning disability. Auditory processing disorder can be associated with conditions affected by genetic traits, such as various developmental disorders. Inheritance of auditory processing disorder refers to whether the condition is inherited from your parents or "runs" in families. Central auditory processing disorder may be hereditary neurological traits from the mother or the father. Developmental
In the majority of cases of developmental APD, the cause is unknown. An exception is acquired epileptic aphasia or Landau-Kleffner syndrome, where a childs development regresses, with language comprehension severely affected. The child is often thought to be deaf, but normal peripheral hearing is found. In other cases, suspected or known causes of APD in children include delay in myelin maturation, ectopic (misplaced) cells in the auditory cortical areas, or genetic predisposition. In a family with autosomal dominant epilepsy, seizures which affected the left temporal lobe seemed to cause problems with auditory processing. In another extended family with a high rate of APD, genetic analysis showed a haplotype in chromosome 12 that fully co-segregated with language impairment.Hearing begins in utero, but the central auditory system continues to develop for at least the first decade. There is considerable interest in the idea that disruption to hearing during a sensitive period may have long-term consequences for auditory development. | This can include problems with: "...sound localization and lateralization (see also binaural fusion); auditory discrimination; auditory pattern recognition; temporal aspects of audition, including temporal integration, temporal discrimination (e.g., temporal gap detection), temporal ordering, and temporal masking; auditory performance in competing acoustic signals (including dichotic listening); and auditory performance with degraded acoustic signals".The Committee of UK Medical Professionals Steering the UK Auditory Processing Disorder Research Program have developed the following working definition of auditory processing disorder: "APD results from impaired neural function and is characterized by poor recognition, discrimination, separation, grouping, localization, or ordering of speech sounds. It does not solely result from a deficit in general attention, language or other cognitive processes." Types of testing
The SCAN-C for children and SCAN-A for adolescents and adults are the most common tools for screening and diagnosing APD in the USA. Both tests are standardized on a large number of subjects and include validation data on subjects with auditory processing disorders. The SCAN test batteries include screening tests: norm-based criterion-referenced scores; diagnostic tests: scaled scores, percentile ranks and ear advantage scores for all tests except the Gap Detection test. The four tests include four subsets on which the subject scores are derived include: discrimination of monaurally presented single words against background noise (speech in noise), acoustically degraded single words (filtered words), dichotically presented single words and sentences. Random Gap Detection Test (RGDT) is also a standardized test. It assesses an individuals gap detection threshold of tones and white noise. | 11
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IBS-D is associated with elevated hydrogen numbers on breath tests while IBS-C is associated with elevated methane numbers on breath tests. Subsequent studies demonstrated statistically significant reduction in IBS symptoms following therapy for SIBO.Various mechanisms are involved in the development of diarrhea and IBS-D in bacterial overgrowth. First, the excessive bacterial concentrations can cause direct inflammation of the small bowel cells, leading to an inflammatory diarrhea. The malabsorption of lipids, proteins and carbohydrates may cause poorly digestible products to enter into the colon. This can cause diarrhea by the osmotic drive of these molecules, but can also stimulate the secretory mechanisms of colonic cells, leading to a secretory diarrhea.There is a lack of consensus however, regarding the suggested link between IBS and SIBO. Other authors concluded that the abnormal breath results so common in IBS patients do not suggest SIBO, and state that "abnormal fermentation timing and dynamics of the breath test findings support a role for abnormal intestinal bacterial distribution in IBS." There is general consensus that breath tests are abnormal in IBS; however, the disagreement lies in whether this is representative of SIBO. Etiology and risk factors
Certain people are more predisposed to the development of bacterial overgrowth because of certain risk factors. | Zinc sulfate is an inorganic compound. It is used as a dietary supplement to treat zinc deficiency and to prevent the condition in those at high risk. Side effects of excess supplementation may include abdominal pain, vomiting, headache, and tiredness.The most common form includes water of crystallization as the heptahydrate, with the formula ZnSO4·7H2O. It was historically known as "white vitriol". Zinc sulfate and its hydrates are colourless solids. Uses
Medicine
In medicine it is used together with oral rehydration therapy (ORT) and an astringent. Manufacturing
The hydrates, especially the heptahydrate, are the primary forms used commercially. The main application is as a coagulant in the production of rayon. It is also a precursor to the pigment lithopone. It is also used as an electrolyte for zinc electroplating, as a mordant in dyeing, and as a preservative for skins and leather. Other
Zinc sulfate is used to supply zinc in animal feeds, fertilizers, toothpaste, and agricultural sprays. Zinc sulfate, like many zinc compounds, can be used to control moss growth on roofs.Zinc sulfate can be used to supplement zinc in the brewing process. Zinc is a necessary nutrient for optimal yeast health and performance, although it is not a necessary supplement for low-gravity beers, as the grains commonly used in brewing already provide adequate zinc. It is a more common practice when pushing yeast to their limit by increasing alcohol content beyond their comfort zone. Before modern stainless steel, brew Kettles, fermenting vessels and after wood, zinc was slowly leached by the use of copper kettles. | 0-1
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Ebanga is an Angolan commune. It belongs to the municipality of Ganda, in the province of Benguela. == References == | Nabumetone is a nonsteroidal anti-inflammatory drug (NSAID). Nabumetone was developed by Beecham and first received regulatory approval in 1991. It is available under numerous brand names, such as Relafen, Relifex, and Gambaran. Nabumetone is a nonacidic NSAID prodrug that is rapidly metabolized in the liver to the active metabolite, 6-methoxy-2-naphthyl acetic acid. As found with previous NSAIDs, nabumetones active metabolite inhibits the cyclooxygenase enzyme and preferentially blocks COX-2 activity (which is indirectly responsible for the production of inflammation and pain during arthritis). The active metabolite of nabumetone is felt to be the compound primarily responsible for therapeutic effect. Comparatively, the parent drug is a poor inhibitor of COX-2 byproducts, particularly prostaglandins. It may be less nephrotoxic than indomethacin. There are two known polymorphs of the compound.Nabumetone has little effect on renal prostaglandin secretion and less of an association with heart failure than other traditional drugs of the class. Effects of nabumetone on blood pressure control in hypertensive patients on ACE inhibitors is also good—equivalent to paracetamol. Medical uses
Similar in action to other NSAIDs, Nabumetone is used to treat pain and inflammation. | 0-1
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Retinoblastoma (Rb) is a rare form of cancer that rapidly develops from the immature cells of a retina, the light-detecting tissue of the eye. It is the most common primary malignant intraocular cancer in children, and it is almost exclusively found in young children.Though most children survive this cancer, they may lose their vision in the affected eye(s) or need to have the eye removed.Almost half of children with retinoblastoma have a hereditary genetic defect associated with retinoblastoma. In other cases, it is caused by a congenital mutation in the chromosome 13 gene 13q14 (retinoblastoma protein). Signs and symptoms
Retinoblastoma is universally known as the most intrusive intraocular cancer among children. The chance of survival and preservation of the eye depends fully on the severity. Retinoblastoma is extremely rare as there are only about 200 to 300 cases every year in the United States. Looking at retinoblastoma globally, only 1 in about 15,000 children have this malignancy but these numbers continuously increase.Intraocular malignancies are more curable rather than extraocular malignancies due to early diagnosis and an early treatment prognosis. During infant screenings, if they incorporate an eye screening like they do a hearing screening, it can be detected at an earlier age, therefore, preventing its spread. Leucocoria is the primary indication of retinoblastoma and is when the cancer is still intraocular, meaning inside the eye. When light is reflected by the white tumor, the view of the red retina is blocked. | Microscopically, both undifferentiated and differentiated elements may be present. Undifferentiated elements appear as collections of small, round cells with hyperchromatic nuclei; differentiated elements include Flexner-Wintersteiner rosettes, Homer Wright rosettes, and fleurettes from photoreceptor differentiation. Genetic testing
Identifying the RB1 gene mutation that led to a childs retinoblastoma can be important in the clinical care of the affected individual and in the care of (future) siblings and offspring. It may run in the family. Bilaterally affected individuals and 13-15% of unilaterally affected individuals, are expected to show an RB1 mutation in blood. By identifying the RB1 mutation in the affected individual, (future) siblings, children, and other relatives can be tested for the mutation; if they do not carry the mutation, child relatives are not at risk of retinoblastoma, so need not undergo the trauma and expense of examinations under anaesthetic. For the 85% of unilaterally affected patients found not to carry either of their eye tumor RB1 mutations in blood, neither molecular testing nor clinical surveillance of siblings is required. If the RB1 mutation of an affected individual is identified, amniotic cells in an at-risk pregnancy can be tested for the family mutation; any fetus that carries the mutation can be delivered early, allowing early treatment of any eye tumors, leading to better visual outcomes. For cases of unilateral retinoblastoma where no eye tumor is available for testing, if no RB1 mutation is detected in blood after high-sensitivity molecular testing (i.e. | 11
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Posterior septal perforations, which mainly occur iatrogenically, are often managed with simple observation and are at times intended portions of skull base surgery. Septal perforations that are not bothersome can be managed with simple observation. While no septal perforation will spontaneously close, for the majority of septal perforations that are unlikely to get larger observation is an appropriate form of management. For perforations that bleed or are painful, initial management should include humidification and application of salves to the perforation edges to promote healing. Mucosalization of the perforation edges will help prevent pain and recurrent epistaxis and majority of septal perforations can be managed without surgery. For perforations in which anosmia, or the loss of smell, and a persistent whistling are a concern, the use of a silicone septal button is a treatment option. These can be placed while the patient is awake and usually in the clinic setting. While complications of button insertion are minimal, the presence of the button can be bothersome to most patients. For patients who desire definitive close, surgery is the only option. Prior to determining candidacy for surgical closure, the etiology of the perforation must be determined. Often this requires a biopsy of the perforation to rule out autoimmune causes. If a known cause such as cocaine is the offending agent, it must be ensured that the patient is not still using the irritant. For those that are determined to be medically cleared for surgery, the anatomical location and size of the perforation must be determined. | A nasal septum perforation is a medical condition in which the nasal septum, the bony/cartilaginous wall dividing the nasal cavities, develops a hole or fissure. This may be brought on directly, as in the case of nasal piercings, or indirectly, as by long-term topical drug application, including intranasal ethylphenidate, methamphetamine, cocaine, crushed prescription pills, or decongestant nasal sprays, chronic epistaxis, excessive nose picking and as a complication of nasal surgery like septoplasty or rhinoplasty. Much less common causes for perforated nasal septums include rare granulomatous inflammatory conditions like granulomatosis with polyangiitis. It has been reported as a side effect of anti-angiogenesis drugs like bevacizumab. Signs and symptoms
A perforated septum can vary in size and location, and is usually found deep inside the nose. It may be asymptomatic, or cause a variety of signs and symptoms. Small perforations can cause a whistling noise when breathing. Larger perforations usually have more severe symptoms. These can be a combination of crusting, blood discharge, difficulty breathing, nasal pressure and discomfort. The closer the perforation is to the nostrils, the more likely it is to cause symptoms. Cause
Infective causes include syphilis, leprosy, and rhinoscleroma. Non-infective causes include cocaine abuse, an in situ foreign body, chronic use of topical nasal decongestants, methamphetamine, facial trauma, or may develop as a consequence of nasal surgery. Treatment
Septal perforations are managed with a multitude of options. The treatment often depends on the severity of symptoms and the size of the perforations. Generally speaking anterior septal perforations are more bothersome and symptomatic. | 11
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However these babies usually have uncomplicated heart defects, like a ventricular septal defect, which may not require any surgery. Kidneys
Kidney defects are seen in approximately 50 percent of patients with VACTERL association. In addition, up to 35 percent of patients with VACTERL association have a single umbilical artery (there are usually two arteries and one vein) which is often associated with additional kidney or urologic problems. Renal abnormalities in VACTERL association can be severe, with incomplete formation of one or both kidneys or urologic abnormalities such as obstruction of outflow of urine from the kidneys or severe reflux (backflow) of urine into the kidneys from the bladder. These problems can cause kidney failure early in life and may require kidney transplant. Many of these problems can be corrected surgically before any damage can occur. Limbs
Limb defects occur in up to 70 percent of babies with VACTERL association and include a displaced or hypoplastic thumb, extra digits (polydactyly), fusion of digits (syndactyly) and forearm defects such as radial aplasia. Babies with limb defects on both sides tend to have kidney or urologic defects on both sides, while babies with limb defects on only one side of the body tend to have kidney problems on that same side. Extension
Features secondary to VACTERL components are frequent enough to be considered an extension of VACTERL. These include: single umbilical artery, ambiguous genitalia, abdominal wall defects, diaphragmatic hernia, intestinal and respiratory anomalies, and oligohydramnios sequence defects. Cardiac defects are thought to fit in this category. | Nephroptosis, is rare and abnormal condition in which the kidney drops down into the pelvis when the patient stands up. It is more common in women than in men. It has been one of the most controversial conditions in terms of both its diagnosis and its treatments. Symptoms and signs
Nephroptosis is asymptomatic in most persons. However, nephroptosis can be characterized by violent attacks of colicky flank pain, nausea, chills, hypertension, hematuria and proteinuria. Persons with symptomatic nephroptosis often complain of sharp pains that radiate into the groin. Many persons also suggest a weighing feeling on the abdomen. Pain is typically relieved by lying down. It is believed that flank pain on standing that is relieved by lying down is due to movement of the kidney causing intermittent renal tract obstruction. The attack of colic pain is called Dietls crisis or renal paroxysm. Cause
It is believed to result from deficiency of supporting inferior pararenal fasciae. Diagnosis
Diagnosis is contemplated based upon patient symptoms. Diagnosis is confirmed during intravenous urography, by obtaining erect and supine films. The renal DMSA scan may show decreased counts in the sitting position compared with supine scan. Treatment
Nephropexy was performed in the past to stabilize the kidney, but presently surgery is not recommended in asymptomatic patients. A Nephropexy does not guarantee the symptoms will go away. Laparoscopic nephropexy has recently become available for selected symptomatic patients. References
Further reading
Barber N, Thompson P (2004). "Nephroptosis and nephropexy--hung up on the past?". Eur Urol. 46 (4): 428–33. doi:10.1016/j.eururo.2004.03.023. PMID 15363554. == External links == | 0-1
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Presence of an ape hand deformity when the hand is at rest, due to an hyperextension of index finger and thumb, and an adducted thumb
Presence of benediction sign when attempting to form a fist, due to loss of flexion of radial half of digits
Sensory deficit: Loss of sensation in lateral 3+1⁄2 digits including their nail beds, and the thenar areaAt the elbow
Entrapment at the level of the elbow or the proximal forearm could be due to the pronator teres syndrome.Within the proximal forearm: Anterior interosseous syndrome
Injury to the anterior interosseous branch in the forearm causes the anterior interosseous syndrome
Common mechanisms: Tight cast, forearm bone fracture
Motor deficit: Loss of pronation of forearm, loss of flexion of radial half of digits and thumb
Sensory deficit: NoneAt the wrist
Common mechanism: Wrist laceration
Motor deficit:
Weakness in flexion of radial half of digits and thumb, loss of abduction and opposition of thumb
Presence of an ape hand deformity when the hand is at rest may be likely, due to an hyperextension of index finger and thumb, and an adducted thumb. Nevertheless, an ape hand deformity is not a requirement for a carpal tunnel syndrome diagnosis. | A cervical rib in humans is an extra rib which arises from the seventh cervical vertebra. Their presence is a congenital abnormality located above the normal first rib. A cervical rib is estimated to occur in 0.2% to 0.5% (1 in 200 to 500) of the population. People may have a cervical rib on the right, left or both sides.Most cases of cervical ribs are not clinically relevant and do not have symptoms; cervical ribs are generally discovered incidentally, most often during x-rays and CT scans. However, they vary widely in size and shape, and in rare cases, they may cause problems such as contributing to thoracic outlet syndrome, because of pressure on the nerves that may be caused by the presence of the rib.A cervical rib represents a persistent ossification of the C7 lateral costal element. During early development, this ossified costal element typically becomes re-absorbed. Failure of this process results in a variably elongated transverse process or complete rib that can be anteriorly fused with the T1 first rib below. Diagnosis
On imaging, cervical ribs can be distinguished because their transverse processes are directed inferolaterally, whereas those of the adjacent thoracic spine are directed anterolaterally. Associated conditions
The presence of a cervical rib can cause a form of thoracic outlet syndrome due to compression of the lower trunk of the brachial plexus or subclavian artery. These structures become encroached upon by the cervical rib and scalene muscles. | 0-1
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Although such strategies have shown to be able to reduce the burden of scabies in these kinds of communities, debate remains about the best strategy to adopt, including the choice of drug.The resources required to implement such large-scale interventions in a cost-effective and sustainable way are significant. Furthermore, since endemic scabies is largely restricted to poor and remote areas, it is a public health issue that has not attracted much attention from policy makers and international donors. Epidemiology
Scabies is one of the three most common skin disorders in children, along with tinea and pyoderma. As of 2010, it affects about 100 million people (1.5% of the population) and its frequency is not related to gender. The mites are distributed around the world and equally infect all ages, races, and socioeconomic classes in different climates. Scabies is more often seen in crowded areas with unhygienic living conditions. Globally as of 2009, an estimated 300 million cases of scabies occur each year, although various parties claim the figure is either over- or underestimated. About 1–10% of the global population is estimated to be infected with scabies, but in certain populations, the infection rate may be as high as 50–80%. History
Scabies has been observed in humans since ancient times. Archeological evidence from Egypt and the Middle East suggests scabies was present as early as 494 BC. In the fourth century BC, Aristotle reported on "lice" that "escape from little pimples if they are pricked" – a description consistent with scabies. | In 2012, the United States Department of Justice fined GlaxoSmithKline $3 billion for withholding data, unlawfully promoting use in those under 18, and preparing an article that misleadingly reported the effects of paroxetine in adolescents with depression following its clinical trial study 329. Medical uses
Paroxetine is primarily used to treat major depressive disorder, obsessive-compulsive disorder, post-traumatic stress disorder, social anxiety disorder, and panic disorder. It is also occasionally used for agoraphobia, generalized anxiety disorder, premenstrual dysphoric disorder and menopausal hot flashes. Depression
A variety of meta analyses have been conducted to evaluate the efficacy of paroxetine in depression. They have variously concluded that paroxetine is superior or equivalent to placebo and that it is equivalent or inferior to other antidepressants. Despite this, there was no clear evidence that paroxetine was better or worse compared with other antidepressants at increasing response to treatment at any point in time. Anxiety disorders
Paroxetine was the first antidepressant approved in the United States for the treatment of panic disorder. Several studies have concluded that paroxetine is superior to placebo in the treatment of panic disorder.Paroxetine has demonstrated efficacy for the treatment of social anxiety disorder in adults and children. It is also beneficial for people with co-occurring social anxiety disorder and alcohol use disorder. It appears to be similar to a number of other SSRIs.Paroxetine is used in the treatment of obsessive-compulsive disorder. Comparative efficacy of paroxetine is equivalent to that of clomipramine and venlafaxine. | 0-1
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Low-income women are frequently trapped in a cycle of poverty, unable to advance, affecting their ability to access and receive quality healthcare to diagnose and treat postpartum depression.Studies have also shown a correlation between a mothers race and postpartum depression. African American mothers have been shown to have the highest risk of PPD at 25%, while Asian mothers had the lowest at 11.5%, after controlling for social factors such as age, income, education, marital status, and babys health. The PPD rates for First Nations, Caucasian and Hispanic women fell in between.Migration away from a cultural community of support can be a factor in PPD. Traditional cultures around the world prioritize organized support during postpartum care to ensure the mothers mental and physical health, wellbeing, and recovery.One of the strongest predictors of paternal PPD is having a partner who has PPD, with fathers developing PPD 50% of the time when their female partner has PPD.Sexual orientation has also been studied as a risk factor for PPD. In a 2007 study conducted by Ross and colleagues, lesbian and bisexual mothers were tested for PPD and then compared with a heterosexual sample group. It was found that lesbian and bisexual biological mothers had significantly higher Edinburgh Postnatal Depression Scale scores than did the heterosexual women in the sample. Postpartum depression is more common among lesbian women than heterosexual women, which can be attributed to lesbian womens higher depression prevalence. | Codeine/paracetamol, also known as codeine/acetaminophen and co-codamol, is a compound analgesic consisting of a combination of codeine phosphate and paracetamol (acetaminophen). Codeine/paracetamol is used for the relief of mild to moderate pain when paracetamol or non-steroidal anti-inflammatory drug (NSAIDs) such as ibuprofen, aspirin or naproxen alone do not sufficiently relieve symptoms.In 2019, it was the 173rd most commonly prescribed medication in the United States, with more than 3 million prescriptions. Combination products containing codeine are available over the counter in Barbados, United Kingdom, Israel and Costa Rica. Of the European Union (EU) member states, 12 countries (Bulgaria, Cyprus, Denmark, Estonia, France, Ireland, Latvia, Lithuania, Malta, Poland, Romania, Slovenia) allow the sale of OTC codeine solid dosage forms. Side effects
The most common side effects of co-codamol are constipation and feeling sick (nausea) or sleepy. Other side effects may include blood from mouth, skin rashes, dizziness, sedation, shortness of breath, hypersensitivity reaction, fainting (syncope or near syncope), confusion, loss of short-term memory, changes in blood, allergic reactions, euphoria, dysphoria, abdominal pain, itchiness, easy bruising, bleeding gums, vivid dreams, dry mouth and addiction.Genetic differences between people give rise to differing rates of metabolism of codeine to morphine. In about 5% of people this may happen particularly fast, leading to higher levels of morphine being passed through breast milk in amounts potentially able to cause fatal respiratory depression of a breastfed baby. References
External links
"Acetaminophen mixture with codeine phosphate". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Microphthalmia in newborns is sometimes associated with fetal alcohol spectrum disorder or infections during pregnancy, particularly herpes simplex virus, rubella and cytomegalovirus (CMV), but the evidence is inconclusive.The following genes, many of which are transcription and regulatory factors, have been implicated in microphthalmia, anophthalmia, and coloboma:
SOX2 has been implicated in a substantial number (10–15%) of cases and in many other cases failure to develop the ocular lens often results in microphthalmia.Microphthalmia-associated transcription factor (MITF), located on chromosome 14q32, is associated with one form of isolated microphthalmia (MCOP1). In mammals, the failure of expression of MITF in the retinal pigment epithelium prevents this structure from fully differentiating, causing a malformation of the choroid fissure of the eye and drainage of vitreous body fluid. Without this fluid, the eye fails to enlarge, resulting in microphthalmia. Waardenburg syndrome type 2 in humans may also be caused by mutations in MITF The human MITF gene is homologous to the mouse microphthalmia gene (gene symbol mi); mouse with mutations in this gene are hypopigmented in their fur. The identification of the genetics of WS type 2 owes a lot to observations of phenotypes of MITF-mutant mice. Diagnosis
Microphthalmia is often diagnosed soon after birth. An initial diagnosis usually occurs after the eyes are inspected through the lids. In addition to visual examinations, measurements of the cornea are used in the diagnosis of this condition. An ultrasound may also be conducted to confirm whether the axial length of the eye is clinically below average (i.e. | In these unilateral cases, eye glasses may be worn to offer a measure of physical protection.A key aspect of managing this condition is accounting for the small volume of the eye. The small orbit size characteristic of microphthalmia can impact the growth and structural development of the face after birth. As a result, microphthalmia can cause hemifacial asymmetry. This possibility is a particular concern for individuals with unilateral cases of microphthalmia. With one eye of average size, the asymmetry often becomes much more severe as the child ages. An axial length of less than 16 mm (0.63 in) indicates that a microphthalmic eyes growth will not be sufficient, and intervention will be necessary to reduce the degree of facial asymmetry.Minimizing facial asymmetry is important for cosmetic and structural reasons. In order to address the size discrepancy of the affected eye(s), it is important to begin eye socket expansion early in life. The face reaches 70% of its adult size by roughly 2 years of age, and 90% of its adult size by about 5.5 years of age. Additionally, the symmetry fostered by early socket expansion allows for a better prosthetic fit later in life. Typically, an infant begins wearing a conformer, or an unpainted ocular prosthesis, in the first weeks of life. The conformer is repeatedly replaced with a prothesis of a slightly larger size. This process, which takes place during the first 5 years of life, gradually enlarges the eye socket. | 11
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Many other factors also affect nerve recovery. The use of autologous nerve grafting procedures that involve redirection of regenerative donor nerve fibers into the graft conduit has been successful in restoring target muscle function. Localized delivery of soluble neurotrophic factors may help promote the rate of axon regeneration observed within these graft conduits.An expanding area of nerve regeneration research deals with the development of scaffolding and bio-conduits. Scaffolding developed from bio-compatible material would be useful in nerve regeneration if they successfully exhibit essentially the same role as the endoneurial tubes and Schwann cells do in guiding regrowing axons. Prevention of nerve injuries
Methods to help prevent peripheral nerve injuries include injection pressure monitoring. The presence of a high opening injection pressure (> 20 PSI) is a sensitive sign of intrafascicular/intraneural needle tip placement. Extrafascicular needle tip placement is associated with low pressures (< 20 PSI). Also, high pressure injection was associated with neurologic deficits and severe axonal damage after the block. Other methods of preventing peripheral nerve injury include electrical nerve stimulation and ultrasonography. Electrical stimulation with a motor response at < 0.2 mA only can occur with an intraneural/intrafasciular needle tip location. See also
Brain injury
References
== External links == | Complications
Arrhythmias
Pulmonary edema
Peripheral emboli
Spread (metastasis) of the tumor
Blockage of the mitral heart valve
Stroke
Fusiform cerebral aneurysms
Causes
Myxomata are the most common type of adult primary heart tumor. Most myxomata arise sporadically (90%), and only about 10% are thought to arise due to inheritance.About 10% of myxomata are inherited, as in Carney syndrome. Such tumors are called familial myxomata. They tend to occur in more than one part of the heart at a time, and often cause symptoms at a younger age than other myxomata. Other abnormalities are observed in people with Carney syndrome include skin myxomata, pigmentation, endocrine hyperactivity, schwannomas and epithelioid blue nevi. Myxomata are more common in women than men. Diagnosis
A doctor will listen to the heart with a stethoscope. A "tumor plop" (a sound related to movement of the tumor), abnormal heart sounds, or a murmur similar to the mid-diastolic rumble of mitral stenosis may be heard. These sounds may change when the patient changes position.Right atrial myxomata rarely produce symptoms until they have grown to be at least 13 cm (about 5 inches) wide.Tests may include:
Echocardiogram and Doppler study
Chest x-ray
CT scan of chest
Heart MRI
Left heart angiography
Right heart angiography
ECG—may show atrial fibrillationBlood tests:
Blood tests: An FBC may show anemia and increased WBCs (white blood cells). The erythrocyte sedimentation rate (ESR) is usually increased. Blood tests: An FBC may show anemia and increased WBCs (white blood cells). The erythrocyte sedimentation rate (ESR) is usually increased. Treatment
The surgery is treatment of choice, tumor must be surgically removed. Some patients will also need their mitral valve replaced. | 0-1
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High frequency of bowel movements, weight loss, nausea, fatigue, and fever are also common during disease flares. Chronic bleeding from the GI tract, chronic inflammation, and iron deficiency often leads to anemia, which can affect quality of life.The clinical presentation of ulcerative colitis depends on the extent of the disease process. Up to 15% of individuals may have severe disease upon initial onset of symptoms. A substantial proportion (up to 45%) of people with a history of UC without any ongoing symptoms (clinical remission) have objective evidence of ongoing inflammation. Ulcerative colitis is associated with a generalized inflammatory process that can affect many parts of the body. Sometimes, these associated extra-intestinal symptoms are the initial signs of the disease. Extent of involvement
In contrast to Crohns disease, which can affect areas of the gastrointestinal tract outside of the colon, ulcerative colitis is usually confined to the colon. Inflammation in ulcerative colitis is usually continuous, typically involving the rectum, with involvement extending proximally (to sigmoid colon, ascending colon, etc.). In contrast, inflammation with Crohns disease is often patchy, with so-called "skip lesions" (intermittent regions of inflamed bowel).The disease is classified by the extent of involvement, depending on how far the disease extends: proctitis (rectal inflammation), left sided colitis (inflammation extending to descending colon), and extensive colitis (inflammation proximal to the descending colon). Proctosigmoiditis describes inflammation of the rectum and sigmoid colon. Pancolitis describes involvement of the entire colon, extending from the rectum to the cecum. | Male adrenoleukodystrophy phenotypes
Female adrenoleukodystrophy phenotypes
Genetics
ALD is caused by mutations in ABCD1, located at Xq28 and demonstrates X-linked recessive inheritance. The gene ABCD1 encodes a peroxisomal membrane transporter which is responsible for transporting very long chain fatty acid substrate into the peroxisomes for degradation. Mutations in this gene that interfere with this process cause this syndrome.Males with an ABCD1 mutation are hemizygous, as they only have a single X chromosome. Female carriers will typically avoid the most severe manifestations of the disease, but often become symptomatic later in life. Although the detection of an ABCD1 mutation identifies an individual who is affected with a form of ALD, there is no genotype–phenotype correlation. Within a family, there will often be several different phenotypes, despite the presence of the same causative mutation. In one case, a family with six affected members displayed five different phenotypes. There are no common mutations that cause ALD, most are private or familial. Almost 600 different mutations have been identified, approximately half are missense mutations, one quarter are frameshifts, with in-frame deletions and splicing defects making up the remainder. The incidence of new mutations in ALD (those occurring spontaneously, rather than being inherited from a carrier parent) is estimated at 4.1%, with the possibility that these are due to germline mosaicism. Pathogenesis
The exact cause for the varied collection of symptoms found in the different ALD phenotypes is not clear. The white matter of the brain, the Leydig cells of the testes and the adrenal cortex are the most severely affected systems. | 0-1
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Proximal bilateral pudendal neuropathy has been demonstrated in patients with rectal prolapse who have fecal incontinence. This finding was shown to be absent in healthy subjects, and may be the cause of denervation-related atrophy of the external anal sphincter. Some authors suggest that pudendal nerve damage is the cause for pelvic floor and anal sphincter weakening, and may be the underlying cause of a spectrum of pelvic floor disorders.Sphincter function in rectal prolapse is almost always reduced. This may be the result of direct sphincter injury by chronic stretching of the prolapsing rectum. Alternatively, the intussuscepting rectum may lead to chronic stimulation of the rectoanal inhibitory reflex (RAIR - contraction of the external anal sphincter in response to stool in the rectum). The RAIR was shown to be absent or blunted. Squeeze (maximum voluntary contraction) pressures may be affected as well as the resting tone. This is most likely a denervation injury to the external anal sphincter.The assumed mechanism of fecal incontinence in rectal prolapse is by the chronic stretch and trauma to the anal sphincters and the presence of a direct conduit (the intussusceptum) connecting rectum to the external environment which is not guarded by the sphincters.The assumed mechanism of obstructed defecation is by disruption to the rectum and anal canals ability to contract and fully evacuate rectal contents. | Cystica profunda is characterized by formation of mucin cysts in the muscle layers of the gut lining, and it can occur anywhere along the gastrointestinal tract. When it occurs in the rectum, some believe to be an interchangeable diagnosis with SRUS since the histologic features of the conditions overlap. Indeed, CCP is managed identically to SRUS.Electromyography may show pudendal nerve motor latency. Complications
Complications are uncommon, but include massive rectal bleeding, ulceration into the prostate gland or formation of a stricture. Very rarely, cancer can arise on the section of prolapsed rectal lining. Diagnosis and investigations
SRUS is commonly misdiagnosed, and the diagnosis is not made for 5–7 years. Clinicians may not be familiar with the condition, and treat for Inflammatory bowel disease, or simple constipation.The thickened lining or ulceration can also be mistaken for types of cancer.The differential diagnosis of SRUS (and CCP) includes:
polyps
endometriosis
inflammatory granulomas
infectious disorders
drug-induced colitis
mucus-producing adenocarcinomaDefecography, sigmoidoscopy, transrectal ultrasound, mucosal biopsy, anorectal manometry and electromyography have all been used to diagnose and study SRUS. Some recommend biopsy as essential for diagnosis since ulcerations may not always be present, and others state defecography as the investigation of choice to diagnose SRUS. Treatment
Although SRUS is not a medically serious disease, it can be the cause of significantly reduced quality of life for patients. It is difficult to treat, and treatment is aimed at minimizing symptoms. Stopping straining during bowel movements, by use of correct posture, dietary fiber intake (possibly included bulk forming laxatives such as psyllium), stool softeners (e.g. | 11
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amalgam particles can contaminate dental floss and lead to linear amalgam tattoos in between the teeth, especially if flossing is carried out immediately after placement of an amalgam filling with a mesial or distal aspect
Polishing of an amalgam filling
The pressure from high speed turbine dental drills can be enough to force amalgam particles into soft tissue, as may occur when an old amalgam filling is being removed
When a tooth with an amalgam filling is extracted,: 183 e.g. broken bits of amalgam filling falling into an extraction socket unnoticed
When an amalgam filling is placed in the same appointment as a tooth extracted, as may occur in "quadrant dentistry"
Apicectomies are common causes of amalgam tattoo, since the amalgam is being placed inside the alveolus and the soft tissues are replaced on topOver time, the amalgam particles embedded in the soft tissues corrode. : 183 Macrophages take up the exogenous particles, and the silver in amalgam leads to staining of collagen fibers. : 183 A similar appearance can be caused by implantation of graphite (e.g. from pencil leads), and is sometimes termed a graphite tattoo, although this is less common than tattooing with amalgam. : 138
Diagnosis
The diagnosis is clinical. : 138 Amalgam tattoo can be distinguished from other causes of localized oral pigmentation because it does not change significantly in size or color,: 138 although it may appear to slowly enlarge for several months after the initial implantation of the metal particles. : 183 Some amalgam tattoos appear radio-opaque on radiographs (i.e. | Telangiectasia macularis eruptiva perstans is persistent, pigmented, asymptomatic eruption of macules usually less than 0.5 cm in diameter with a slightly reddish-brown tinge. : 616
See also
Mastocytosis
Skin lesion
List of cutaneous conditions
References
== External links == | 0-1
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The ICD-10 specifies that mild forms of sadomasochism "are commonly used to enhance otherwise normal sexual activity" (p. 172), and that the diagnosis would apply only if the behavior is preferred or required for sexual gratification. The condition is classified as one of the disorders of sexual preference, which includes the paraphilias (p. 170). Paraphilic coercive disorder refers to the preference for non-consenting over consenting sexual partners. It differs from sexual sadism disorder in that although the individual with this disorder may inflict pain or threats of pain in order to gain the compliance of the victim, the infliction of pain is not the individuals actual goal. The condition is typically described as a paraphilia and continues to undergo research, but does not appear in the current DSM or ICD. Alternate terms for the condition have included Biastophilia, Coercive Paraphilic Disorder, and Preferential Rape.BDSM or "bondage/discipline dominance/submission sadomasochism" is a colloquial term referring to the subculture of individuals who willingly engage in consenting forms of mild or simulated pain or humiliation. It is not currently a diagnosable condition in either the DSM or ICD system. Alternative terms have included Bondage and Discipline (B&D), Domination and Submission (D&S), and Sadism and Masochism (S&M). In scientific research, this sexual preference has also been called the hyperdominance pattern of sexual behavior. Unlike individuals with sexual sadism disorder or paraphilic coercive disorder, individuals with hyperdominance seek to provoke pleasure in their partner(s) with the pain/humiliation. | Most of the people diagnosed with sexual sadism disorder come to the attention of authorities by committing sexually motivated crimes. Surveys have also been conducted to include people who are interested in only mild and consensual forms of sexual pain/humiliation (BDSM).Most people with full-blown sexual sadism disorder are male, whereas the sex ratio of people interested in BDSM is closer to 2:1 male-to-female.People with sexual sadism disorder are at an elevated likelihood of having other paraphilic sexual interests. Typology
Criminologist Lee Mellor created a six typology of sexually sadistic homicide offenders, based upon a combination of three binary factors: Destructive versus Preservative: Destructive sex sadists mutilate the bodies of their living victims, while Preservative sex sadists do not. Prolonged versus Brief: The Prolonged sex sadist tortures their victim for an hour or more, while the Brief sex sadist does so over less time. Elaborate versus Simple: Where Simple sex sadists tend to use one or two methods of torture, Elaborate sadists have three of the following four characteristics, (i) variation in torture methods, (ii) complex torture apparatus, (iii) psychological torture, (iv) record making (e.g., using notes/media to document the process). | 11
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These chemicals promote the migration of different kinds of cells that are heterozygous for the NF1 gene into the hyperplastic lesions created by the nonmyelinating Schwann cells. These cell types include fibroblasts, perineurial cells, endothelial cells, and mast cells. The mast cells then secrete mitogens or survival factors that alter the developing tumor microenvironment and result in neurofibroma formation. Dermal and plexiform neurofibromas differ in later development stages, but the details are unclear at this point. Diagnosis
Dermal neurofibromas may be 2 to 20 mm in diameter, is soft, flaccid, and pinkish-white, and frequently this soft small tumor can be invaginated, as if through a ring in the skin by pressure with the finger, a maneuver called "button-holing". : 619 A blood test for protein melanoma inhibitory activity may be used to detect the presence of neurofibromas.A biopsy can be used for histopathology diagnosis. Treatments
Dermal neurofibroma
Dermal neurofibromas are not usually surgically removed unless they are painful or disfiguring, because there are generally so many of them and they are not dangerous. CO2 lasers have been used to remove dermal neurofibromas. In a paper titled Hypertrophic Scars After Therapy with CO2 Laser for Treatment of Multiple Cutaneous Neurofibromas Ostertag et al. said this about treatment by laser: "The cosmetic disfigurement is the most important issue in the decision to treat cutaneous symptoms of neurofibromatosis. Treating patients with extensive neurofibromas with [a] CO2 laser is still the best choice. | Cause
This section discusses the tumorigenesis of neurofibroma in terms of genetics, cell signaling, histology and the cell cycle. Neurofibromin 1 gene
The NF1 gene is composed of 60 exons spanning 350kb of genomic data, and maps to chromosomal region 17qll.2. This gene codes for neurofibromin which is a large 220-250 KDa cytoplasmic protein that is composed of 2,818 amino acids with three alternatively spliced exons (9a, 23a and 48a) in the encoding gene. The functional part of neurofibromin is a GAP, or GTPase-activating protein. GAP accelerates the conversion of the active GTP-bound RAS to its inactive GDP-bound form, inactivating RAS and reducing RAS-mediated growth signaling. Loss of RAS control leads to increased activity of other signaling pathways including RAF, ERK1/2, PI3K, PAK and mTOR-S6 kinase. This increased activity of downstream RAS pathways might work together to increase cell growth and survival. Genes that code for proteins that regulate cell growth, such as NF1 and TP53, are referred to as tumor suppressor genes. Neurofibromin has other growth-regulatory properties besides its ability to regulate RAS activity, but these other functions are poorly understood at this time. Schwann cells
There are two kinds of Schwann cells, myelinating and nonmyelinating. While myelinating Schwann cells cover large diameter (>1 micrometer) peripheral nervous system (PNS) axons with myelin, nonmyelinating Schwann cells encapsulate small diameter PNS axons with their cytoplasmic processes. Nonmyelinating Schwann cells are the neoplastic element in neurofibromas. This conglomeration of nonmyelinating Schwann cells and axons is called a Remak bundle. | 11
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When removing gloves, “grasp outer edge of glove near wrist, peel away from hand turning inside out, hold removed glove in opposite gloved hand, slide ungloved finger under wrist of gloved hand so finger is inside gloved area, peel off the glove from inside creating a ‘bag’ for both gloves, dispose of gloves in proper waste receptacle”.The inappropriate use of PPE equipment such as gloves, has been linked to an increase in rates of the transmission of infection, and the use of such must be compatible with the other particular hand hygiene agents used. Research studies in the form of randomized controlled trials and simulation studies are needed to determine the most effective types of PPE for preventing the transmission of infectious diseases to healthcare workers. There is low quality evidence that supports making improvements or modifications to personal protective equipment in order to help decrease contamination. Examples of modifications include adding tabs to masks or gloves to ease removal and designing protective gowns so that gloves are removed at the same time. In addition, there is weak evidence that the following PPE approaches or techniques may lead to reduced contamination and improved compliance with PPE protocols: Wearing double gloves, following specific doffing (removal) procedures such as those from the CDC, and providing people with spoken instructions while removing PPE. Antimicrobial surfaces
Microorganisms are known to survive on non-antimicrobial inanimate touch surfaces (e.g., bedrails, over-the-bed trays, call buttons, bathroom hardware, etc.) for extended periods of time. | Prednicarbate is a relatively new topical corticosteroid drug. It is similar in potency to hydrocortisone. Corticosteroids have always been an important part of the pharmacological arsenal of dermatology; however, their tendency to produce side-effects has caused the need to search for new preparations.It is nonhalogenated. == References == | 0-1
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In the whole midgut, activity rises from a baseline of approximately three enzyme units (EU) per midgut to a maximum of 12 EU at 30 hours after the blood meal, subsequently falling to baseline levels by 60 hours. A similar cycle of activity occurs in the posterior midgut and posterior midgut lumen, whereas aminopeptidase in the posterior midgut epithelium decreases in activity during digestion. Aminopeptidase in the anterior midgut is maintained at a constant, low level, showing no significant variation with time after feeding. Alpha-glucosidase is active in anterior and posterior midguts before and at all times after feeding. In whole midgut homogenates, alpha-glucosidase activity increases slowly up to 18 hours after the blood meal, then rises rapidly to a maximum at 30 hours after the blood meal, whereas the subsequent decline in activity is less predictable. All posterior midgut activity is restricted to the posterior midgut lumen. Depending on the time after feeding, greater than 25% of the total midgut activity of alpha-glucosidase is located in the anterior midgut. After blood meal ingestion, proteases are active only in the posterior midgut. Trypsin is the major primary hydrolytic protease and is secreted into the posterior midgut lumen without activation in the posterior midgut epithelium. Aminopeptidase activity is also luminal in the posterior midgut, but cellular aminopeptidases are required for peptide processing in both anterior and posterior midguts. | In many species, the female needs to obtain nutrients from a blood meal before it can produce eggs, whereas in many other species, obtaining nutrients from a blood meal enables the mosquito to lay more eggs. A mosquito has a variety of ways of finding nectar or its prey, including chemical, visual, and heat sensors. Both plant materials and blood are useful sources of energy in the form of sugars, and blood also supplies more concentrated nutrients, such as lipids, but the most important function of blood meals is to obtain proteins as materials for egg production.When a female reproduces without such parasitic meals, it is said to practice autogenous reproduction, as in Toxorhynchites; otherwise, the reproduction may be termed anautogenous, as occurs in mosquito species that serve as disease vectors, particularly Anopheles and some of the most important disease vectors in the genus Aedes. In contrast, some mosquitoes, for example, many Culex, are partially anautogenous: they do not need a blood meal for their first cycle of egg production, which they produce autogenously; subsequent clutches of eggs are produced anautogenously, at which point their disease vectoring activity becomes operative.Among humans, the feeding preferences of mosquitoes typically include: those with type O blood, heavy breathers, an abundance of skin bacteria, high body heat, and pregnant women. Individuals attractiveness to mosquitoes also has a heritable, genetically-controlled component.Female mosquitoes hunt their blood host by detecting organic substances such as carbon dioxide (CO2) and 1-octen-3-ol (mushroom alcohol, found in exhaled breath) produced from the host, and through visual recognition. | 11
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In the same year, WSS was established as a new heritable disorder of connective tissue that appeared to be transmitted as an
. In 1993, WSS was diagnosed in a mother and her son. Both patients displayed decreased elastic recoil of the skin and an increase in the number of palmar creases. In 1999, there were up to nine reported cases of WSS. In 2008, Kornak et al. investigated glycosylation of serum proteins with individuals with WSS and found that they had defects in N-glycosylation at the level of the Golgi apparatus. References
NIH GARD (Genetic and Rare Diseases Information Center)
Monarch Initiative
Online Mendelian Inheritance in Man Database
See also
Ehlers–Danlos syndrome
Cutis Laxa Type II
List of cutaneous conditions
References
== External links == | In amyloidoma, there will be low T1 signal with gadolinium injection and low T2 signal.The type of the amyloid protein can be determined in various ways: the detection of abnormal proteins in the bloodstream (on protein electrophoresis or light chain determination); binding of particular antibodies to the amyloid found in the tissue (immunohistochemistry); or extraction of the protein and identification of its individual amino acids. Immunohistochemistry can identify AA amyloidosis the majority of the time, but can miss many cases of AL amyloidosis. Laser microdissection with mass spectrometry is the most reliable method of identifying the different forms of amyloidosis.AL was previously considered the most common form of amyloidosis, and a diagnosis often begins with a search for plasma cell dyscrasia, memory B cells producing aberrant immunoglobulins or portions of immunoglobulins. Immunofixation electrophoresis of urine or serum is positive in 90% of people with AL amyloidosis. Immunofixation electrophoresis is more sensitive than regular electrophoresis but may not be available in all centers. Alternatively immunohistochemical staining of a bone marrow biopsy looking for dominant plasma cells can be sought in people with a high clinical suspicion for AL amyloidosis but negative electrophoresis.ATTR is now considered to be the most common form of amyloidosis, and no longer considered as a rare disease. It may be either age related in wild-type ATTR (ATTRv) or familial transthyretin-associated amyloidosis, is suspected in people with family history of idiopathic neuropathies or heart failure who lack evidence of plasma cell dyscrasias. | 0-1
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The International Study of Unruptured Intracranial Aneurysms (ISUIA) provided prognostic data both in people having previously had a subarachnoid hemorrhage and people who had aneurysms detected by other means. Those having previously had a SAH were more likely to bleed from other aneurysms. In contrast, those having never bled and had small aneurysms (smaller than 10 mm) were very unlikely to have a SAH and were likely to sustain harm from attempts to repair these aneurysms. On the basis of the ISUIA and other studies, it is now recommended that people are considered for preventive treatment only if they have a reasonable life expectancy and have aneurysms that are highly likely to rupture. Moreover, there is only limited evidence that endovascular treatment of unruptured aneurysms is actually beneficial. Treatment
Management involves general measures to stabilize the person while also using specific investigations and treatments. These include the prevention of rebleeding by obliterating the bleeding source, prevention of a phenomenon known as vasospasm, and prevention and treatment of complications.Stabilizing the person is the first priority. Those with a depressed level of consciousness may need to be intubated and mechanically ventilated. Blood pressure, pulse, respiratory rate, and Glasgow Coma Scale are monitored frequently. Once the diagnosis is confirmed, admission to an intensive care unit may be preferable, especially since 15 percent may have further bleeding soon after admission. Nutrition is an early priority, mouth or nasogastric tube feeding being preferable over parenteral routes. | History
The introduction and use of ampicillin alone started in 1961. The development and introduction of this drug allowed the use of targeted therapies against gram-negative bacteria. With the rise of beta-lactamase producing bacteria, ampicillin and the other penicillin-derivatives became ineffective to these resistant organisms. With the introduction of beta-lactamase inhibitors such as sulbactam, combined with ampicillin made beta-lactamase producing bacteria susceptible. Formulation
Ampicillin-sulbactam only comes in a parenteral formulation to be either used as intravenous or intramuscular injections, and can be formulated for intravenous infusion. It is formulated in a 2:1 ratio of ampicillin:sulbactam. The commercial preparations available include:
1.5 grams (1 gram ampicillin and 0.5 gram sulbactam)→Brand names: Unasyn, Unasyn ADD-Vantage, Unasyn Piggyback
3 grams (2 grams ampicillin and 1 gram sulbactam)→Brand names: Unasyn, Unasyn ADD-Vantage, Unasyn Piggyback
15 grams (10 grams ampicillin and 5 grams sulbactam)→Brand name: Unasyn
Society and culture
Names
Unasyn (US)
Subacillin (Taiwan)
Unictam (Egypt)
Ultracillin (Egypt)
Fortibiotic
Sulbin (Egypt)
Novactam (Egypt)
Sulbacin (Kenya)
References
External links
"Ampicillin mixture with Sulbactam". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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In E. coli, glucose catabolite repression is regulated by the phosphotransferase system, a multi-protein phosphorylation cascade that couples glucose uptake and metabolism. Culture growth
Optimum growth of E. coli occurs at 37 °C (99 °F), but some laboratory strains can multiply at temperatures up to 49 °C (120 °F). E. coli grows in a variety of defined laboratory media, such as lysogeny broth, or any medium that contains glucose, ammonium phosphate monobasic, sodium chloride, magnesium sulfate, potassium phosphate dibasic, and water. Growth can be driven by aerobic or anaerobic respiration, using a large variety of redox pairs, including the oxidation of pyruvic acid, formic acid, hydrogen, and amino acids, and the reduction of substrates such as oxygen, nitrate, fumarate, dimethyl sulfoxide, and trimethylamine N-oxide. E. coli is classified as a facultative anaerobe. It uses oxygen when it is present and available. It can, however, continue to grow in the absence of oxygen using fermentation or anaerobic respiration. The ability to continue growing in the absence of oxygen is an advantage to bacteria because their survival is increased in environments where water predominates. Cell cycle
The bacterial cell cycle is divided into three stages. The B period occurs between the completion of cell division and the beginning of DNA replication. The C period encompasses the time it takes to replicate the chromosomal DNA. The D period refers to the stage between the conclusion of DNA replication and the end of cell division. The doubling rate of E. coli is higher when more nutrients are available. | This may be done by using formate to reduce electron carriers and supply the ATP required in anabolic pathways inside of these synthetic autotrophs.E. coli have three native glycolytic pathways: EMPP, EDP, and OPPP. The EMPP employs ten enzymatic steps to yield two pyruvates, two ATP, and two NADH per glucose molecule while OPPP serves as an oxidation route for NADPH synthesis. Although the EDP is the more thermodynamically favourable of the three pathways, E. coli do not use the EDP for glucose metabolism, relying mainly on the EMPP and the OPPP. The EDP mainly remains inactive except for during growth with gluconate. Catabolite repression
When growing in the presence of a mixture of sugars, bacteria will often consume the sugars sequentially through a process known as catabolite repression. By repressing the expression of the genes involved in metabolizing the less preferred sugars, cells will usually first consume the sugar yielding the highest growth rate, followed by the sugar yielding the next highest growth rate, and so on. In doing so the cells ensure that their limited metabolic resources are being used to maximize the rate of growth. The well-used example of this with E. coli involves the growth of the bacterium on glucose and lactose, where E. coli will consume glucose before lactose. Catabolite repression has also been observed in E. coli in the presence of other non-glucose sugars, such as arabinose and xylose, sorbitol, rhamnose, and ribose. | 11
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Acquired idiopathic generalized anhidrosis (AIGA) is characterized by generalized absence of sweating without other autonomic and neurologic dysfunction.AIGA is classified into 3 subgroups: idiopathic pure sudomotor failure (IPSF), sweat gland failure (SGF), and sudomotor neuropathy, with each subgroup presenting a different pathogenesis. Diagnosis
Quantitative sudomotor axon reflex test and microneurography are used in the diagnosis of AIGA. However, these refined methods are mostly used for research purposes and not generally available.Skin biopsy analysis may play a crucial role in the identification of AIGA subgroups. See also
Hypohidrosis
References
== External links == | Tobacco use is associated with an increase in keratinization of the oral mucosa. In extreme forms, this may manifest as leukoplakia or stomatitis nicotina (smokers keratosis). This increased keratinization may mechanically reinforce the mucosa and reduce the tendency of ulcers to form after minor trauma, or present a more substantial barrier to microbes and antigens, but this is unclear. Nicotine is also known to stimulate production of adrenal steroids and reduce production of TNF-α, interleukin-1 and interleukin-6. Smokeless tobacco products also seem to protect against aphthous stomatitis. Cessation of smoking is known to sometimes precede the onset of aphthous stomatitis in people previously unaffected, or exacerbate the condition in those who were already experiencing aphthous ulceration. Despite this correlation, starting smoking again does not usually lessen the condition. Antigenic sensitivity
Various antigenic triggers have been implicated as a trigger, including L forms of streptococci, herpes simplex virus, varicella-zoster virus, adenovirus, and cytomegalovirus. Some people with aphthous stomatitis may show herpes virus within the epithelium of the mucosa, but without any productive infection. In some persons, attacks of ulceration occur at the same time as asymptomatic viral shedding and elevated viral titres.In some instances, recurrent mouth ulcers may be a manifestation of an allergic reaction. Possible allergens include certain foods (e.g., chocolate, coffee, strawberries, eggs, nuts, tomatoes, cheese, citrus fruits, benzoates, cinnamaldehyde, and highly acidic foods), toothpastes, and mouthwashes. | 0-1
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Women with gestational diabetes who receive lifestyle interventions seem to have less postpartum depression, and were more likely to reach their weight loss targets after giving birth, than women who had no intervention. Their babies are also less likely to be large for their gestational age, and have less percentage of fat when they are born. More research is needed to find out which lifestyle interventions are best. Some women with GDM use probiotics but it is very uncertain if there are any benefits in terms of blood glucose levels, high blood pressure disorders or induction of labour.If a diabetic diet or G.I. Diet, exercise, and oral medication are inadequate to control glucose levels, insulin therapy may become necessary. The development of macrosomia can be evaluated during pregnancy by using sonography. Women who use insulin, with a history of stillbirth, or with hypertension are managed like women with overt diabetes. Lifestyle
Counselling before pregnancy (for example, about preventive folic acid supplements) and multidisciplinary management are important for good pregnancy outcomes. Most women can manage their GDM with dietary changes and exercise. Self monitoring of blood glucose levels can guide therapy. Some women will need antidiabetic drugs, most commonly insulin therapy. Any diet needs to provide sufficient calories for pregnancy, typically 2,000–2,500 kcal with the exclusion of simple carbohydrates. The main goal of dietary modifications is to avoid peaks in blood sugar levels. This can be done by spreading carbohydrate intake over meals and snacks throughout the day, and using slow-release carbohydrate sources—known as the G.I. Diet. | Sclerema neonatorum is a rare and severe skin condition that is characterized by diffuse hardening of the subcutaneous tissue with minimal inflammation. It usually affects premature, ill newborns. Prognosis is poor. Minimal inflammation helps distinguish sclerema neonaturum from subcutaneous fat necrosis of the newborn. See also
Panniculitis
Skin lesion
List of cutaneous conditions
References
== External links == | 0-1
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They can cause vasospasm including coronary vasospasm and are contraindicated in people with coronary artery disease. Magnesium
Magnesium is recognized as an inexpensive, over-the-counter supplement which some studies have shown to be effective in both preventing and treating migraine in intravenous form. Other
Intravenous metoclopramide, intravenous prochlorperazine, or intranasal lidocaine are other potential options. Metoclopramide or prochlorperazine are the recommended treatment for those who present to the emergency department. Haloperidol may also be useful in this group. A single dose of intravenous dexamethasone, when added to standard treatment of a migraine attack, is associated with a 26% decrease in headache recurrence in the following 72 hours. Spinal manipulation for treating an ongoing migraine headache is not supported by evidence. It is recommended that opioids and barbiturates not be used due to questionable efficacy, addictive potential, and the risk of rebound headache. There is tentative evidence that propofol may be useful if other measures are not effective.Occipital nerve stimulation, may be effective but has the downsides of being cost-expensive and has a significant amount of complications.There is modest evidence for the effectiveness of non-invasive neuromodulatory devices, behavioral therapies and acupuncture in the treatment of migraine headaches. There is little to no evidence for the effectiveness of physical therapy, chiropractic manipulation and dietary approaches to the treatment of migraine headaches. | Neurostimulation uses noninvasive or implantable neurostimulators similar to pacemakers for the treatment of intractable chronic migraine with encouraging results for severe cases. A transcutaneous electrical nerve stimulator and a transcranial magnetic stimulator are approved in the United States for the prevention of migraines. There is also tentative evidence for transcutaneous electrical nerve stimulation decreases the frequency of migraines. Migraine surgery, which involves decompression of certain nerves around the head and neck, may be an option in certain people who do not improve with medications. Management
There are three main aspects of treatment: trigger avoidance, acute symptomatic control, and medication for prevention. Medications are more effective if used earlier in an attack. The frequent use of medications may result in medication overuse headache, in which the headaches become more severe and more frequent. This may occur with triptans, ergotamines, and analgesics, especially opioid analgesics. Due to these concerns simple analgesics are recommended to be used less than three days per week at most. Analgesics
Recommended initial treatment for those with mild to moderate symptoms are simple analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs) or the combination of paracetamol (also known as acetaminophen), aspirin, and caffeine. Several NSAIDs, including diclofenac and ibuprofen have evidence to support their use. Aspirin (900 to 1000 mg) can relieve moderate to severe migraine pain, with an effectiveness similar to sumatriptan. Ketorolac is available in intravenous and intramuscular formulations.Paracetamol, either alone or in combination with metoclopramide, is another effective treatment with a low risk of adverse effects. Intravenous metoclopramide is also effective by itself. | 11
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Second line anti-epileptic medications include levetiracetam, benzodiazepines (such as clonazepam), lamotrigine, carbamazepine, brivaracetam, ethosuximide, and topiramate.Photosensitive reflex epilepsy tends to decrease with age, especially in ones thirties. In 25-50% of people, seizures may spontaneously subside or disappear. Epidemiology
In 2015 epilepsy was present in about 1.3% of the population of the United States, approximately 3 million adults and 470,000 children. Reflex epilepsy is found in approximately 5% of people who have epilepsy. Photosensitive epilepsy is the most common type of reflex epilepsy, accounting for 75-80% of cases. In addition, reflex epilepsies may show preferential distribution between the two sexes or certain age groups. Photosensitive epilepsy, for example, is more common in females (60% of cases) and is also more common in younger people (7–19 years old). History
Triggering seizures in epilepsy has been a phenomenon that has been observed since ancient times. The Apologia records instances of a spinning potters wheel causing seizures in epileptic slaves. In 1850 Marshal Hall described the role of specific stimuli on causing seizures. Since then, many types of stimuli that can trigger seizures have been identified. The International League Against Epilepsy (ILAE) identified epilepsy caused by a specific stimuli in 1989 in their official definition of epilepsy and more recently, has updated this definition to recognize new types of focal and generalized seizures. Currently reflex epilepsies are classified as miscellaneous types of epilepsy and are identified by the type of triggering stimulus. References
External links
Reflex Epilepsy Overview Medscape Reference | A study regarding the efficacy of treatment with nitisinone and dietary restrictions found that 93% of people survived at two years, four years, and six years indicating the prognosis of stabilizing the HT1 disease state is positive. Epidemiology
Tyrosinemia type I affects males and females in equal numbers. Its prevalence has been estimated to be 1 in 100,000 to 120,000 births worldwide. HT1 is especially prevalent in the Saguenay-Lac Saint-Jean region of Quebec is one in 1,850 births. The elevated frequency of this disorder within individuals of French-Canadian ancestry in Quebec is believed to be due to reduced genetic heterogeneity within the original founder population for the Saguenay-Lac Saint-Jean region. The initial settlement of Saguenay Lac-Saint-Jean (SLSJ) occurred between 1838 and 1911. From a total of 28,656 settlers, 75 percent originated from the neighboring Charlevoix region. The settling of the Charlevoix region itself started in 1675 when 599 founders of mostly French descent moved to this region from the Quebec City area.Worldwide, type I tyrosinemia affects about 1 person in 100,000. This type of tyrosinemia is much more common in Quebec, Canada. The overall incidence in Quebec is about 1 in 16,000 individuals. In the Saguenay-Lac-Saint-Jean region of Quebec, type 1 tyrosinemia affects 1 person in 1,846. The carrier rate has been estimated to be between 1 in 20 and 1 in 31. History
Nitisinone was first used to clinically treat tyrosinemia type I in 1991. Nitisinone was approved by the European Medicine Agency (EMA) under exceptional circumstances in 2005. | 0-1
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The United Nations special rapporteur on the right to food, Jean Ziegler proposes that agricultural waste, such as corn cobs and banana leaves, should be used as fuel instead of crops.In some developing countries, overnutrition (in the form of obesity) is beginning to appear in the same communities where malnutrition occurs. Overnutrition increases with urbanisation, food commercialisation and technological developments and increases physical inactivity. Variations in the health status of individuals in the same society are associated with the societal structure and an individuals socioeconomic status which leads to income inequality, racism, educational differences and lack of opportunities. Diseases & conditions
Infectious diseases which increase nutrient requirements, such as gastroenteritis, pneumonia, malaria, and measles, can cause malnutrition. So can some chronic illnesses, especially HIV/AIDS.Malnutrition can also result from abnormal nutrient loss due to diarrhea or chronic small bowel illnesses, like Crohns disease or untreated coeliac disease. "Secondary malnutrition" can result from increased energy expenditure.In infants, a lack of breastfeeding may contribute to undernourishment. Anorexia nervosa and bariatric surgery can also cause malnutrition. Dietary practices
Undernutrition
Undernutrition due to lack of adequate breastfeeding is associated with the deaths of an estimated one million children annually. Illegal advertising of breast-milk substitutes contributed to malnutrition and continued three decades after its 1981 prohibition under the WHO International Code of Marketing Breast Milk Substitutes.Maternal malnutrition can also factor into the poor health or death of a baby. | Malnutrition can cause vitamin-deficiency-related diseases like scurvy and rickets. As malnutrition worsens, those affected have less energy and experience impairment in brain functions. This can make it difficult (or impossible) for them to perform the tasks needed to acquire food, earn an income, or gain an education. Malnutrition can also cause acute problems, like hypoglycemia (low blood sugar). This condition can cause lethargy, limpness, seizures, and loss of consciousness. Children are particularly at risk and can become hypoglycemic after 4 to 6 hours without food. Dehydration can also occur in malnourished people, and can be life-threatening, especially in babies and small children. Signs
There are many different signs of dehydration in malnourished people. These can include sunken eyes; a very dry mouth; decreased urine output and/or dark urine; increased heart rate with decreasing blood pressure; and altered mental status. Cognitive development
Protein-calorie malnutrition can cause cognitive impairments. This most commonly occurs in people who were malnourished during a "critical period ... from the final third of gestation to the first 2 years of life". For example, in children under two years of age, iron deficiency anemia is likely to affect brain function acutely, and probably also chronically. Similarly, folate deficiency has been linked to neural tube defects.Iodine deficiency is "the most common preventable cause of mental impairment worldwide." "Even moderate [iodine] deficiency, especially in pregnant women and infants, lowers intelligence by 10 to 15 I.Q. points, shaving incalculable potential off a nations development." | 11
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In clinical context, increased platelet and endothelial activation may be detected before symptoms appear.Hypoperfusion of the placenta is associated with abnormal modelling of the fetal–maternal placental interface that may be immunologically mediated. The pathogenesis of pre-eclampsia is poorly understood and may be attributed to factors related to the woman and placenta since pre-eclampsia is seen in molar pregnancies absent of a fetus or fetal tissue. The placenta normally produces the potent vasodilator adrenomedullin but it is reduced in pre-eclampsia and eclampsia. Other vasodilators, including prostacyclin, thromboxane A2, nitric oxide, and endothelins, are reduced in eclampsia and may lead to vasoconstriction.Eclampsia is associated with hypertensive encephalopathy in which cerebral vascular resistance is reduced, leading to increased blood flow to the brain, cerebral edema and resultant convulsions. An eclamptic convulsion usually does not cause chronic brain damage unless intracranial haemorrhage occurs. Diagnosis
If a pregnant woman has already been diagnosed with pre-eclampsia during the current pregnancy and then develops a seizure, she may be assigned a clinical diagnosis of eclampsia without further workup. While seizures are most common in the third trimester, they may occur any time from 20 weeks of pregnancy until 6 weeks after birth. Because pre-eclampsia and eclampsia are common conditions in women, eclampsia can be assumed to be the correct diagnosis until proven otherwise in pregnant or postpartum women who experience seizures. However, if a woman has a seizure and it is unknown whether or not they have pre-eclampsia, testing can help make the diagnosis clear. | The placenta may bleed (hemorrhage) or begin to separate early from the wall of the uterus. It is normal for the placenta to separate from the uterine wall during delivery, but it is abnormal for it to separate prior to delivery; this condition is called placental abruption and can be dangerous for the fetus. Placental insufficiency may also occur, a state in which the placenta fails to support appropriate fetal development because it cannot deliver the necessary amount of oxygen or nutrients to the fetus. During an eclamptic seizure, the beating of the fetal heart may become slower than normal (bradycardia). If any of these complications occurs, fetal distress may develop. Treatment of the mothers seizures may also manage fetal bradycardia. If the risk to the health of the fetus or the mother is high, the definitive treatment for eclampsia is delivery of the baby. Delivery by cesarean section may be necessary, especially if the instance of fetal bradycardia does not resolve after 10 to 15 minutes of resuscitative interventions. It may be safer to deliver the infant preterm than to wait for the full 40 weeks of fetal development to finish, and as a result prematurity is also a potential complication of eclampsia.In the mother, changes in vision may occur as a result of eclampsia, and these changes may include blurry vision, one-sided blindness (either temporary due to amaurosis fugax or potentially permanent due to retinal detachment), or cortical blindness, which affects the vision from both eyes. There are also potential complications in the lungs. | 11
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But in either form of myotonia congenita, the terms strictest sense reflects that the disease is genetically present from birth, although the clinical onset may be delayed.With the advent of genetic testing, it has recently been found that some typically recessive mutations may occur in a dominant fashion in some individuals. The reason for this is not known.Because several CLCN1 mutations can cause either Becker disease or Thomsen disease, doctors usually rely on characteristic signs and symptoms to distinguish the two forms of myotonia congenita. However, myotonia caused by CLCN1 mutations can occasionally be clinically indistinguishable from myotonia caused by sodium channel mutations (SCN4A mutations) resulting in the similar disease paramyotonia congenita.A so-called Finnish heritage disease, congenital myotonia is more common in Finland and among ethnic Finns. A molecular study of the CLCN1 gene in 24 families in northern Finland, including 46 affected individuals, showed that although the inheritance appeared to be dominant (Thomsen type), in fact it is recessive (Becker type). Differential diagnosis
Sodium channel myotonias (SCN4A)
Potassium-aggravated myotonia (acetazolamide responsive myotonia)
Paramyotonia congenita
Hyperkalemic periodic paralysisDystrophies
Myotonic dystrophy (myotonic muscular dystrophy: Type 1 and Type 2)Potassium channel disorders (KCNJ2)
Andersen-Tawil syndromeOther disorders
Thyroid disorders
Neuromyotonia (Isaacs Syndrome)
Schwartz–Jampel syndrome
Stiff person syndrome
Brody myopathy (Brody Disease, Brodys Disease, Brodys Myopathy)
Treatment
Some cases of myotonia congenita do not require treatment, or it is determined that the risks of the medication outweigh the benefits. If necessary, however, symptoms of the disorder may be relieved with quinine, ranolazine, procainamide, flecainide, phenytoin, carbamazepine, mexiletine and other anticonvulsant drugs. | This may be partly because there are over 130 currently known different mutations that can cause the disorder, each with their own specifics, and also because myotonia congenita is an ion channel disorder, and ion channels are sensitive to internal and external environmental factors. It has been shown that pregnancy and the use of diuretics aggravate myotonia, and both these conditions are linked to the loss of divalent cations such as magnesium and calcium. It has further been shown that in chemically-induced myotonia in isolated rat muscle, myotonia could be dampened by increasing the magnesium and calcium content of the extracellular medium. This has also been shown for isolated human muscle.Adrenaline/epinephrine is well known to make myotonia worse in most individuals with the disorder, and a person with myotonia congenita may experience a sudden increase in difficulty with mobility in a particularly stressful situation during which adrenaline is released.Due to the invisible nature of the disorder, the fact that those with myotonia congenita often appear very fit and able bodied, the general lack of knowledge about the disorder by the general and medical community, and often by the individual themselves, and the potential for inconsistency with the symptoms, many people with myotonia congenita have experienced a degree of social persecution at one time or another because of the effects of their disorder. | 11
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Complications
Locoregional complications include pancreatic pseudocyst (most common, occurring in up to 25% of all cases, typically after 4–6 weeks) and phlegmon/abscess formation, splenic artery pseudoaneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic vein, superior mesenteric vein and portal veins (in descending order of frequency), duodenal obstruction, common bile duct obstruction, progression to chronic pancreatitis, pancreatic ascites, pleural effusion, sterile/infected pancreatic necrosis.Systemic complications include ARDS, multiple organ dysfunction syndrome, DIC, hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin-producing beta cell damage), malabsorption due to exocrine failure
MetabolicHypocalcemia, hyperglycemia, hypertriglyceridemiaRespiratoryHypoxemia, atelectasis, Effusion, pneumonitis, Acute respiratory distress syndrome (ARDS)Renal
Renal artery or vein thrombosis
Kidney failure
Circulatory
Arrhythmias
Hypovolemia and shock
myocardial infarction
Pericardial effusion
vascular thrombosis
Gastrointestinal
Gastrointestinal hemorrhage from stress ulceration;
gastric varices (secondary to splenic vein thrombosis)
Gastrointestinal obstruction
Hepatobiliary
Jaundice
Portal vein thrombosis
Neurologic
Psychosis or encephalopathy (confusion, delusion and coma)
Cerebral Embolism
Blindness (angiopathic retinopathy with hemorrhage)
Hematologic
Anemia
DIC
Leucocytosis
Dermatologic
Painful subcutaneous fat necrosis
Miscellaneous
Subcutaneous fat necrosis
Arthalgia
Causes
Most common
Biliary pancreatitis due to gallstones or constriction of ampulla of Vater in 40% of cases
Alcohol in 30% of cases
Idiopathic in 15-25% of cases
Metabolic disorders: hereditary pancreatitis, hypercalcemia, elevated triglycerides, malnutrition
Post-ERCP
Abdominal trauma
Penetrating ulcers
Carcinoma of the head of pancreas, and other cancer
Drugs: diuretics (e.g., thiazides, furosemide), gliptins (e.g., vildagliptin, sitagliptin, saxagliptin, linagliptin), tetracycline, sulfonamides, estrogens, azathioprine and mercaptopurine, pentamidine, salicylates, steroids, Depakote
Infections: mumps, viral hepatitis, coxsackie B virus, cytomegalovirus, Mycoplasma pneumoniae, Ascaris
Structural abnormalities: choledochocele, pancreas divisum
Radiotherapy
Autoimmune pancreatitis
Severe hypertriglyceridemia
Less common
Scorpion venom
Chinese liver fluke
Ischemia from bypass surgery
Heart valve surgery
Fat necrosis
Pregnancy
Infections other than mumps, including varicella zoster
Hyperparathyroidism
Valproic acid
Cystic fibrosis
Anorexia or bulimia
Codeine phosphate reaction
Pathology
Pathogenesis
Acute pancreatitis occurs when there is abnormal activation of digestive enzymes within the pancreas. | Some physicians favor administering the maximum safe dose (calculated based on a number of factors), while others favor administering smaller doses, which may still be effective in ablating all thyroid tissue. I-131 is used for ablation of the thyroid tissue. Minimally invasive thyroidectomy has been used in recent years in cases where the nodules are small. Finding disease recurrence
Some studies have shown that thyroglobulin (Tg) testing combined with neck ultrasound is more productive in finding disease recurrence than full- or whole-body scans (WBS) using radioactive iodine. However, current protocol (in the USA) suggests a small number of clean annual WBS are required before relying on Tg testing plus neck ultrasound. When needed, whole body scans consist of withdrawal from thyroxine medication and/or injection of recombinant human Thyroid stimulating hormone (TSH). In both cases, a low iodine diet regimen must also be followed to optimize the takeup of the radioactive iodine dose. Low dose radioiodine of a few millicuries is administered. Full body nuclear medicine scan follows using a gamma camera. Scan doses of radioactive iodine may be I131 or I123. Recombinant human TSH, commercial name Thyrogen, is produced in cell culture from genetically engineered hamster cells. | 0-1
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It is 75% monohydrate and 25% macrocrystals. Contraindications
Nitrofurantoin is contraindicated in patients with decreased renal function (CrCl < 60 ml/min) due to systemic accumulation and subtherapeutic levels reached in the urinary tract. However, a retrospective chart review suggests the data for this cutoff are slim and a cutoff of CrCl < 40 ml/min would be more appropriate. Many of the severe side effects of this drug are more common in the elderly and those with renal impairment, as this causes the drug to be retained in the body and reach higher systemic levels. Thus, the drug is not recommended for the elderly population according to 2012 AGS Beers criteria.Nitrofurantoin is also contraindicated in babies up to the age of one month, as they have immature enzyme systems in their red blood cells (glutathione instability), so nitrofurantoin must not be used because it can cause haemolytic anaemia. For the same reason, nitrofurantoin should not be given to pregnant women after 38 weeks of pregnancy. Nitrofurantoin is contraindicated in patients with glucose-6-phosphate dehydrogenase deficiency (G6PD) because of risk of intravascular hemolysis resulting in anemia. Adverse effects
The most common side effects with nitrofurantoin are nausea, headache, and flatulence. | Japan did not allocate MRLs for nitrofurans leading to the implementation of a "zero tolerance or no residue standard". In Thailand, the Ministry of Health issued in 2001 Proclamation No. 231 MRL of veterinary drug in food which did not allocate MRL for nitrofurans. The Ministry of Agriculture and Cooperatives had already prohibited importation and use of furazolidone and nitrofurazone in animal feed in 1999 which was extended to all nitrofurans in 2002. Several metabolites of nitrofurans, such as furazolidone, furaltadone and nitrofurazone cause cancer or genetic damage in rats. References
External links
"Nitrofurantoin". Drug Information Portal. U.S. National Library of Medicine. | 11
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Execution of the parallel squat will develop the lower body muscles that will strengthen the hips, knees, and ankles. Technique
The last major way to prevent a tear in the meniscus is learning proper technique for the movement that is taking place. For the sports involving quick powerful movements it is important to learn how to cut, turn, land from a jump, and stop correctly. It is important to take the time out to perfect these techniques when used. These three major techniques will significantly prevent and reduce the risk of a meniscus tear. Treatment
Presently, treatments make it possible for quicker recovery. If the tear is not serious, physical therapy, compression, elevation and icing the knee can heal the meniscus. Meniscus tears are more likely to heal on their own if they are in what physicians call the "red zone," or the outer edge of the meniscus where blood supply is present. More serious tears may require surgical procedures. Surgery, however, does not appear to be better than non-surgical care. In the long term, degenerative meniscal tears are often associated with osteoarthritis. This leads to poor outcomes regardless of treatment type. In the short term, studies have shown arthroscopic partial meniscectomy (APM) is a more effective treatment with regards to function and pain management. | Radiology
X-ray images (normally during weightbearing) can be obtained to rule out other conditions or to see if the patient also has osteoarthritis. The menisci themselves cannot be visualised with plain radiographs. If the diagnosis is not clear from the history and examination, the menisci can be imaged with magnetic resonance imaging (an MRI scan). This technique has replaced previous arthrography, which involved injecting contrast medium into the joint space. In straightforward cases, knee arthroscopy allows quick diagnosis and simultaneous treatment. Recent clinical data shows that MRI and clinical testing are comparable in sensitivity and specificity when looking for a meniscal tear. Classification
A meniscal tear can be classified in various ways, such as by anatomic location or by proximity to blood supply. Various tear patterns and configurations have been described. These include:
Radial tears
Flap or parrot-beak tears
Peripheral, longitudinal tears
Bucket-handle tears
Horizontal cleavage tears
Complex, degenerative tearsThese tears can then be further classified by their proximity to the meniscus blood supply, namely whether they are located in the “red-red,” “red-white,” or “white-white” zones. The functional importance of these classifications, however, is to ultimately determine whether a meniscus is repairable. The repairability of a meniscus depends on a number of factors. These include:
Age/strength
Activity level
Tear pattern
Chronicity of the tear
Associated injuries (anterior cruciate ligament injury)
Healing potential
Prevention
Tear of a meniscus is a common injury in many sports. The menisci hold 30–50% of the body load in standing position. Some sports where a meniscus tear is common are American football, association football, ice hockey and tennis. | 11
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The de novo pathway is stimulated due to an excess of PRPP (5-phospho-D-ribosyl-1-pyrophosphate or simply phosphoribosyl-pyrophosphate).It was previously unclear whether the neurological abnormalities in LNS were due to uric acid neurotoxicity or to a relative shortage in "new" purine nucleotides during essential synthesis steps. Genetic mutations affecting the enzymes of the de novo synthesis pathway may possibly contribute to the disease, although these are rare or unknown. Uric acid has been suggested as a possible cause of neurotoxicity but this is unproven.Importantly, evidence suggests that one or more lesions in striatal dopaminergic pathways may be central to the neurological deficits, especially the choreoathetoid dyskinesia and self-mutilation. 6-hydroxydopamine toxicity in rodents may be a useful animal model for the syndrome, although this is not proven. However, the link between dopamine and purine synthesis is a nucleotide called guanosine triphosphate or GTP. The first step of dopamine synthesis is GTP cyclohydrolase, and significantly a deficiency of this step produces a syndrome that has a neuropathology similar to LNS. Thus a lack of HGPRT may produce a nucleotide deficiency (specifically: GTP deficiency) disorder, resulting in dopamine deficiency.Another animal model for LNS has been proposed to arise from oxidative damage, caused by the hyperuricemia accompanying LNS. This is based on the theory that uric acid is a powerful reducing agent and likely an important human antioxidant, in high concentration in blood. | Nizatidine is a histamine H2 receptor antagonist that inhibits stomach acid production, and is commonly used in the treatment of peptic ulcer disease and gastroesophageal reflux disease.It was patented in 1980 and approved for medical use in 1988. It was developed by Eli Lilly. Brand names include Tazac and Axid. Medical use
Nizatidine is used to treat duodenal ulcers, gastric ulcers, and gastroesophageal reflux disease (GERD/GORD), and to prevent stress ulcers. Adverse effects
Side effects are uncommon, usually minor, and include diarrhea, constipation, fatigue, drowsiness, headache, and muscle aches. History and development
Nizatidine was developed by Eli Lilly, and was first marketed in 1988. It is considered to be equipotent with ranitidine and differs by the substitution of a thiazole ring in place of the furan ring in ranitidine. In September 2000, Eli Lilly announced they would sell the sales and marketing rights for Axid to Reliant Pharmaceuticals. Subsequently, Reliant developed the oral solution of Axid, marketing this in 2004, after gaining approval from the U.S. Food and Drug Administration (FDA). However, a year later, they sold rights of the Axid Oral Solution (including the issued patent protecting the product) to Braintree Laboratories.Nizatidine proved to be the last new histamine H2 receptor antagonist introduced prior to the advent of proton pump inhibitors.Axid (nizatidine) drug recalled due to presence of NDMA. See also
Famotidine (Pepcid) — another popular H2 receptor antagonist
References
External links
"Nizatidine". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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For example, ICD-10 classifies "vasculitis limited to skin" with skin conditions (under "L"), and "necrotizing vasculopathies" (corresponding to systemic vasculitis) with musculoskeletal system and connective tissue conditions (under "M"). Arteritis/phlebitis on their own are classified with circulatory conditions (under "I"). Type or size of the blood vessels that they predominantly affect. Apart from the arteritis/phlebitis distinction mentioned above, vasculitis is often classified by the caliber of the vessel affected. However, there can be some variation in the size of the vessels affected.A small number have been shown to have a genetic basis. These include adenosine deaminase 2 deficiency and haploinsufficiency of A20. According to the size of the vessel affected, vasculitis can be classified into:
Large vessel: Takayasus arteritis, Temporal arteritis
Medium vessel: Buergers disease, Kawasaki disease, Polyarteritis nodosa
Small vessel: Behçets syndrome, Eosinophilic granulomatosis with polyangiitis, Cutaneous vasculitis, granulomatosis with polyangiitis, Henoch–Schönlein purpura, and microscopic polyangiitis. Condition of some disorders have vasculitis as their main feature. The major types are given in the table below:Takayasus arteritis, polyarteritis nodosa and giant cell arteritis mainly involve arteries and are thus sometimes classed specifically under arteritis. There are also many conditions that have vasculitis as an accompanying or atypical feature, including:
Rheumatic diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and dermatomyositis
Cancer, such as lymphomas
Infections, such as hepatitis C
Primary Immunodeficiencies, such as DADA2, GATA2, and RAG deficiency
Exposure to chemicals and drugs, such as amphetamines, cocaine, and anthrax vaccines which contain the Anthrax Protective Antigen as the primary ingredient. | Bleb or bulla
The most common disease causing blebs or bullae is paraseptal emphysema though centrilobular emphysema may sometimes be involved. Other conditions associated with lung bullae are:
Other conditions associated with lung bullae are:
Alpha 1-antitrypsin deficiency
Marfan syndrome
Ehlers–Danlos syndromes
Cocaine smoking
Sarcoidosis
HIV/AIDS
Intravenous substance abuse
Cyst
A pulmonary cyst is not necessarily the same type of cyst seen in many cystic lung diseases. The cyst for example in pneumocystis pneumonia is not the same as the pulmonary cyst. Cystic lung diseases include:
Langerhans cell histiocytosis (LCH)
Lymphangioleiomyomatosis (LAM)
Lymphocytic interstitial pneumonia (LIP)
Birt–Hogg–Dubé syndrome
Pneumocystis pneumonia
Pulmonary amyloidosis
Light chain deposition disease
Lung metastases rarely cause multiple cystic lung lesions. This form of presentation has been described in metastatic sarcomas. Incidental blebs and cysts
A focal lung pneumatosis that is an incidental imaging finding such as on a CT scan, without suspicious findings (such as findings indicating any of the diseases listed above), generally does not indicate further follow-up. Cavity
Two infectious diseases that are commonly associated with cavities of lung tissue are Mycobacterium tuberculosis and Klebsiella pneumoniae. The formation of cavities is due to tissue necrosis and creates an environment that allows the pathogen to expand in numbers and spread further.In the absence of infectious symptoms, a lung nodule with cavitation is a suspected lung cancer. == References == | 0-1
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The Turing test is commonly cited in discussions of artificial intelligence as a proposed criterion for machine consciousness; it has provoked a great deal of philosophical debate. For example, Daniel Dennett and Douglas Hofstadter argue that anything capable of passing the Turing test is necessarily conscious, while David Chalmers argues that a philosophical zombie could pass the test, yet fail to be conscious. A third group of scholars have argued that with technological growth once machines begin to display any substantial signs of human-like behavior then the dichotomy (of human consciousness compared to human-like consciousness) becomes passé and issues of machine autonomy begin to prevail even as observed in its nascent form within contemporary industry and technology. Jürgen Schmidhuber argues that consciousness is the result of compression. As an agent sees representation of itself recurring in the environment, the compression of this representation can be called consciousness. In a lively exchange over what has come to be referred to as "the Chinese room argument", John Searle sought to refute the claim of proponents of what he calls "strong artificial intelligence (AI)" that a computer program can be conscious, though he does agree with advocates of "weak AI" that computer programs can be formatted to "simulate" conscious states. His own view is that consciousness has subjective, first-person causal powers by being essentially intentional due to the way human brains function biologically; conscious persons can perform computations, but consciousness is not inherently computational the way computer programs are. | Also, it is difficult to reason objectively about the question, because a denial that an animal is conscious is often taken to imply that it does not feel, its life has no value, and that harming it is not morally wrong. Descartes, for example, has sometimes been blamed for mistreatment of animals due to the fact that he believed only humans have a non-physical mind. Most people have a strong intuition that some animals, such as cats and dogs, are conscious, while others, such as insects, are not; but the sources of this intuition are not obvious, and are often based on personal interactions with pets and other animals they have observed. Philosophers who consider subjective experience the essence of consciousness also generally believe, as a correlate, that the existence and nature of animal consciousness can never rigorously be known. Thomas Nagel spelled out this point of view in an influential essay titled What Is it Like to Be a Bat?. He said that an organism is conscious "if and only if there is something that it is like to be that organism—something it is like for the organism"; and he argued that no matter how much we know about an animals brain and behavior, we can never really put ourselves into the mind of the animal and experience its world in the way it does itself. Other thinkers, such as Douglas Hofstadter, dismiss this argument as incoherent. | 11
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Osteochondrodysplasia is a general term for a disorder of the development (dysplasia) of bone ("osteo") and cartilage ("chondro"). Osteochondrodysplasias are rare diseases. About 1 in 5,000 babies are born with some type of skeletal dysplasia. Nonetheless, if taken collectively, genetic skeletal dysplasias or osteochondrodysplasias comprise a recognizable group of genetically determined disorders with generalized skeletal affection. Osteochondrodysplasias can result in marked functional limitation and even mortality. Osteochondrodysplasias subtypes can overlap in clinical aspects, therefore plain radiography is absolutely necessary to establish an accurate diagnosis. Magnetic resonance imaging can provide further diagnostic insights and guide treatment strategies especially in cases of spinal involvement. Early diagnosis, and timely management of skeletal dysplasia are important to combat functional deterioration. Types
Achondroplasia
Achondroplasia is a type of autosomal dominant genetic disorder that is the most common cause of dwarfism. It is also the most common type of non-lethal osteochondrodysplasia or skeletal dysplasia. The prevalence is approximately 1 in 25,000 births. Achondroplastic dwarfs have short stature, with an average adult height of 131 cm (4 feet, 3 inches) for males and 123 cm (4 feet, 0 inches) for females. In achondroplasia the dwarfism is readily apparent at birth. likewise, craniofacial abnormalities in the form of macrocephaly and mid-face hypoplasia are present at birth. The previous clinical findings differentiate between achondroplasia and pseudoachondroplasia in which dwarfism is not recognizable at birth and craniofacial abnormalities are not considered a disease feature. Plain radiography plays an additional and important role in the differential diagnosis of achondroplasia. | They are caused by an abnormal function of the lysosomal enzymes, which blocks degradation of mucopolysaccharides and leads to accumulation of harmful byproducts, namely, heparan sulfate, dermatan sulfate, and keratan sulfate. The resulting cellular malfunction can lead to a diverse array of skeletal and visceral manifestations. MPS have been subcategorized according to the type of enzyme inadequacy and glycoprotein accumulated. Cleidocranial dysostosis
Cleidocranial dysostosis is a general skeletal condition named for the collarbone (cleido-) and cranium deformities which people with it often have. Common features include:
Partly or completely missing collarbones. A soft spot or larger soft area in the top of the head where the fontanelle failed to close. Bones and joints are underdeveloped. The permanent teeth include supernumerary teeth. Permanent teeth not erupting
Bossing (bulging) of the forehead. Hypertelorism
Fibrous dysplasia
Fibrous dysplasia causes bone thinning and growths or lesions in one or more bones of the human body. These lesions are tumor-like growths that consist of replacement of the medullary bone with fibrous tissue, causing the expansion and weakening of the areas of bone involved. Especially when involving the skull or facial bones, the lesions can cause externally visible deformities. The skull is often, but not necessarily, affected, and any other bones can be involved. Langer–Giedion syndrome
Langer–Giedion syndrome is a very rare genetic disorder caused by a deletion of chromosomal material. Diagnosis is usually made at birth or in early childhood. | 11
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However, its androgen synthesis inhibition is probably clinically insignificant.Spironolactone has been found in some studies to increase levels of estradiol, an estrogen, although many other studies have found no changes in estradiol levels. The mechanism of how spironolactone increases estradiol levels is unclear, but it may involve inhibition of the inactivation of estradiol into estrone and enhancement of the peripheral conversion of testosterone into estradiol. It is notable that spironolactone has been found in vitro to act as a weak inhibitor of 17β-hydroxysteroid dehydrogenase 2, an enzyme that is involved in the conversion of estradiol into estrone. Increased levels of estradiol with spironolactone may be involved in its preservation of bone density and in its side effects such as breast tenderness, breast enlargement, and gynecomastia in women and men.In response to the antimineralocorticoid activity spironolactone, and in an attempt to maintain homeostasis, the body increases aldosterone production in the adrenal cortex. Some studies have found that levels of cortisol, a glucocorticoid hormone that is also produced in the adrenal cortex, are increased as well. However, other clinical studies have found no change in cortisol levels with spironolactone, and those that have found increases often have observed only small changes. In accordance, spironolactone has not been associated with conventional glucocorticoid medication effects or side effects.Other activities of spironolactone may include very weak interactions with the estrogen and progesterone receptors and agonism of the pregnane X receptor. These activities could contribute to the menstrual irregularities and breast side effects of spironolactone and to its drug interactions, respectively. | For this reason, men are typically not prescribed spironolactone for any longer than a short period of time, e.g., for an acute exacerbation of heart failure. A newer medication, eplerenone, has been approved by the U.S. Food and Drug Administration for the treatment of heart failure, and lacks the antiandrogenic effects of spironolactone. As such, it is far more suitable for men for whom long-term medication is being chosen. However, eplerenone may not be as effective as spironolactone or the related medication canrenone in reducing mortality from heart failure.The clinical benefits of spironolactone as a diuretic are typically not seen until 2–3 days after dosing begins. Likewise, the maximal antihypertensive effect may not be seen for 2–3 weeks.Unlike with some other diuretics, potassium supplementation should not be administered while taking spironolactone, as this may cause dangerous elevations in serum potassium levels resulting in hyperkalemia and potentially deadly abnormal heart rhythms. High blood pressure
About 1 in 100 people with hypertension have elevated levels of aldosterone; in these people, the antihypertensive effect of spironolactone may exceed that of complex combined regimens of other antihypertensives since it targets the primary cause of the elevated blood pressure. However, a Cochrane review found adverse effects at high doses and little effect on blood pressure at low doses in the majority of people with high blood pressure. There is no evidence of person-oriented outcome at any dose in this group. High aldosterone levels
Spironolactone is used in the treatment of hyperaldosteronism (high aldosterone levels or mineralocorticoid excess), for instance primary aldosteronism (Conns syndrome). | 11
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Adults can more easily compensate and correct for the loss of tissue use and therefore the mortality likelihood in an adult with cerebral softening is less than in an infant. Documented cases
In this late 19th-century case study, a 10-year-old boy was found to have cerebral softening in specific parts of the brain, limiting specific sensory function. The identifiable softening enabled researchers to detect and partition cerebral areas related to different sensory perceptions.Another case in the late 19th century showed that cerebral softening, when caused by hemorrhaging, can affect various neural pathways leading to convulsions, spasms, coma and death.A third case in 1898 followed the ten-day decline of a 66-year-old woman with cerebral softening. She had yellow softening which led to symptoms that started slowly with transient facial paralysis on the right side of the face. The limbs later became cold and the right side of the body transiently progressed between semi-paralysis and tetanus. Her heart rate and respiration rate became slow by days three and four. Later she developed a yellow jaundiced appearance in the sclera and skin that the doctor proposed as paroxysmal hemoglobinuria upon autopsy. On the last days, the paralysis became more frequent, respiration rose and she developed tachycardia. She died on the evening of the tenth day. The autopsy revealed that the top of the brain down to the lateral ventricle were healthy, but below that there was a 2.5 × 2 × 1 inch area on the left side of the brain that was softened and yellow. | Cerebral softening, also known as encephalomalacia, is a localized softening of the substance of the brain, due to bleeding or inflammation. Three varieties, distinguished by their color and representing different stages of the disease progress, are known respectively as red, yellow, and white softening. Causes
Stroke
Ischemia: A decreased or restriction of circulating blood flow to a region of the brain which deprives neurons of the necessary substrates (primarily glucose); represents 80% of all strokes. A thrombus or embolus plugs an artery so there is a reduction or cessation of blood flow. This hypoxia or anoxia leads to neuronal injury, which is known as a stroke. The death of neurons leads to a so-called softening of the cerebrum in the affected area.Hemorrhage: Intracerebral hemorrhage occurs in deep penetrating vessels and disrupts the connecting pathways, causing a localized pressure injury and in turn injury to brain tissue in the affected area. Hemorrhaging can occur in instances of embolic ischemia, in which the previously obstructed region spontaneously restores blood flow. This is known as a hemorrhagic infarction and a resulting red infarct occurs, which points to a type of cerebral softening known as red softening. Circle of Willis
In a study on the circle of Willis and its relation to cerebral vascular disorders, a comparison on various anomalies between normal brains (those without the condition of cerebral softening) and brains with cerebral softening were looked at to observe trends in the differences of the anatomical structure of the circle of Willis. | 11
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In 1929, Fritz Lickint of Dresden, Germany, published a paper containing formal statistical evidence of a lung cancer–tobacco link. During the Great Depression Adolf Hitler condemned his earlier smoking habit as a waste of money, and later with stronger assertions. This movement was further strengthened with Nazi reproductive policy as women who smoked were viewed as unsuitable to be wives and mothers in a German family. In the 20th century, smoking was common. There were social events like the smoke night which promoted the habit. The anti-tobacco movement in Nazi Germany did not reach across enemy lines during the Second World War, as anti-smoking groups quickly lost popular support. By the end of the Second World War, American cigarette manufacturers quickly reentered the German black market. Illegal smuggling of tobacco became prevalent, and leaders of the Nazi anti-smoking campaign were silenced. As part of the Marshall Plan, the United States shipped free tobacco to Germany; with 24,000 tons in 1948 and 69,000 tons in 1949. Per capita yearly cigarette consumption in post-war Germany steadily rose from 460 in 1950 to 1,523 in 1963. By the end of the 20th century, anti-smoking campaigns in Germany were unable to exceed the effectiveness of the Nazi-era climax in the years 1939–41 and German tobacco health research was described by Robert N. Proctor as "muted". In 1950, Richard Doll published research in the British Medical Journal showing a close link between smoking and lung cancer. | The results suggest either, that the consumption in bars and restaurants is not affected by smoking bans in the long run, or, that negative revenue impacts by smokers are compensated by increasing revenues through non-smokers. Ignition safety
An indirect public health problem posed by cigarettes is that of accidental fires, usually linked with consumption of alcohol. Enhanced combustion using nitrates was traditionally used but cigarette manufacturers have been silent on this subject claiming at first that a safe cigarette was technically impossible, then that it could only be achieved by modifying the paper. Roll your own cigarettes contain no additives and are fire safe. Numerous fire safe cigarette designs have been proposed, some by tobacco companies themselves, which would extinguish a cigarette left unattended for more than a minute or two, thereby reducing the risk of fire. Among American tobacco companies, some have resisted this idea, while others have embraced it. RJ Reynolds was a leader in making prototypes of these cigarettes in 1983 and will make all of their U.S. market cigarettes to be fire-safe by 2010. Phillip Morris is not in active support of it. Lorillard (purchased by RJ Reynolds), the US 3rd-largest tobacco company, seems to be ambivalent. Gateway drug theory
The relationship between tobacco and other drug use has been well-established, however the nature of this association remains unclear. The two main theories are the phenotypic causation (gateway) model and the correlated liabilities model. | 11
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Management
The goals of short-term hormone therapy are to induce the beginning of sexual development and induce a growth spurt, but should be limited to children with severe distress or anxiety secondary to their delayed puberty. Bone age must be monitored frequently to prevent precocious closure of the bone plates, thereby stunting growth. Constitutional and physiologic delay
If a child is healthy with a constitutional delay of growth and puberty, reassurance and prediction based on the bone age can be provided. No other intervention is usually necessary, but repeat evaluation by measuring serum testosterone or estrogen is recommended. Furthermore, the diagnosis of hypogonadism can be excluded once the adolescent has started puberty by age 16–18.Boys aged >14 years old whose growth is severely stunted or are experiencing severe distress secondary to their lack of puberty can be started on testosterone to increase their height. Testosterone treatment can also be used to stimulate sexual development, but it can close bone plates prematurely stopping growth altogether if not carefully administered. Another therapeutic option is the use of aromatase inhibitors to inhibit the conversion of androgens to estrogens as estrogens are responsible for stopping bone growth plate development and thus growth. However, due to side effects, therapy with testosterone alone is most often used. | Others
Growth hormone is another option that has been described, however it should only be used in proven growth hormone deficiency such as idiopathic short stature. Children with a constitutional delay have not been shown to benefit from growth hormone therapy. Although serum growth hormone levels are low in constitutional delay of puberty, they increase after treatment with sex hormones and in those cases, growth hormone is not suggested to accelerate growth.Subnormal vitamin A intake is one of the etiological factors in delayed pubertal maturation. Supplementation of both vitamin A and iron to normal constitutionally delayed children with subnormal vitamin A intake is as efficacious as hormonal therapy in the induction of growth and puberty.More therapies are being developed to target the more discreet modulators of the HPG axis including kisspeptin and neurokinin B.In cases of severe delayed puberty secondary to hypogonadism, evaluation by a psychologist or psychiatrist, as well as counseling and a supportive environment are an important supplemental therapy for the child. Transition from pediatric to adult care is also vital as many children are lost during transition of care. Outlook
Constitutional delay of growth and puberty is a variation of normal development with no long-term health consequences, however it can have lasting psychological effects. Adolescent boys with delayed puberty have a higher level of anxiety and depression relative to their peers. | 11
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Sub-Saharan Africa, the Americas, Western Europe, the UK, and Ireland still face many challenges combating this disease. Other types
As with any gram-negative bacterium, N. meningitidis can infect a variety of sites.Meningococcal pneumonia can appear during influenza pandemics and in military camps. This is a multilobar, rapidly evolving pneumonia, sometimes associated with septic shock. With prompt treatment, the prognosis is excellent. Another alternative is dexamethasone with vancomycin and meropenem. Pericarditis can appear, either as a septic pericarditis with grave prognosis or as a reactive pericarditis in the wake of meningitis or septicaemia. Signs and symptoms
Meningitis
The patient with meningococcal meningitis typically presents with high fever, nuchal rigidity (stiff neck), Kernigs sign, severe headache, vomiting, purpura, photophobia, and sometimes chills, altered mental status, or seizures. Diarrhea or respiratory symptoms are less common. Petechiae are often also present, but do not always occur, so their absence should not be used against the diagnosis of meningococcal disease. Anyone with symptoms of meningococcal meningitis should receive intravenous antibiotics before the results of lumbar puncture, as delay in treatment worsens the prognosis. Meningococcemia
Symptoms of meningococcemia are, at least initially, similar to those of influenza. Typically, the first symptoms include fever, nausea, myalgia, headache, arthralgia, chills, diarrhea, stiff neck, and malaise. Later symptoms include septic shock, purpura, hypotension, cyanosis, petechiae, seizures, anxiety, and multiple organ dysfunction syndrome. Acute respiratory distress syndrome and altered mental status may also occur. The petechial rash appear with the star-like shape. | A small amount of acetoacetate is a value under 20 mg/dL; a moderate amount is a value of 30–40 mg/dL, and a finding of 80 mg/dL or greater is reported as a large amount. One 2010 study admits that though ketonurias relation to general metabolic health is ill-understood, there is a positive relationship between the presence of ketonuria after fasting and positive metabolic health. Causes
Metabolic abnormalities such as diabetes, renal glycosuria, or glycogen storage disease. Dietary conditions such as starvation, fasting, low-carbohydrate diets, prolonged vomiting, and anorexia including caused by hyperemesis gravidarum. Conditions in which metabolism is increased, such as hyperthyroidism, fever, pregnancy or lactation.In non-diabetic persons, ketonuria may occur during acute illness or severe stress. Approximately 15% of hospitalized patients may have ketonuria, even though they do not have diabetes. In a diabetic patient, ketone bodies in the urine suggest that the patient is not adequately controlled and that adjustments of medication, diet, or both should be made promptly. In the non diabetic patient, ketonuria reflects a reduced carbohydrate metabolism and an increased fat metabolism. Diagnosis
A wide variety of companies manufacture ketone screening strips. A strip consists of a thin piece of plastic film slightly larger than a matchstick, with a reagent pad on one end that is either dipped into a urine sample or passed through the stream while the user is voiding. | 0-1
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However, Gurd and Wilsons criteria for fat embolism become more commonly used when compared to the other two diagnostic criteria. Gurd and Wilsons criteria
Major criteria
Axillary or subconjunctival petechiae
Hypoxaemia PaO2 <60 mm Hg, FIO2 = 0.4
Central nervous system depression disproportionate to hypoxaemia
Pulmonary oedemaMinor criteria
Tachycardia more than 110 beats per minute
Pyrexia more than 38.5 °C
Fat globules present in urine
Changes in renal function (reduced urine output)
Drop in haemoglobin values (more than 20% of the value upon admission)
Drop in haematocrit values
Drop in platelet values (more than 50% of the value upon admission)
Increasing erythrocyte sedimentation rate (ESR) (greater than 71 mm per hour)
Fat globules present in the sputum
Emboli present in the retina on fundoscopyA least two positive major criteria plus one minor criteria or four positive minor criteria are suggestive of fat embolism syndrome. Fat embolism syndrome is a clinical diagnosis. There are no laboratory tests sensitive or specific enough to diagnose FES. Such laboratory tests are only used to support the clinical diagnosis only. Chest X-ray may show diffuse interstitial infiltrates while chest CT scan will show diffuse vascular congestion and pulmonary oedema. Bronchoalveolar lavage has been proposed to look for fat droplets in alveolar macrophages however it is time-consuming and is not specific to fat embolism syndrome. Looking for fat globules in sputum and urine is also not specific enough to diagnose FES. Prevention
For those treated conservatively with immobilisation of long bone fractures, the incidence of FES is 22%. | Early operative fixation of long bone fractures can reduce the incidence of FES especially with the usage of internal fixation devices. Patients undergoing urgent fixation of long bone fractures has a rate of 7% of acute respiratory distress syndrome (ARDS) when compared to those undergoing fixation after 24 hours (39% with ARDS). However, movement of the fracture ends of the long bones during the operative fixation can cause transient increase of fat emboli in the blood circulation. Cytokines are persistently elevated if the long bone fractures is treated conservatively using immobilisation. The cytokine levels would return to normal after operative fixation. Although ream nailing increases pressure in the medullary cavity of the long bones, it does not increase the rates of FES. Other methods such as drilling of holes in the bony cortex, lavaging bone marrow prior to fixation, and the use of tourniquets to prevent embolisation have not been shown to reduce the rates of FES.Corticosteroid therapy such as methylprednisolone (6 to 90 mg/kg) has been proposed for the treatment of FES, however, it is controversial. Corticosteroid can be used to limit free fatty acid levels, stabilising membranes, and inhibit leukocyte aggregation. A meta-analysis conducted in 2009 reported prophylactic corticosteroids can reduce the risk of FES by 77%. However, there is no difference in mortality, infection, and avascular necrosis when compared to the control group. However, a randomised trial conducted in 2004 reported no differences in FES incidence when comparing treatment with the control group. | 11
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Ethanol (abbr. EtOH; also called ethyl alcohol, grain alcohol, drinking alcohol, or simply alcohol) is an organic compound. It is a simple alcohol with the chemical formula C2H6O. Its formula can be also written as CH3−CH2−OH or C2H5OH (an ethyl group linked to a hydroxyl group). Ethanol is a volatile, flammable, colorless liquid with a characteristic wine-like odor and pungent taste. It is a psychoactive recreational drug, the active ingredient in alcoholic drinks. Ethanol is naturally produced by the fermentation process of sugars by yeasts or via petrochemical processes such as ethylene hydration. It has medical applications as an antiseptic and disinfectant. It is used as a chemical solvent and in the synthesis of organic compounds, and as a fuel source. Ethanol also can be dehydrated to make ethylene, an important chemical feedstock. Etymology
Ethanol is the systematic name defined by the International Union of Pure and Applied Chemistry (IUPAC) for a compound consisting of an alkyl group with two carbon atoms (prefix "eth-"), having a single bond between them (infix "-an-") and an attached functional group −OH group (suffix "-ol").The "eth-" prefix and the qualifier "ethyl" in "ethyl alcohol" originally come from the name "ethyl" assigned in 1834 to the group C2H5− by Justus Liebig. He coined the word from the German name Aether of the compound C2H5−O−C2H5 (commonly called "ether" in English, more specifically called "diethyl ether"). | Vulvar vestibulitis
Vulvar vestibulitis syndrome (VVS), vestibulodynia, or simply vulvar vestibulitis or "localized (to the vestibule) provoked vulvodynia" refers to pain localized to the vestibular region. It tends to be associated with a highly localized "burning" or "cutting" type of pain. The pain of vulvodynia may extend into the clitoris; this is referred to as clitorodynia.Vulvar vestibulitis syndrome is the most common subtype of vulvodynia that affects premenopausal women – the syndrome has been cited as affecting about 10%–15% of women seeking gynecological care. Causes
A wide variety of possible causes and treatments for vulvodynia are currently being explored. Moreover, there are probably several causes of vulvodynia, and some may be individual to the patient.Possible causes include Sjögren syndrome, the symptoms of which include chronic vaginal dryness. Others include genetic predisposition to inflammation, allergy or other sensitivity (for example: oxalates in the urine), an autoimmune disorder similar to lupus erythematosus or to eczema or to lichen sclerosus, infection (e.g., yeast infections, bacterial vaginosis, HPV, HSV), injury, and neuropathy—including an increased number of nerve endings in the vaginal area. Some cases seem to be negative outcomes of genital surgery, such as a labioplasty. Initiation of hormonal contraceptives that contain low- dose estrogen before the age of 16 could predispose women to vulvar vestibulitis syndrome. A significantly lower pain threshold, especially in the posterior vestibulum, has also been associated with the use of hormonal contraceptives in women without vulvar vestibulitis syndrome. Pelvic floor dysfunction may be the underlying cause of some womens pain. | 0-1
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Cerebral granulomatous infection may also be caused by S. mansoni. In situ egg deposition following the anomalous migration of the adult worm, which appears to be the only mechanism by which Schistosoma can reach the central nervous system in people with schistosomiasis. The destructive action on the nervous tissue and the mass effect produced by a large number of eggs surrounded by multiple, large granulomas in circumscribed areas of the brain characterize the pseudotumoral form of neuroschistosomiasis and are responsible for the appearance of clinical manifestations: headache, hemiparesis, altered mental status, vertigo, visual abnormalities, seizures, and ataxia. Similarly, granulomatous lesions from S. mansoni and S. haematobium eggs in the spinal cord can lead to transverse myelitis (inflammation of the spinal cord) with flaccid paraplegia. In cases with advanced hepatosplenic and urinary schistosomiasis, the continuous embolization of eggs from the portal mesenteric system (S. mansoni) or portal mesenteric-pelvic system (S. haematobium) to the brain, results in a sparse distribution of eggs associated with scant periovular inflammatory reaction, usually with little or no clinical significance.Spinal cord inflammation (transverse myelitis) symptoms may include:
Paralysis of the lower extremities
Loss of bowel or urinary control
Loss of sensation below the level of the lesion
Pain below the level of the lesionCerebral granulomatous infection symptoms may include:
Seizures
Headaches
Motor impairment
Sensory impairment
Cerebellar symptomsUnsteady gait
Inability to stand or sit without support
Uncoordinated movements
Scanning speech
Irregular eye movementsCorticosteroids is used to prevent permanent neurological damage from the inflammatory response to the eggs, and sometimes anticonvulsant is needed to stop the seizures. Corticosteroid is given prior to administration of Praziquantel. | In one 6-year-old patient antibodies to GABA-producing enzyme glutamate decarboxylase were detected. See also
Stiff person syndrome
References
== External links == | 0-1
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The main form of fat that is commonly ingested is triglycerides, which are composed of three fatty acids bound together. In this state, triglycerides are able to give fatty foods unique textures that are often described as creaminess. But this texture is not an actual taste. It is only during ingestion that the fatty acids that make up triglycerides are hydrolysed into fatty acids via lipases. The taste is commonly related to other, more negative, tastes such as bitter and sour due to how unpleasant the taste is for humans. Richard Mattes, a co-author of the study, explained that low concentrations of these fatty acids can create an overall better flavor in a food, much like how small uses of bitterness can make certain foods more rounded. However, a high concentration of fatty acids in certain foods is generally considered inedible. To demonstrate that individuals can distinguish fat taste from other tastes, the researchers separated volunteers into groups and had them try samples that also contained the other basic tastes. Volunteers were able to separate the taste of fatty acids into their own category, with some overlap with savory samples, which the researchers hypothesized was due to poor familiarity with both. The researchers note that the usual "creaminess and viscosity we associate with fatty foods is largely due to triglycerides", unrelated to the taste; while the actual taste of fatty acids is not pleasant. | In contrast, rubidium and caesium ions are far larger, so their salty taste differs accordingly. The saltiness of substances is rated relative to sodium chloride (NaCl), which has an index of 1. Potassium, as potassium chloride (KCl), is the principal ingredient in salt substitutes and has a saltiness index of 0.6.Other monovalent cations, e.g. ammonium (NH4+), and divalent cations of the alkali earth metal group of the periodic table, e.g. calcium (Ca2+), ions generally elicit a bitter rather than a salty taste even though they, too, can pass directly through ion channels in the tongue, generating an action potential. But the chloride of calcium is saltier and less bitter than potassium chloride, and is commonly used in pickle brine instead of KCl. Bitterness
Bitterness is one of the most sensitive of the tastes, and many perceive it as unpleasant, sharp, or disagreeable, but it is sometimes desirable and intentionally added via various bittering agents. Common bitter foods and beverages include coffee, unsweetened cocoa, South American mate, coca tea, bitter gourd, uncured olives, citrus peel, some varieties of cheese, many plants in the family Brassicaceae, dandelion greens, horehound, wild chicory, and escarole. The ethanol in alcoholic beverages tastes bitter, as do the additional bitter ingredients found in some alcoholic beverages including hops in beer and gentian in bitters. Quinine is also known for its bitter taste and is found in tonic water. | 11
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This device is a mouthguard similar to those used in sports to protect the teeth. It is designed to hold the lower jaw slightly down and forward relative to the natural, relaxed position. This position holds the tongue farther away from the back of the airway and may be enough to relieve apnea or improve breathing. Many people benefit from sleeping at a 30-degree elevation of the upper body or higher, as if in a recliner. Doing so helps prevent the gravitational collapse of the airway. Sleeping on a side as opposed to sleeping on the back is also recommended.Some studies have suggested that playing a wind instrument may reduce snoring and apnea incidents. This may be especially true of double reed instruments. Rapid Palatal Expansion
In children, orthodontic treatment to expand the volume of the nasal airway, such as nonsurgical Rapid Palatal expansion is common. Since the palatal suture is fused in adults, regular RPE using tooth-borne expanders cannot be performed. Mini-implant assisted rapid palatal expansion (MARPE) has been recently developed as a non-surgical option for the transverse expansion of the maxilla in adults. This method increases the volume of the nasal cavity and nasopharynx, leading to increased airflow and reduced respiratory arousals during sleep. Changes are permanent with minimal complications. Surgery
Surgical treatments to modify airway anatomy, known as sleep surgery, are varied and must be tailored to the specific airway obstruction needs of a patient. Surgery is not considered a first line treatment for obstructive sleep apnea in adults. | Moreover, in diseases such as Alzheimers disease, Picks disease, and Creutzfeldt-Jakob disease, progressive deterioration of comprehension and production of language is just one of the many possible types of mental deterioration, such as the progressive decline of memory, motor skills, reasoning, awareness, and visuospatial skills. Causes
Currently, the specific causes for PPA and other degenerative brain disease similar to PPA are unknown. Autopsies have revealed a variety of brain abnormalities in people who had PPA. These autopsies, as well as imaging techniques such as CT scans, MRI, EEG, single photon emission computed tomography (SPECT), and positron emission tomography (PET), have generally revealed abnormalities to be almost exclusively in the left hemisphere. Risk factors
There have been no large epidemiological studies on the incidence and prevalence of the PPA variants. Though it most likely has been underestimated, onset of PPA has been found to occur in the sixth or seventh decade.There are no known environmental risk factors for the progressive aphasias. However, one observational, retrospective study suggested that vasectomy could be a risk factor for PPA in men. These results have yet to be replicated or demonstrated by prospective studies.PPA is not considered a hereditary disease. However, relatives of a person with any form of frontotemporal lobar degeneration, including PPA, are at slightly greater risk of developing PPA or another form of the condition. In a quarter of patients diagnosed with PPA, there is a family history of PPA or one of the other disorders in the FTLD spectrum of disorders. | 0-1
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Nonetheless, they are useful when used in adjunct with other voice assessment measures, or as a tool for monitoring therapeutic effects over time. Prevention
Given that certain occupations are more at risk for developing dysphonia (e.g. teachers) research into prevention studies have been conducted. Research into the effectiveness of prevention strategies for dysphonia have yet to produce definitive results, however, research is still ongoing. Primarily, there are two types of vocal training recognized by professionals to help with prevention: direct and indirect. Direct prevention describes efforts to reduce conditions that may serve to increase vocal strain (such as patient education, relaxation strategies, etc. ), while indirect prevention strategies refer to changes in the underlying physiological mechanism for voice production (e.g., adjustments to the manner in which vocal fold adduction occurs, respiratory training, shifting postural habits, etc.). Treatment
Although there is no universal classification of voice problems, voice disorders can be separated into certain categories: organic (structural or neurogenic), functional, neurological (psychogenic) or iatrogenic, for example. Depending on the diagnosis and severity of the voice problem, and depending on the category that the voice disorder falls into, there are various treatment methods that can be suggested to the patient. The professional has to keep in mind there is not one universal treatment, but rather the clinical approach must find what the optimal effective course of action for that particular patient is.There are three main type of treatments: medical treatments, voice therapy and surgical treatments. When necessary, certain voice disorders use a combination of treatment approaches. | These causes can range from vocal abuse and misuse to systemic diseases. Causes of dysphonia can be divided into five basic categories, although overlap may occur between categories. (Note that this list is not exhaustive):
Employment
It has been suggested that certain occupational groups may be at increased risk of developing dysphonia due to the excessive or intense vocal demands of their work. Research on this topic has primarily focused on teachers and singers, although some studies have examined other groups of heavy voice users (e.g. actors, cheerleaders, aerobic instructors, etc.). At present, it is known that teachers and singers are likely to report dysphonia. Moreover, physical education teachers, teachers in noisy environments, and those who habitually use a loud speaking voice are at increased risk. The term clergymans throat or dysphonia clericorum was previously used for painful dysphonia associated with public speaking, particularly among preachers. However, the exact prevalence rates for occupational voice users are unclear, as individual studies have varied widely in the methodologies used to obtain data (e.g. employing different operational definitions for "singer"). Mechanism
Located in the anterior portion of the neck is the larynx (also known as the voice box), a structure made up of several supporting cartilages and ligaments, which houses the vocal folds. In normal voice production, exhaled air moves out of the lungs and passes upward through the vocal tract. At the level of the larynx, the exhaled air causes the vocal folds to move toward the midline of the tract (a process called adduction). | 11
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Moreover, animal studies and at least three human case reports have found no interaction between ketamine and the monoamine oxidase inhibitor (MAOI) tranylcypromine, which is of importance as the combination of a monoamine reuptake inhibitor with an MAOI can produce severe toxicity such as serotonin syndrome or hypertensive crisis. Collectively, these findings shed doubt on the involvement of monoamine reuptake inhibition in the effects of ketamine in humans. Ketamine has been found to increase dopaminergic neurotransmission in the brain, but instead of being due to dopamine reuptake inhibition, this may be via indirect/downstream mechanisms, namely through antagonism of the NMDA receptor.Whether ketamine is an agonist of D2 receptors is controversial. Early research by the Philip Seeman group found ketamine to be a D2 partial agonist with the potency similar to that of its NMDA receptor antagonism. However, later studies by different researchers found the affinity of ketamine of >10 μM for the regular human and rat D2 receptors, Moreover, whereas D2 receptor agonists such as bromocriptine are able to rapidly and powerfully suppress prolactin secretion, subanesthetic doses of ketamine have not been found to do this in humans and in fact, have been found to dose-dependently increase prolactin levels. Imaging studies have shown mixed results on inhibition of striatal [11C] raclopride binding by ketamine in humans, with some studies finding a significant decrease and others finding no such effect. However, changes in [11C] raclopride binding may be due to changes in dopamine concentrations induced by ketamine rather than binding of ketamine to the D2 receptor. | Steroid therapy may also be considered. In cases when all conservative treatment fails, surgical therapy may be necessary. In a bursectomy the bursa is cut out either endoscopically or with open surgery. The bursa grows back in place after a couple of weeks but without any inflammatory component. See also
Calcific bursitis
Snapping scapula syndrome
References
External links
Bursitis treatment from NHS Direct
Questions and Answers about Bursitis and Tendinitis – US National Institute of Arthritis and Musculoskeletal and Skin Diseases | 0-1
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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. | However, it is argued that the numbers are far greater than accounted by the point in time method. For example, while the Census of 2011 counted 46.724 homeless individuals in Delhi, the Indo-Global Social Service Society counted them to be 88,410, and another organization called the Delhi Development Authority counted them to be 150,000. Furthermore, there is a high proportion of mentally ill and street children in the homeless population. There are 18 million street children in India, the largest number of any country in the world, with 11 million being urban. Finally, more than three million men and women are homeless in Indias capital city of New Delhi; the same population in Canada would make up approximately 30 electoral districts. A family of four members has an average of five homeless generations in India.There is a shortage of 18.78 million houses in the country. Total number of houses has increased from 52.06 million to 78.48 million (as per 2011 census). However, the country still ranks as the 124th wealthiest country in the world as of 2003. More than 90 million people in India make less than US$1 per day, thus setting them below the global poverty threshold. The ability of the Government of India to tackle urban homelessness and poverty may be affected in the future by both external and internal factors. The number of people living in slums in India has more than doubled in the past two decades and now exceeds the entire population of Britain, the Indian Government has announced. | 11
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In an outbreak, the virus in a nerve cell becomes active and is transported via the neurons axon to the skin, where virus replication and shedding occur and may cause new sores. Transmission
HSV-1 and HSV-2 are transmitted by contact with an infected person who has reactivations of the virus. HSV-2 is periodically shed, most often asymptomatically. Most sexual transmissions occur during periods of asymptomatic shedding. Asymptomatic reactivation means that the virus causes atypical, subtle, or hard-to-notice symptoms that are not identified as an active herpes infection, so acquiring the virus is possible even if no active HSV blisters or sores are present. In one study, daily genital swab samples detected HSV-2 at a median of 12–28% of days among those who had an outbreak, and 10% of days among those with asymptomatic infection (no prior outbreaks), with many of these episodes occurring without visible outbreak ("subclinical shedding").In another study, 73 subjects were randomized to receive valaciclovir 1 g daily or placebo for 60 days each in a two-way crossover design. A daily swab of the genital area was self-collected for HSV-2 detection by polymerase chain reaction, to compare the effect of valaciclovir versus placebo on asymptomatic viral shedding in immunocompetent, HSV-2 seropositive subjects without a history of symptomatic genital herpes infection. The study found that valaciclovir significantly reduced shedding during subclinical days compared to placebo, showing a 71% reduction; 84% of subjects had no shedding while receiving valaciclovir versus 54% of subjects on placebo. | Four of these occur in East Africa, one in East Asia and one in Europe and North America. This suggests that the virus may have originated in East Africa. The most recent common ancestor of the Eurasian strains appears to have evolved ~60,000 years ago. The East Asian HSV-1 isolates have an unusual pattern that is currently best explained by the two waves of migration responsible for the peopling of Japan.Herpes simplex 2 genomes can be divided into two groups: one is globally distributed and the other is mostly limited to sub Saharan Africa. The globally distributed genotype has undergone four ancient recombinations with herpes simplex 1. It has also been reported that HSV-1 and HSV-2 can have contemporary and stable recombination events in hosts simultaneously infected with both pathogens. All of the cases are HSV-2 acquiring parts of the HSV-1 genome, sometimes changing parts of its antigen epitope in the process.The mutation rate has been estimated to be ~1.38×10−7 substitutions/site/year. In clinical setting, the mutations in either the thymidine kinase gene or DNA polymerase gene has caused resistance to aciclovir. However, most of the mutations occur in the thymidine kinase gene rather than the DNA polymerase gene.Another analysis has estimated the mutation rate in the herpes simplex 1 genome to be 1.82×10−8 nucleotide substitution per site per year. This analysis placed the most recent common ancestor of this virus ~710,000 years ago.Herpes simplex 1 and 2 diverged about 6 million years ago. | 11
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Use in turtles is particularly contraindicated.A characteristic of the antinematodal action of ivermectin is its potency: for instance, to combat Dirofilaria immitis in dogs, ivermectin is effective at 0.001 milligram per kilogram of body weight when administered orally.For dogs, the insecticide spinosad may have the effect of increasing the toxicity of ivermectin. Pharmacology
Mechanism of action
Ivermectin and its related drugs act by interfering with the nerve and muscle functions of helminths and insects. The drug binds to glutamate-gated chloride channels common to invertebrate nerve and muscle cells. The binding pushes the channels open, which increases the flow of chloride ions and hyper-polarizes the cell membranes, paralyzing and killing the invertebrate. Ivermectin is safe for mammals (at the normal therapeutic doses used to cure parasite infections) because mammalian glutamate-gated chloride channels only occur in the brain and spinal cord: the causative avermectins usually do not cross the blood–brain barrier, and are unlikely to bind to other mammalian ligand-gated channels. Pharmacokinetics
Ivermectin can be given by mouth, topically, or via injection. It does not readily cross the blood–brain barrier of mammals due to the presence of P-glycoprotein (the MDR1 gene mutation affects the function of this protein). Crossing may still become significant if ivermectin is given at high doses, in which case brain levels peak 2–5 hours after administration. In contrast to mammals, ivermectin can cross the blood–brain barrier in tortoises, often with fatal consequences. Chemistry
Fermentation of Streptomyces avermitilis yields eight closely related avermectin homologues, of which B1a and B1b form the bulk of the products isolated. | Signs and symptoms
Fear, discomfort or anxiety may be triggered both by the presence and the anticipation of the specific object or situation. The main behavioral sign of a specific phobia is avoidance. The fear or anxiety associated with specific phobia can also manifest in physical symptoms such as an increased heart rate, shortness of breath, muscle tension, sweating, or a desire to escape the situation. Causes
The exact cause of specific phobias is not known. The mechanisms for development of specific phobias can be distinguished between innate (genetic and neurobiological) factors, and learned factors. In neurobiology, one explanation proposed for specific phobia is that the typical activation of the amygdala in response to stimuli may be exaggerated due to pathological changes. According to this theory, a deficiency in amygdala habituation may also contribute to the persistence of non-experiential phobia. Certain phobias that are less lethal (e.g. dogs) seem to be more frequently observed and easily acquired in comparison to potentially lethal fears which are more relevant to developed human society (e.g. cars and guns). This was theorised to be due to biological adaptation being passed through evolution which makes recent threats less prone to easy acquisition. However, a 2014 study found evidence against this evolutionary theory, which stated: "Our findings are inconsistent with the hypothesis that fears/phobias of individual stimuli result from genetic and environmental factors unique to that stimulus. Instead, we observed substantial sharing of risk factors across individual fears." | 0-1
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One reason why women are more affected is the weakening of pelvic floor muscles by pregnancy. Men
Men tend to experience incontinence less often than women, and the structure of the male urinary tract accounts for this difference. Stress incontinence is common after prostate cancer treatments.While urinary incontinence affects older men more often than younger men, the onset of incontinence can happen at any age. Estimates around 2007 suggested that 17 percent of men over age 60, an estimated 600,000 men in the US, experienced urinary incontinence, with this percentage increasing with age. Children
Incontinence happens less often after age 5: About 10 percent of 5-year-olds, 5 percent of 10-year-olds, and 1 percent of 18-year-olds experience episodes of incontinence. It is twice as common in girls as in boys. History
The management of urinary incontinence with pads is mentioned in the earliest medical book known, the Ebers Papyrus (1500 BC).Incontinence has historically been a taboo subject in Western culture. However, this situation changed some when Kimberly-Clark aggressively marketed adult diapers in the 1980s with actor June Allyson as spokeswoman. Allyson was initially reticent to participate, but her mother, who had incontinence, convinced her that it was her duty in light of her successful career. The product proved a success. Law
The case Hiltibran et al v. Levy et al in the United States District Court for the Western District of Missouri resulted in that court issuing an order in 2011. | Metageria is a cutaneous condition characterized by premature aging. See also
Hutchinson–Gilford syndrome
List of cutaneous conditions
References
== External links == | 0-1
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Gonadal dysgenesis is classified as any congenital developmental disorder of the reproductive system
in the male or female. It is the atypical development of the gonads in an embryo,
with reproductive tissue replaced with functionless, fibrous tissue, termed streak gonads. Streak gonads are a form of aplasia, resulting in hormonal failure that manifests as sexual infantism and infertility, with no initiation of puberty and secondary sex characteristics.Gonadal development is a genetically controlled process by the chromosomal sex (XX or XY) which directs the formation of the gonad (ovary or testis).Differentiation of the gonads requires a tightly regulated cascade of genetic, molecular and morphogenic events. At the formation of the developed gonad, steroid production influences local and distant receptors for continued morphological and biochemical changes. This results in the appropriate phenotype corresponding to the karyotype (46,XX for females and 46,XY for males).Gonadal dysgenesis arises from the failure of signalling in this tightly regulated process during early foetal development.Manifestations of gonadal dysgenesis are dependent on the aetiology and severity of the underlying defect. Causes
Pure gonadal dysgenesis 46,XX also known as XX gonadal dysgenesis
Pure gonadal dysgenesis 46,XY also known as XY gonadal dysgenesis
Mixed gonadal dysgenesis also known as partial gonadal dysgenesis, and 45,X/46,XY mosaicism
Turner syndrome also known as 45,X or 45,X0
Endocrine disruptions
Pathogenesis
46,XX gonadal dysgenesis
46,XX gonadal dysgenesis is characteristic of female hypogonadism with a karyotype of 46,XX. Streak ovaries are present with non-functional tissues unable to produce the required sex steroid oestrogen. | Society and culture
In a 1987 study by the International Conference of Symphony and Opera Musicians, it was reported that 27% of interviewed members said they used beta blockers such as propranolol for musical performances. For about 10–16% of performers, their degree of stage fright is considered pathological. Propranolol is used by musicians, actors, and public speakers for its ability to treat anxiety symptoms activated by the sympathetic nervous system. It has also been used as a performance-enhancing drug in sports where high accuracy is required, including archery, shooting, golf, and snooker. In the 2008 Summer Olympics, 50-metre pistol silver medalist and 10-metre air pistol bronze medalist Kim Jong-su tested positive for propranolol and was stripped of his medals. Brand names
Propranolol was first marketed under the brand name Inderal, manufactured by ICI Pharmaceuticals (now AstraZeneca), in 1965. Propranolol is also marketed under brand names Avlocardyl, Deralin, Dociton, Inderalici, InnoPran XL, Indoblok, Sumial, Anaprilin, and Bedranol SR (Sandoz). In India it is marketed under brand names such as Ciplar and Ciplar LA by Cipla. Hemangeol, a 4.28 mg/mL solution of propranolol, is indicated for the treatment of proliferating infantile hemangioma. References
External links
Stapleton MP (1997). "Sir James Black and propranolol. The role of the basic sciences in the history of cardiovascular pharmacology". Texas Heart Institute Journal. 24 (4): 336–342. PMC 325477. PMID 9456487. "Propranolol". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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However, ABA has been strongly criticised by the autistic community, who view it as abusive and detrimental to autistic childrens growth. Sensory integration therapy
Sensory integration therapy helps people with autism adapt to different kinds of sensory stimuli. Many with autism can be oversensitive to certain stimuli, such as lights or sounds, causing them to overreact. Others may not react to certain stimuli, such as someone speaking to them. Many types of therapy activities involve a form of play, such as using swings, toys and trampolines to help engage people with sensory stimuli. Therapists will create a plan that focuses on the type of stimulation the person needs integration with. Medication
There are no medications specifically designed to treat autism. Medication is usually used for symptoms associated with autism, such as depression, anxiety, or behavioral problems. Medicines are usually used after other alternative forms of treatment have failed. Criticism of functioning labels
Many medical professionals, autistic people, and supporters of autistic rights disagree with the categorisation of individuals into "high-functioning autism" and "low-functioning autism", stating that the "low-functioning" label causes people to put low expectations on a child and view them as lesser. Furthermore, critics of functioning labels state that an individuals functioning can fluctuate from day to day, and categories do not take this into consideration. Levels of functioning are unrelated to intellectual disability. | Additionally, individuals with "medium-functioning autism" are typically left out of the discussion entirely, and due to the non-linear nature of the autistic spectrum, individuals can be high-functioning in some areas while at the same time being medium or low functioning in other areas. See also
Asperger syndrome and neuroscience
Autism-spectrum quotient, a self-administered test for high-functioning autism
Historical figures sometimes considered autistic
Low-functioning autism
Nonverbal learning disorder
Lorna Wing
References
Further reading
Robison, John Elder (2007). Look Me in the Eye: My Life with Aspergers. Three Rivers Press. ISBN 9780307395986. | 11
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Nicotine inhalers are metered-dose inhalers that administer nicotine through the lungs and mucous membranes of the throat quickly, lasting for a short amount of time. For example, blood nicotine levels are the highest 5–10 minutes after using the nicotine nasal spray, 20 minutes after using a nicotine inhaler or chewing nicotine gum, and 2–4 hours after using a nicotine patch. Society and culture
NRT products were first approved for use in the United States in 1984. Nicotine replacement products are on the World Health Organizations List of Essential Medicines.. They are available as generic medication. Formulations
The nicotine patch is a once-daily, longer-acting form of NRT. An advantage of the nicotine patch is its simple compliance; it does not require active use throughout the day. The gum, lozenge, sublingual tablet, oral inhaler, oral spray, and nasal spray are acutely dosed products, providing the user with the benefit and ability of self-titrating based on cravings.Brand names include Commit Lozenge, Nicoderm, Nicogum, Nicorette, Nicotex, Nicotinell, and Thrive. NRT products contain similar pharmaceutical grade nicotine as is used in e-cigarettes. Medicines
In 2015, the United States Public Health Service listed seven agents for the stopping of tobacco, which included five nicotine replacement treatments (nicotine patches, gum, lozenges, inhalers, and nasal sprays) and two oral medications (bupropion and varenicline). Other NRT options are available, including nicotine mouth sprays and sublingual tablets. Dosing
The dose of nicotine replacement therapy products is generally based on if the user is considered a heavy, average, or light smoker. | A persistent thyroglossal duct is a usually benign medical condition in which the thyroglossal duct, a structure usually only found during embryonic development, fails to atrophy. The duct persists as a midline structure forming an open connection between the back of the tongue and the thyroid gland. This opening can lead to fluid accumulation and infection, which necessitate the removal of the duct. Signs and symptoms
Studies done on cadavers claim persistent thyroglossal ducts can be completely asymptomatic and found in 7% of the human adult population. However, the continued presence of the duct can often lead to complications due to infections and fluid buildup. The glands in the mucosa of the duct will continue their secretions until the fluid forms a cyst or exit the duct via the opening in the foramen cecum. Local infections, such as colds, tonsillitis, or inflammation of the lymph nodes in the area can also lead to the accumulation of fluid within the duct. Even if the cyst forms as secondary to another infection and improved after antibiotics, it will often reoccur and require treatment. Three-fourths of abnormalities within a persistent thyroglossal duct involve the formation of a cyst. If a persistent thyroglossal duct becomes fluid filled it will form a thyroglossal duct cyst, which accounts for 70% of congenital neck masses and is the most likely diagnosis if the mass is along the midline of the neck. These cysts are often diagnosed in children under the age of ten and have no particular gender prevalence. | 0-1
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