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Some common factors which were pointed to include: the shift of focus from vocal music to instrumental music; changes in performance practice, including the loss of the continuo.Crucial to most interpretations of the sonata form is the idea of a tonal center; and, as the Grove Concise Dictionary of Music puts it: "The main form of the group embodying the sonata principle, the most important principle of musical structure from the Classical period to the 20th century: that material first stated in a complementary key be restated in the home key". (The sonata idea has been thoroughly explored by William Newman in his monumental three-volume work Sonata in the Classic Era (A History of the Sonata Idea), begun in the 1950s and published in what has become the standard edition of all three volumes in 1972. 20th-century theory
Heinrich Schenker argued that there was an Urlinie or basic tonal melody, and a basic bass figuration. He held that when these two were present, there was basic structure, and that the sonata represented this basic structure in a whole work with a process known as interruption.As a practical matter, Schenker applied his ideas to the editing of the piano sonatas of Beethoven, using original manuscripts and his own theories to "correct" the available sources. The basic procedure was the use of tonal theory to infer meaning from available sources as part of the critical process, even to the extent of completing works left unfinished by their composers. | Types
An overview of types 1, 2, and 4 is presented below (type 3 is usually excluded from modern classifications):
Type 1: distal
Distal RTA (dRTA) is the classical form of RTA, being the first described. Distal RTA is characterized by a failure of H+ secretion into lumen of nephron by the alpha intercalated cells of the medullary collecting duct of the distal nephron.This failure of acid secretion may be due to a number of causes, and it leads to an inability to acidify the urine to a pH of less than 5.3. Because renal excretion is the primary means of eliminating H+ from the body, there is consequently a tendency towards acidemia. There is an inability to excrete H+ while K+ cannot be reclaimed by the cell, leading to acidemia (as H+ builds up in the body) and hypokalemia (as K+ cannot be reabsorbed by the alpha cell).This leads to the clinical features of dRTA; In other words, the intercalated cells apical H+/K+ antiporter is non-functional, resulting in proton retention and potassium excretion. Since calcium phosphate stones demonstrate a proclivity for deposition at higher pHs (alkaline), the substance of the kidney develops stones bilaterally; this does not occur in the other RTA types. Normal anion gap metabolic acidosis/acidemia
Hypokalemia, Hypocalcemia, Hyperchloremia
Urinary stone formation (related to alkaline urine, hypercalciuria, and low urinary citrate). | 0-1
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Determining when death has occurred is difficult, as cessation of life functions is often not simultaneous across organ systems. Such determination, therefore, requires drawing precise conceptual boundaries between life and death. This is difficult, due to there being little consensus on how to define life. It is possible to define life in terms of consciousness. When consciousness ceases, an organism can be said to have died. One of the flaws in this approach is that there are many organisms that are alive but probably not conscious (for example, single-celled organisms). Another problem is in defining consciousness, which has many different definitions given by modern scientists, psychologists and philosophers. Additionally, many religious traditions, including Abrahamic and Dharmic traditions, hold that death does not (or may not) entail the end of consciousness. In certain cultures, death is more of a process than a single event. It implies a slow shift from one spiritual state to another. Other definitions for death focus on the character of cessation of organismic functioning and a human death which refers to irreversible loss of personhood. More specifically, death occurs when a living entity experiences irreversible cessation of all functioning. As it pertains to human life, death is an irreversible process where someone loses their existence as a person.Historically, attempts to define the exact moment of a humans death have been subjective, or imprecise. | Goltz-Gorlin
Besides its formal name, it is most commonly referred to as Goltz-Gorlin syndrome, after Robert Goltz and Robert Gorlin. Goltz and Gorlin worked together at the University of Minnesota and are credited for describing the symptoms of the disorder in more detail than ever before and tracking its genetic trends. The name became popular during the second half of the 20th century. See also
List of cutaneous conditions
List of radiographic findings associated with cutaneous conditions
References
External links
http://www.orpha.net/consor/www/cgi-bin/OC_Exp.php?lng=EN&Expert=2092
GeneReview/NIH/UW entry on Focal dermal hypoplasia | 0-1
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Tension headache, also known as stress headache, or tension-type headache (TTH), is the most common type of primary headache. The pain can radiate from the lower back of the head, the neck, eyes or other muscle groups in the body typically affecting both sides of the head. Tension-type headaches account for nearly 90% of all headaches. Pain medications, such as paracetamol and ibuprofen, are effective for the treatment of tension headache. Tricyclic antidepressants appear to be useful for prevention. Evidence is poor for SSRIs, propranolol and muscle relaxants.As of 2016, tension headaches affect about 1.89 billion people and are more common in women than men (23% to 18% respectively). Signs and symptoms
According to the third edition of the International Classification of Headache Disorders, the attacks must meet the following criteria:
A duration of between 30 minutes and 7 days. At least two of the following four characteristics:
bilateral location
pressing or tightening (non-pulsating) quality
mild or moderate intensity
not aggravated by routine physical activity such as walking or climbing stairs
Both of the following:
no nausea or vomiting
no more than one of photophobia (sensitivity to bright light) or phonophobia (sensitivity to loud sounds)Tension-type headaches may be accompanied by tenderness of the scalp on manual pressure during an attack. Risk factors
Various precipitating factors may cause tension-type headaches in susceptible individuals:
Anxiety
Stress
Sleep problems
Young age
Poor health
Mechanism
Although the musculature of the head and neck and psychological factors such as stress may play a role in the overall pathophysiology of TTH, neither is currently believed to be the sole cause of the development of TTH. | The head becomes so enlarged that they eventually may be bedridden.About 80–90% of fetuses or newborn infants with spina bifida—often associated with meningocele or myelomeningocele—develop hydrocephalus. Acquired
This condition is acquired as a consequence of CNS infections, meningitis, brain tumors, head trauma, toxoplasmosis, or intracranial hemorrhage (subarachnoid or intraparenchymal), and is usually painful. Type
The cause of hydrocephalus is not known with certainty and is probably multifactorial. It may be caused by impaired CSF flow, reabsorption, or excessive CSF production. Obstruction to CSF flow hinders its free passage through the ventricular system and subarachnoid space (e.g., stenosis of the cerebral aqueduct or obstruction of the interventricular foramina secondary to tumors, hemorrhages, infections or congenital malformations) and can cause increases in ICP. Hydrocephalus can also be caused by overproduction of CSF (relative obstruction) (e.g., choroid plexus papilloma, villous hypertrophy). Bilateral ureteric obstruction is a rare, but reported, cause of hydrocephalus.Hydrocephalus can be classified into communicating and noncommunicating (obstructive). Both forms can be either congenital or acquired. Communicating
Communicating hydrocephalus, also known as nonobstructive hydrocephalus, is caused by impaired CSF reabsorption in the absence of any obstruction of CSF flow between the ventricles and subarachnoid space. This may be due to functional impairment of the arachnoidal granulations (also called arachnoid granulations or Pacchionis granulations), which are located along the superior sagittal sinus, and is the site of CSF reabsorption back into the venous system. Various neurologic conditions may result in communicating hydrocephalus, including subarachnoid/intraventricular hemorrhage, meningitis, and congenital absence of arachnoid villi. | 0-1
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Final maturation induction
Final maturation induction and release, such as by human chorionic gonadotropin (HCG or hCG) or recombinant luteinizing hormone, results in a predictable time of ovulation, with the interval from drug administration to ovulation depending on the type of drug. This avails for sexual intercourse or intrauterine insemination to conveniently be scheduled at ovulation, the most likely time to achieve pregnancy.As evidenced by clomifene-induced cycles, however, triggering oocyte release has been shown to decrease pregnancy chances compared to frequent monitoring with LH surge tests. Therefore, in such cases, triggering oocyte release is best reserved for women who require intrauterine insemination and in whom luteinizing hormone monitoring proves difficult or unreliable. It may also be used when luteinizing hormone monitoring has no shown an luteinizing hormone surge by cycle day 18 (where cycle day 1 is the first day of the preceding menstruation) and there is an ovarian follicle of over 20 mm in size. Repeat cycles
Ovulation induction can be repeated every menstrual cycle. For clomifene, the dosage may be increased by 50-mg increments in subsequent cycles until ovulation is achieved. However, at a dosage of 200 mg, further increments are unlikely to increase pregnancy chances.It is not recommended by the manufacturer of clomifene to use it for more than 6 consecutive cycles. | Many patients with ventriculitis also experience some degree of hydrocephalus, which is the buildup of cerebrospinal fluid due to the inability of the ventricles to reabsorb and correctly circulate the fluid. Brain abscess is another common disorder resulting from the inflammation. If left untreated, ventriculitis can lead to serious inhibition of mental function and even death. The symptoms vary greatly, in part, because of the underlying or causing infection. While the inflammation can cause a number of effects such as those mentioned previously, the base infection could cause other symptoms that dont necessarily have to do with the ventriculitis, itself. One of the challenges doctors face in diagnosing ventriculitis is distinguishing indicative symptoms, in spite of the wide variety of possible presentations of the disease. A great deal of emphasis is being put on research into better and faster ways to diagnose ventriculitis without the delay inherent with microbiological testing of the cerebrospinal fluid.The progression of the disease is also largely dependent on the nature of the specific case. Depending on the underlying infection, the way it entered the brain, and the type and timing of treatment, the infection may spread or withdraw on the order of months or days. Ventriculitis is a very serious condition and should be treated early to ensure as little lasting damage as possible. Cause
Ventriculitis is caused by an infection of the ventricles, causing an immune response in the lining, which in turn, leads to inflammation. The ventriculitis, is in truth, a complication of the initial infection or abnormality. | 0-1
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Such individual differences may be due to genetic polymorphisms, which code for D2 receptor binding site affinity, or prior exposure to environmental toxins. Decreased functional reserve or cognitive dysfunction, associated with aging, intellectual disability, alcohol and drug use, or traumatic head injuries, has also been shown to increase risk of developing the disorder among those treated with neuroleptics. Antipsychotic drugs can sometimes camouflage the signs of tardive dyskinesia from occurring in the early stages; this can happen from the individual having an increased dose of an antipsychotic drug. Often the symptoms of tardive dyskinesia are not apparent until the individual comes off of the antipsychotic drugs; however, when tardive dyskinesia worsens, the signs become visible.Other dopamine antagonists and antiemetics can cause tardive dyskinesia, such as metoclopramide and promethazine, used to treat gastrointestinal disorders. Atypical antipsychotics are considered lower-risk for causing TD than their typical counterparts with their relative rates of TD of 13.1% and 32.4% respectively in short-term trials with haloperidol being the main typical antipsychotic utilised in said trials. Quetiapine and clozapine are considered the lowest risk agents for precipitating TD. From 2008, there have been reported cases of the anti-psychotic medication aripiprazole, a partial agonist at D2 receptors, leading to tardive dyskinesia. As of 2013, reports of tardive dyskinesia in aripiprazole have grown in number. The available research seems to suggest that the concurrent prophylactic use of a neuroleptic and an antiparkinsonian drug is useless to avoid early extrapyramidal side-effects and may render the person more sensitive to tardive dyskinesia. | Tardive dyskinesia (TD) is a disorder that results in involuntary, repetitive body movements, which may include grimacing, sticking out the tongue, or smacking the lips. Additionally, there may be rapid jerking movements or slow writhing movements. In about 20% of people with TD, the disorder interferes with daily functioning.Tardive dyskinesia occurs in some people as a result of long-term use of dopamine-receptor-blocking medications such as antipsychotics and metoclopramide. These medications are usually used for mental illness but may also be given for gastrointestinal or neurological problems. The condition typically develops only after months to years of use. The diagnosis is based on the symptoms after ruling out other potential causes.Efforts to prevent the condition include either using the lowest possible dose or discontinuing use of neuroleptics. Treatment includes stopping the neuroleptic medication if possible or switching to clozapine. Other medications such as valbenazine, tetrabenazine, or botulinum toxin may be used to lessen the symptoms. With treatment, some see a resolution of symptoms, while others do not.Rates in those on atypical antipsychotics are about 20%, while those on typical antipsychotics have rates of about 30%. The risk of acquiring the condition is greater in older people, for women, as well as patients with mood disorders and/or medical diagnoses receiving antipsychotic medications. The term "tardive dyskinesia" first came into use in 1964. Signs and symptoms
Tardive dyskinesia is characterized by repetitive, involuntary movements. | 11
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Hematinic deficiencies can cause anemia, which is also associated with aphthous-like ulceration.Gastrointestinal disorders are sometimes associated with aphthous-like stomatitis, e.g. most commonly celiac disease, but also inflammatory bowel disease such as Crohns disease or ulcerative colitis. The link between gastrointestinal disorders and aphthous stomatitis is probably related to nutritional deficiencies caused by malabsorption. Less than 5% of people with RAS have celiac disease, which usually presents with severe malnutrition, anemia, abdominal pain, diarrhea and glossitis (inflammation of the tongue). Sometimes aphthous-like ulcerations can be the only sign of celiac disease. Despite this association, a gluten-free diet does not usually improve the oral ulceration.Other examples of systemic conditions associated with aphthous-like ulceration include reactive arthritis, and recurrent erythema multiforme. Diagnosis
Diagnosis is mostly based on the clinical appearance and the medical history. The most important diagnostic feature is a history of recurrent, self healing ulcers at fairly regular intervals. Although there are many causes of oral ulceration, recurrent oral ulceration has relatively few causes, most commonly aphthous stomatitis, but rarely Behçets disease, erythema multiforme, ulceration associated with gastrointestinal disease, and recurrent intra-oral herpes simplex infection. A systemic cause is more likely in adults who suddenly develop recurrent oral ulceration with no prior history.Special investigations may be indicated to rule out other causes of oral ulceration. These include blood tests to exclude anemia, deficiencies of iron, folate or vitamin B12, or celiac disease. However, the nutritional deficiencies may be latent and the peripheral blood picture may appear relatively normal. | History, society and culture
"Aphthous affectations" and "aphthous ulcerations" of the mouth are mentioned several times in the treatise "Of the Epidemics" (part of the Hippocratic corpus, in the 4th century BCE), although it seems likely that this was oral ulceration as a manifestation of some infectious disease, since they are described as occurring in epidemic-like patterns, with concurrent symptoms such as fever. Aphthous stomatitis was once thought to be a form of recurrent herpes simplex virus infection, and some clinicians still refer to the condition as "herpes" despite this cause having been disproven.The informal term "canker sore" is sometimes used, mainly in North America, either to describe this condition generally, or to refer to the individual ulcers of this condition, or mouth ulcers of any cause unrelated to this condition. The origin of the word "canker" is thought to have been influenced by Latin, Old English, Middle English and Old North French. In Latin, cancer translates to "malignant tumor" or literally "crab" (related to the likening of sectioned tumors to the limbs of a crab). The closely related word in Middle English and Old North French, chancre, now more usually applied to syphilis, is also thought to be involved. Despite this etymology, aphthous stomatitis is not a form of cancer but rather entirely benign. An aphtha (plural aphthae) is a non specific term that refers to an ulcer of the mouth. The word is derived from the Greek word aphtha meaning "eruption" or "ulcer". | 11
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Lower doses again are called for in the elderly to reduce the incidence of side effects and maintain age-dependent normal levels of IGF-1.In many countries, including the UK, the majority view among endocrinologists is that the failure of treatment to provide any demonstrable, measurable benefits in terms of outcomes means treatment is not recommended for all adults with severe GHD, and national guidelines in the UK as set out by NICE suggest three criteria which all need to be met for treatment to be indicated:
Severe GH deficiency, defined as a peak GH response of <9mU/litre during an insulin tolerance test
Perceived impairment of quality of life, as assessed by questionnaire
They are already treated for other pituitary hormone disordersWhere treatment is indicated, duration is dependent upon indication. Cost of adult treatment in the UK is 3000-4000 GBP annually. Side effects
Headaches
Joint pain and muscle pain
Fluid retention, and carpal tunnel syndrome
Mild hypertension
Visual problems
Nausea and vomiting
Paraesthesiae
Antibody formation
Reactions at the injection site
Rarely, benign intracranial hypertension. Prognosis
Child
When treated with GH, a severely deficient child will begin to grow faster within months. In the first year of treatment, the rate of growth may increase from half as fast as other children are growing to twice as fast (e.g., from 1 inch a year to 4 inches, or 2.5 cm to 10). Growth typically slows in subsequent years, but usually remains above normal so that over several years a child who had fallen far behind in his height may grow into the normal height range. Excess adipose tissue may be reduced. | Severe GH deficiency in childhood additionally has the following measurable characteristics:
Proportional stature well below that expected for family heights, although this characteristic may not be present in the case of familial-linked GH deficiency
Below-normal velocity of growth
Delayed physical maturation
Delayed bone age
Low levels of IGF1, IGF2, IGF binding protein 3
Increased growth velocity after a few months of GH treatmentIn childhood and adulthood, the diagnosing doctor will look for these features accompanied by corroboratory evidence of hypopituitarism such as deficiency of other pituitary hormones, a structurally abnormal pituitary, or a history of damage to the pituitary. This would confirm the diagnosis; in the absence of pituitary pathology, further testing would be required. Classification
Growth hormone deficiency can be congenital or acquired in childhood or adult life. It can be partial or complete. It is usually permanent, but sometimes transient. It may be an isolated deficiency or occur in association with deficiencies of other pituitary hormones.The term hypopituitarism is often used interchangeably with GH deficiency but more often denotes GH deficiency plus deficiency of at least one other anterior pituitary hormone. When GH deficiency (usually with other anterior pituitary deficiencies) is associated with posterior pituitary hormone deficiency (usually diabetes insipidus), the condition is termed panhypopituitarism. Treatment
GH deficiency is treated by replacing GH with daily injections under the skin or into muscle. Until 1985, growth hormone for treatment was obtained by extraction from human pituitary glands collected at autopsy. | 11
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Deficient populations
In areas where there is little iodine in the diet, typically remote inland areas and semi-arid equatorial climates where no marine foods are eaten, iodine deficiency gives rise to hypothyroidism, symptoms of which are extreme fatigue, goiter, mental slowing, depression, weight gain, and low basal body temperatures.Iodine deficiency is the leading cause of preventable mental retardation, a result which occurs primarily when babies or small children are rendered hypothyroidic by a lack of the element. The addition of iodine to table salt has largely eliminated this problem in the wealthier nations, but as of March 2006, iodine deficiency remained a serious public health problem in the developing world.Iodine deficiency is also a problem in certain areas of Europe. In Germany it has been estimated to cause a billion dollars in health care costs per year. A modelling analysis suggests universal iodine supplementation for pregnant women in England may save £199 (2013 UK pounds) to the health service per pregnant woman and save £4476 per pregnant woman in societal costs.Iodine deficiency was previously a common disease in Norway, because the content of iodine in the drinking water was low. Before 1950 goiter was a widespread disease caused by iodine deficiency. Up to 80 per cent of the population were affected in inland areas. In the coastal communities, saltwater fish were an important part of the diet, and because of the presence of iodine in seawater, goiter was less common than in the inland districts. From the 1950s, Norwegians started adding iodine to dairy cow feed. | Iodine deficiency is a lack of the trace element iodine, an essential nutrient in the diet. It may result in metabolic problems such as goiter, sometimes as an endemic goiter as well as congenital iodine deficiency syndrome due to untreated congenital hypothyroidism, which results in developmental delays and other health problems. Iodine deficiency is an important global health issue, especially for fertile and pregnant women. It is also a preventable cause of intellectual disability. Iodine is an essential dietary mineral for neurodevelopment among children. The thyroid hormones thyroxine and triiodothyronine contain iodine. In areas where there is little iodine in the diet, typically remote inland areas where no marine foods are eaten, iodine deficiency is common. It is also common in mountainous regions of the world where food is grown in iodine-poor soil. Prevention includes adding small amounts of iodine to table salt, a product known as iodized salt. Iodine compounds have also been added to other foodstuffs, such as flour, water and milk, in areas of deficiency. Seafood is also a well known source of iodine.In the U.S., the use of iodine has decreased over concerns of overdoses since mid-20th century, and the iodine antagonists bromine, perchlorate and fluoride have become more ubiquitous. In particular, around 1980 the practice of using potassium iodate as dough conditioner in bread and baked goods was gradually replaced by the use of other conditioning agents such as bromide.Iodine deficiency resulting in goiter occurs in 187 million people globally as of 2010 (2.7% of the population). | 11
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For example, an egg or sperm cell may gain an extra copy of the chromosome. If one of these atypical reproductive cells contributes to the genetic makeup of a child, the child will have an extra chromosome 13 in each of the bodys cells. Mosaic Patau syndrome is also not inherited. It occurs as a random error during cell division early in fetal development.Patau syndrome due to a translocation can be inherited. An unaffected person can carry a rearrangement of genetic material between chromosome 13 and another chromosome. This rearrangement is called a balanced translocation because there is no extra material from chromosome 13. Although they do not have signs of Patau syndrome, people who carry this type of balanced translocation are at an increased risk of having children with the condition. Recurrence risk
Unless one of the parents is a carrier of a translocation, the chances of a couple having another trisomy 13 affected child is less than 1%, below that of Down syndrome. Diagnosis
Diagnosis is usually based on clinical findings, although fetal chromosome testing will show trisomy 13. While many of the physical findings are similar to Edwards syndrome, there are a few unique traits, such as polydactyly. However, unlike Edwards syndrome and Down syndrome, the quad screen does not provide a reliable means of screening for this disorder. This is due to the variability of the results seen in fetuses with Patau. Treatment
Medical management of children with Trisomy 13 is planned on a case-by-case basis and depends on the individual circumstances of the patient. | Provisional tic disorder approximately replaced transient tic disorder: because initially presenting tics may eventually be diagnosed as chronic tic disorder or Tourettes, transient suggested it could only be defined in retrospect (though that perception did not follow the DSM-IV-TR definition). The term provisional "satisfies experts with a more systematic epidemiological approach to disorders", but should not imply that treatment might not be called for. Differentiation of chronic motor or vocal tic disorder: DSM-5 added a specifier to distinguish between vocal and motor tics that are chronic. This distinction was added because higher rates of comorbid diagnoses are present with vocal tics relative to motor tics. Now includes as Tourettes Disorder patients with tics who experienced a 3-month or longer remission since the first tic, as long as the first tic was at least a year ago. Stimulant use as a cause removed: there is no evidence that the use of stimulants causes tic disorders. New categories, Other specified and Unspecified: for tic disorders that result in significant impairment to the individual yet do not meet the full criteria for other tic disorders. The new categories account for tics with onset in adulthood, or tics triggered by other medical conditions or illicit drug use. References
External links
The Tourette Syndrome Classification Study Group. "Definitions and classification of tic disorders". Arch Neurol. 1993 Oct;50(10):1013-6. PMID 8215958. Retrieved on 2005-03-22
Walkup JT, Ferrão Y, Leckman JF, Stein DJ, Singer H. Tic disorders: some key issues for DSM-V (PDF). Depress Anxiety. 2010 Jun;27(6):600–10. PMID 20533370 doi:10.1002/da.20711 | 0-1
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Magnetic resonance imaging
Magnetic resonance imaging (MRI) use has become increasingly common for diagnosis of appendicitis in children and pregnant patients due to the radiation dosage that, while of nearly negligible risk in healthy adults, can be harmful to children or the developing baby. In pregnancy, it is more useful during the second and third trimester, particularly as the enlargening uterus displaces the appendix, making it difficult to find by ultrasound. The periappendiceal stranding that is reflected on CT by fat stranding on MRI appears as an increased fluid signal on T2 weighted sequences. First trimester pregnancies are usually not candidates for MRI, as the fetus is still undergoing organogenesis, and there are no long-term studies to date regarding its potential risks or side effects. X-ray
In general, plain abdominal radiography (PAR) is not useful in making the diagnosis of appendicitis and should not be routinely obtained from a person being evaluated for appendicitis. Plain abdominal films may be useful for the detection of ureteral calculi, small bowel obstruction, or perforated ulcer, but these conditions are rarely confused with appendicitis. An opaque fecalith can be identified in the right lower quadrant in fewer than 5% of people being evaluated for appendicitis. A barium enema has proven to be a poor diagnostic tool for appendicitis. While failure of the appendix to fill during a barium enema has been associated with appendicitis, up to 20% of normal appendices do not fill. Scoring systems
Several scoring systems have been developed to try to identify people who are likely to have appendicitis. | Computed tomography
Where it is readily available, computed tomography (CT) has become frequently used, especially in people whose diagnosis is not obvious on history and physical examination. Although some concerns about interpretation are identified, a 2019 Cochrane review found that sensitivity and specificity of CT for the diagnosis of acute appendicitis in adults was high. Concerns about radiation tend to limit use of CT in pregnant women and children, especially with the increasingly widespread usage of MRI.The accurate diagnosis of appendicitis is multi-tiered, with the size of the appendix having the strongest positive predictive value, while indirect features can either increase or decrease sensitivity and specificity. A size of over 6 mm is both 95% sensitive and specific for appendicitis.However, because the appendix can be filled with fecal material, causing intraluminal distention, this criterion has shown limited utility in more recent meta-analyses. This is as opposed to ultrasound, in which the wall of the appendix can be more easily distinguished from intraluminal feces. In such scenarios, ancillary features such as increased wall enhancement as compared to adjacent bowel and inflammation of the surrounding fat, or fat stranding, can be supportive of the diagnosis. However, their absence does not preclude it. In severe cases with perforation, an adjacent phlegmon or abscess can be seen. Dense fluid layering in the pelvis can also result, related to either pus or enteric spillage. When patients are thin or younger, the relative absence of fat can make the appendix and surrounding fat stranding difficult to see. | 11
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Additional information can be helpful in diagnosis, including the Dissociative Experiences Scale or other questionnaires, performance-based measures, records from doctors or academic records, and information from partners, parents, or friends. A dissociative disorder cannot be ruled out in a single session and it is common for patients diagnosed with a dissociative disorder to not have a previous dissociative disorder diagnosis due to a lack of clinician training. Some diagnostic tests have also been adapted or developed for use with children and adolescents such as the Adolescent Dissociative Experiences Scale, Childrens Version of the Response Evaluation Measure (REM-Y-71), Child Interview for Subjective Dissociative Experiences, Child Dissociative Checklist (CDC), Child Behavior Checklist (CBCL) Dissociation Subscale, and the Trauma Symptom Checklist for Children Dissociation Subscale.Dissociative disorders have been found to be quite prevalent in outpatient populations, as well as within low-income communities. One study found that in a population of poor inner-city outpatients, there was a 29% prevalence of dissociative disorders.There are problems with classification, diagnosis and therapeutic strategies of dissociative and conversion disorders which can be understood by the historic context of hysteria. Even current systems used to diagnose DD such as the DSM-IV and ICD-10 differ in the way the classification is determined. In most cases mental health professionals are still hesitant to diagnose patients with Dissociative Disorder, because before they are considered to be diagnosed with Dissociative Disorder these patients have more than likely been diagnosed with major depressive disorder, anxiety disorder, and most often post-traumatic stress disorder. | These categories are used for forms of pathological dissociation that do not fully meet the criteria of the other specified dissociative disorders; or if the correct category has not been determined; or the disorder is transient.The ICD11 lists dissociative disorders as:
Dissociative neurological symptom disorder
Dissociative amnesia
Dissociative amnesia with dissociative fugue
Trance disorder
Possession trance disorder
Dissociative identity disorder
Partial dissociative identity disorder
Depersonalization-derealization disorder
Cause and treatment
Dissociative identity disorder
Cause: Dissociative identity disorder is caused by ongoing childhood trauma that occurs before the ages of six to nine. People with dissociative identity disorder usually have close relatives who have also had similar experiences.Treatment: Long-term psychotherapy to improve the patients quality of life. Dissociative amnesia
Cause: A way to cope with trauma. Treatment: Psychotherapy (e.g. talk therapy) counseling or psychosocial therapy which involves talking about your disorder and related issues with a mental health provider. Psychotherapy often involves hypnosis (help you remember and work through the trauma); creative art therapy (using creative process to help a person who cannot express his or her thoughts); cognitive therapy (talk therapy to identify unhealthy and negative beliefs/behaviors); and medications (antidepressants, anti-anxiety medications, or sedatives). These medications help control the symptoms associated with the dissociative disorders, but there are no medications yet that specifically treat dissociative disorders. However, the medication pentothal can sometimes help to restore the memories. The length of an event of dissociative amnesia may be a few minutes or several years. If an episode is associated with a traumatic event, the amnesia may clear up when the person is removed from the traumatic situation. | 11
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In the United States, the marketing approval does not contain these restrictions, though the label contains prominent warnings of skin reactions. The initial approval by the Food and Drug Administration of the United States (December 1999) encompassed these indications:
Acute exacerbations of chronic bronchitis
Acute bacterial sinusitis
Community acquired pneumoniaAdditional indications approved by the Food and Drug Administration:
April 2001: Uncomplicated skin and skin-structure infections
May 2004: Community-acquired pneumonia caused by multidrug-resistant Streptococcus pneumoniae
June 2005: Complicated skin and skin-structure infections
November 2005: Complicated intra-abdominal infectionsThe European Medicines Agency has advised that, for pneumonia, acute bacterial sinusitis, and acute exacerbations of COPD, it should only be used when other antibiotics are inappropriate.Oral and intravenous moxifloxacin have not been approved for children. Several drugs in this class, including moxifloxacin, are not licensed by the Food and Drug Administration for use in children, because of the risk of permanent injury to the musculoskeletal system. Moxifloxacin eye drops are approved for conjunctival infections caused by susceptible bacteria.Recently, alarming reports of moxifloxacin resistance rates among anaerobes have been published. In Austria 36% of Bacteroides have been reported to be reistant to moxifloxacin, while in Italy resistance rates as high as 41% have been reported. Susceptible bacteria
A broad spectrum of bacteria is susceptible, including the following:
Staphylococcus aureus
Staphylococcus epidermidis
Streptococcus pneumoniae
Haemophilus influenzae
Klebsiella spp. Moraxella catarrhalis
Enterobacter spp. Mycobacterium spp. | Ranking 140th within the top 200 prescribed drugs in the United States for 2007, Avelox generated sales of $697.3 million worldwide.Moxifloxacin is also manufactured by Alcon as Vigamox. Patent
A United States patent application was made on 30 June 1989, for Avelox, Bayer A.G. being the assignee, which was subsequently approved on 5 February 1991. This patent was scheduled to expire on 30 June 2009. However, this patent was extended for an additional two and one half years on 16 September 2004, and as such was not expected to expire until 2012. Moxifloxacin was subsequently (ten years later) approved by the FDA for use in the United States in 1999. At least four additional United States patents have been filed regarding moxifloxacin hydrochloride since the 1989 United States application, as well as patents outside of the US. Society and culture
Regulatory actions
Regulatory agencies have taken actions to address certain rare but serious adverse events associated with moxifloxacin therapy. Based on its investigation into reports of rare but severe cases of liver toxicity and skin reactions, the European Medicines Agency recommended in 2008 that the use of the oral (but not the IV) form of moxifloxacin be restricted to infections in which other antibacterial agents cannot be used or have failed. Similarly, the Canadian label includes a warning of the risk of liver injury.The U.S. label does not contain restrictions similar to the European label, but a carries a "black box" warning of the risk of tendon damage and/or rupture and warnings regarding the risk of irreversible peripheral neuropathy. | 11
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Many research groups have begun using techniques such as magnetic resonance spectroscopy, functional imaging and cortical thickness measurements in an attempt to offer an earlier diagnosis to the FTD patient. Fluorine-18-fluorodeoxyglucose positron emission tomography (FDG-PET) scans classically show frontal and/or anterior temporal hypometabolism, which helps differentiate the disease from Alzheimers disease. The PET scan in Alzheimers disease classically shows biparietal hypometabolism. Meta-analyses based on imaging methods have shown that frontotemporal dementia mainly affects a frontomedial network discussed in the context of social cognition or theory of mind. This is entirely in keeping with the notion that on the basis of cognitive neuropsychological evidence, the ventromedial prefrontal cortex is a major locus of dysfunction early on in the course of the behavioural variant of frontotemporal degeneration. The language subtypes of frontotemporal lobar degeneration (semantic dementia and progressive nonfluent aphasia) can be regionally dissociated by imaging approaches in vivo.The confusion between Alzheimers and FTD is justifiable due to the similarities between their initial symptoms. Patients do not have difficulty with movement and other motor tasks. As FTD symptoms appear, it is difficult to differentiate between a diagnosis of Alzheimers disease and FTD. There are distinct differences in the behavioral and emotional symptoms of the two dementias, notably, the blunting of emotions seen in FTD patients. In the early stages of FTD, anxiety and depression are common, which may result in an ambiguous diagnosis. | Types
Supernumerary teeth can be classified by shape and by position. The shapes include the following:
Supplemental (where the tooth has a normal shape for the teeth in that series);
Tuberculate (also called barrel shaped);
Conical (also called peg shaped);
Compound odontoma (multiple small tooth-like forms);
Complex odontoma (a disorganized mass of dental tissue)When classified by position, a supernumerary tooth may be referred to as a mesiodens, a paramolar, or a distomolar. Occasionally, these teeth do not erupt into the oral cavity but manifest as a malocclusion.The most common supernumerary tooth is a mesiodens, which is a malformed, peg-like tooth that occurs between the maxillary central incisors. Fourth and fifth molars that form behind the third molars are another kind of supernumerary teeth. Treatment
Although these teeth are usually asymptomatic and pose no threat to the individual, they are often extracted for aesthetic reasons, to allow the eruption of other teeth, orthodontic reasons and/or suspected pathology. This is done particularly if the mesiodens is positioned in the maxillary central incisor region. The traditional method of removal is done by using bone chisels, although a more advanced technique has been found to be more beneficial, especially if surgery is required. Through the use of piezoelectricity, piezoelectric ultrasonic bone surgery may be more time-consuming than the traditional method but it seems to reduce the post-operative bleeding and associated complications quite significantly. Epidemiology
It is evident that hyperdontia is more common in the permanent dentition than in the primary. | 0-1
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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. | Necrotizing sialometaplasia (NS) is a benign, ulcerative lesion, usually located towards the back of the hard palate. It is thought to be caused by ischemic necrosis (death of tissue due to lack of blood supply) of minor salivary glands in response to trauma. Often painless, the condition is self-limiting and should heal in 6–10 weeks. Although entirely benign and requiring no treatment, due to its similar appearance to oral cancer, it is sometimes misdiagnosed as malignant. Therefore, it is considered an important condition, despite its rarity. Signs and symptoms
The condition most commonly is located at the junction of the hard and soft palate. However, the condition may arise anywhere minor salivary glands are located. It has also been occasionally reported to involve the major salivary glands. It may be present only on one side, or both sides. The lesion typically is 1–4 cm in diameter.Initially, the lesion is a tender, erythematous (red) swelling. Later, in the ulcerated stage, the overlying mucosa breaks down to leave a deep, well-circumscribed ulcer which is yellow-gray in color and has a lobular base.There is usually only minor pain, and the condition is often entirely painless. There may be prodromal symptoms similar to flu before the appearance of the lesion. Causes
The exact cause of the condition is unknown. There is most evidence to support vascular infarction and ischemic necrosis of salivary gland lobules as a mechanism for the condition. | 0-1
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Some preliminary laboratory experiments using the venom extracted from Malo maxima (the Broome Irukandji) on rat cardiovascular tissue in vitro has suggested that magnesium does in fact block many of the actions of this venom. Epidemiology
Reports of Irukandji syndrome have come from Australia, the United States (Hawaii and Florida), the French Antilles, Bonaire, the Caribbean, Timor Leste and Papua New Guinea. Cubozoan species other than Carukia barnesi are presumed to be responsible for envenomations outside Australia. History
In 1964 Jack Barnes confirmed the cause of the syndrome was a sting from a small box jellyfish: the Irukandji jellyfish, which can fire venom-filled stingers out of its body and into passing victims. To prove that the jellyfish was the cause of the syndrome, he captured one and deliberately stung himself, his 9-year-old son and a local lifeguard, then observed the resulting symptoms. Other cubozoans possibly can cause Irukandji syndrome; those positively identified include Carukia barnesi, Alatina mordens, Alatina alata, Malo maxima, Malo kingi, Carybdea xaymacana, Keesingia gigas, an as-yet unnamed "fire jelly", and another unnamed species. Culture and society
A 2005 Discovery Channel program, Killer Jellyfish, portrayed the severity of the pain from an Irukandji jellyfish sting when two Australian researchers (Jamie Seymour and Teresa Carrette) were stung. Another program aired on the Discovery Channel, Stings, Fangs and Spines, featured a 20-minute spot on Irukandji syndrome. | Blood and urine samples are collected for evaluation of kidney and liver function and determination of the presence of a monoclonal protein. Imaging studies such as echocardiography and an ultrasound of the abdomen will be performed. A CT scan, magnetic resonance imaging (MRI) or positron emission tomography (PET) may also be indicated. In patients with LCDD, a biopsy of the affected organ will show deposited light chains. A bone marrow biopsy will be done in order to rule out multiple myeloma. Treatment
Decreasing production of the organ-damaging light chains is the treatment goal. Options include chemotherapy using bortezomib, autologous stem cell transplantation, immunomodulatory drugs, and kidney transplant.There is no standard treatment for LCDD. High-dose melphalan in conjunction with autologous stem cell transplantation has been used in some patients. A regimen of bortezomib and dexamethasone has also been examined. Prognosis
The median time to progression to end stage renal disease is 2.7 years. After 5 years, about 37% of patients with LCDD are alive and do not have end stage renal disease. References
External links
National Institutes of Health Genetic and Rare Diseases Information Center
Emedicine | 0-1
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If the pain is localized, occasionally creams and patches containing compounds such as capsaicin, NSAIDs, or lidocaine may be used. Heat or ice compresses may also be used for treatment.Outpatient follow-up may also be a form of treatment for costochondritis. Manual therapy methods such as myofascial release, muscle energy techniques, balanced ligamentous tension (BLT), rib mobilization techniques, and stretching exercises may be used. Additionally, educating the individual with costochondritis about their body mechanics, posture, and activity modification can be beneficial.In severe cases where symptoms do not resolve and last up to a year or longer, corticosteroids or local anesthetic injections may be considered. Epidemiology
Costochondritis is a common condition that is responsible for approximately 13-36% of acute chest pain-related concerns from adults depending on the setting, with 14-39% for adolescents. It is most often seen in individuals who are older than 40 years of age and occurs more often in women than in men. References
== External links == | Successful surgical correction of strabismus, for adult as well as children, has been shown to have a significantly positive effect on psychological well-being.Very little research exists regarding coping strategies employed by adult strabismics. One study categorized coping methods into three subcategories: avoidance (refraining from participation in an activity), distraction (deflecting attention from the condition), and adjustment (approaching an activity differently). The authors of the study suggested that individuals with strabismus may benefit from psychosocial support such as interpersonal skills training. No studies have evaluated whether psychosocial interventions have had any benefits on individuals undergoing strabismus surgery. Pathophysiology
The extraocular muscles control the position of the eyes. Thus, a problem with the muscles or the nerves controlling them can cause paralytic strabismus. The extraocular muscles are controlled by cranial nerves III, IV, and VI. An impairment of cranial nerve III causes the associated eye to deviate down and out and may or may not affect the size of the pupil. Impairment of cranial nerve IV, which can be congenital, causes the eye to drift up and perhaps slightly inward. Sixth nerve palsy causes the eyes to deviate inward and has many causes due to the relatively long path of the nerve. Increased cranial pressure can compress the nerve as it runs between the clivus and brain stem. Also, if the doctor is not careful, twisting of the babys neck during forceps delivery can damage cranial nerve VI.Evidence indicates a cause for strabismus may lie with the input provided to the visual cortex. | 0-1
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They predict they will have one or more drugs ready for human clinical trials within the next few years. References
External links
GeneReview/NCBI/NIH/UW entry on Progressive Myoclonus Epilepsy, Lafora Type | Carbachol, also known as carbamylcholine and sold under the brand name Miostat among others, is a cholinomimetic drug that binds and activates acetylcholine receptors. Thus it is classified as a cholinergic agonist. It is primarily used for various ophthalmic purposes, such as for treating glaucoma, or for use during ophthalmic surgery. It is generally administered as an ophthalmic solution (i.e., eye drops). Carbachol produces effects comparable to those of sarin if a massive overdose is administered (as may occur following industrial and shipping accidents) and therefore it is classified as an extremely hazardous substance in the United States as defined in Section 302 of the U.S. Emergency Planning and Community Right-to-Know Act (42 U.S.C. 11002), and is subject to strict reporting requirements by facilities which produce, store, or use it in significant quantities.It is on the World Health Organizations List of Essential Medicines. Chemistry and pharmacology
Carbachol is a choline carbamate and a positively charged quaternary ammonium compound. It is not well absorbed in the gastro-intestinal tract and does not cross the blood–brain barrier. It is usually administered topical ocular or through intraocular injection. Carbachol is not easily metabolized by cholinesterase, it has a 2 to 5 minute onset of action and its duration of action is 4 to 8 hours with topical administration and 24 hours for intraocular administration. Since carbachol is poorly absorbed through topical administration, benzalkonium chloride is mixed in to promote absorption.Carbachol is a parasympathomimetic that stimulates both muscarinic and nicotinic receptors. | 0-1
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The archetypical first clinical symptom is weakness of tail tonus that progresses to paralysis of the tail, followed by a progression up the body to affect the hind limbs and finally the forelimbs.However, similar to MS, the disease symptoms reflect the anatomical location of the inflammatory lesions, and may also include emotional lability, sensory loss, optic neuritis, difficulties with coordination and balance (ataxia), and muscle weakness and spasms. Recovery from symptoms can be complete or partial and the time varies with symptoms and disease severity. Depending on the relapse-remission intervals, rats can have up to three bouts of disease within an experimental period. In mice
Demyelination is produced by injection of brain extracts, CNS proteins (such as myelin basic protein), or peptides from such protein emulsified in an adjuvant such as complete Freunds adjuvant. The presence of the adjuvant allows the generation of inflammatory responses to the protein/peptides. In many protocols, mice are coinjected with pertussis toxin to break down the blood-brain barrier and allow immune cells access to the CNS tissue. This immunisation leads to multiple small disseminated lesions of demyelination (as well as micro-necroses) in the brain and spinal cord and the onset of clinical symptoms.Although sharing some features, mostly demyelination, this model, first introduced in the 1930s, differs from human MS in several ways. EAE either kills animals or leaves them with permanent disabilities; animals with EAE also suffer severe nerve inflammation, and the time course of EAE is entirely different from MS, being the main antigen (MBP) in charge. | Experimental autoimmune encephalomyelitis, sometimes experimental allergic encephalomyelitis (EAE), is an animal model of brain inflammation. It is an inflammatory demyelinating disease of the central nervous system (CNS). It is mostly used with rodents and is widely studied as an animal model of the human CNS demyelinating diseases, including multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADEM). EAE is also the prototype for T-cell-mediated autoimmune disease in general.EAE was motivated by observations during the convalescence from viral diseases by Thomas M. Rivers, D. H. Sprunt and G. P. Berry in 1933. Their findings upon a transfer of inflamed patient tissue to primates was published in the Journal of Experimental Medicine. An acute monophasic illness, it has been suggested that EAE is far more similar to ADEM than MS.
Types of EAE
EAE can be induced in a number of species, including mice, rats, guinea pigs, rabbits and primates. The most commonly used antigens in rodents are spinal cord homogenate (SCH), purified myelin, myelin protein such as MBP, PLP, and MOG, or peptides of these proteins, all resulting in distinct models with different disease characteristics regarding both immunology and pathology. It may also be induced by the passive transfer of T cells specifically reactive to these myelin antigens.Depending on the antigen used and the genetic make-up of the animal, rodents can display a monophasic bout of EAE, a relapsing-remitting form, or chronic EAE. The typical susceptible rodent will debut with clinical symptoms around two weeks after immunization and present with a relapsing-remitting disease. | 11
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Glycosuria is the excretion of glucose into the urine. Ordinarily, urine contains no glucose because the kidneys are able to reabsorb all of the filtered glucose from the tubular fluid back into the bloodstream. Glycosuria is nearly always caused by elevated blood glucose levels, most commonly due to untreated diabetes mellitus. Rarely, glycosuria is due to an intrinsic problem with glucose reabsorption within the kidneys (such as Fanconi syndrome), producing a condition termed renal glycosuria. Glycosuria leads to excessive water loss into the urine with resultant dehydration, a process called osmotic diuresis. Alimentary glycosuria is a temporary condition, when a high amount of carbohydrate is taken, it is rapidly absorbed in some cases where a part of the stomach is surgically removed, the excessive glucose appears in urine producing glycosuria. Follow-up
In a patient with glucosuria, diabetes is confirmed by measuring fasting or random plasma glucose and glycated hemoglobin(HbA1c). Pathophysiology
Blood is filtered by millions of nephrons, the functional units that comprise the kidneys. In each nephron, blood flows from the arteriole into the glomerulus, a tuft of leaky capillaries. The Bowmans capsule surrounds each glomerulus, and collects the filtrate that the glomerulus forms. The filtrate contains waste products (e.g. urea), electrolytes (e.g. sodium, potassium, chloride), amino acids, and glucose. The filtrate passes into the renal tubules of the kidney. In the first part of the renal tubule, the proximal tubule, glucose is reabsorbed from the filtrate, across the tubular epithelium and into the bloodstream. | Symptoms
Sheep
Infected sheep experience sunburn at face, ears, teats and vulva. It is the primary symptom of the poisoning caused by sporidesmin. The sunburn is caused by the fact that the lower tissue is swollen. The skin gets crusty, dark and then peels,. making it susceptible to infection. Other symptoms include dullness, weakness, inappetence, and ill-thrift. An affection of the liver results in jaundice. In a worst-case, the sheep die. Cattle
Infected cattle suffer from sunburn. Dark pigmented skin is often affected. Cattle produce less milk. Jaundice is possible and death after some months. Treatment
Convalescence can take a long time, but some animals may not get healthy. External therapy is possible to treat the sunburn. Animals could be protected by the intake of zinc. Zinc reacts with sporidesmin to create a metallic complex, so that the poison can be eliminated from the body. Prevention and control
If animals are sunburned, they should be placed in the stable to protect them from sunlight. Infected cattle should no longer be used in milk production.Reduce flock density (0.45 hectare/ 15 cows or 100 sheep)GGT (enzyme) is released by the damaged liver over the course of this disease and can be tested to indicate disease severity. == References == | 0-1
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The chemicals and structures that make up the brain have similarities across different people, but they vary in certain enzymes and receptors. These variations are not usually enough to cause a problem, but occasionally they do. For example, if a person has a mutation in a gene that creates the sodium channel (a part of the neuron required for firing) it makes it easier for neuronal firing to get out of control. An infection of the brain (encephalitis) can also be a contributing factor. Although this sort of infection is uncommon it can be due to a virus, bacterium, or (very rarely) fungus. If a seizure happens during the infection itself, the person most likely doesnt have epilepsy but has "symptomatic seizures" or seizures occurring because of a known injury to the brain. Once the infection is stopped the seizures will stop. Another more common infection is "meningitis", infection of the membranes surrounding the brain. Since this infection does not directly involve the brain it might not appear as a possible cause of epilepsy, but has been shown that meningitis can cause epilepsy, which would give rise to the possibility of developing epilepsy partialis continua. These infections are most likely to result in epilepsy when they occur at an early age. Problems with brain development can also be a factor. The brain undergoes a complicated process during development in which neurons are born and must travel to the surface of the brain. Here they wind up carefully placed in six distinct layers of the cerebral cortex. | This can be caused by damage to the sphincter itself, the muscles that support it, or nerves that supply it. In men, the damage usually happens after prostate surgery or radiation, and in women, its usually caused by childbirth and pregnancy. The pressure inside the abdomen (from coughing and sneezing) is normally transmitted to both urethra and bladder equally, leaving the pressure difference unchanged, resulting in continence. When the sphincter is incompetent, this increase in pressure will push the urine against it, leading to incontinence.Another example is urge incontinence. This incontinence is associated with sudden forceful contractions of the detrusor muscle (bladder muscle), leading to an intense feeling of urination, and incontinence if the person does not reach the bathroom on time. The syndrome is known as overactive bladder syndrome, and its related to dysfunction of the detrusor muscle. Children
Urination, or voiding, is a complex activity. The bladder is a balloon-like muscle that lies in the lowest part of the abdomen. The bladder stores urine then releases it through the urethra, the canal that carries urine to the outside of the body. Controlling this activity involves nerves, muscles, the spinal cord and the brain.The bladder is made of two types of muscles: the detrusor, a muscular sac that stores urine and squeezes to empty, and the sphincter, a circular group of muscles at the bottom or neck of the bladder that automatically stays contracted to hold the urine in and automatically relax when the detrusor contracts to let the urine into the urethra. | 0-1
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Vital sign stability and vascular assessment are the most important determinants of management in extremity injuries. As with other traumatic cases, those with uncontrolled bleeding require immediate surgical intervention. If surgical intervention is not readily available and direct pressure is insufficient to control bleeding, tourniquets or direct clamping of visible vessels may be used temporarily to slow active bleeding. People with hard signs of vascular injury also require immediate surgical intervention. Hard signs include active bleeding, expanding or pulsatile hematoma, bruit/thrill, absent distal pulses and signs of extremity ischemia.For stable people without hard signs of vascular injury, an injured extremity index (IEI) should be calculated by comparing the blood pressure in the injured limb compared to an uninjured limb in order to further evaluate for potential vascular injury. If the IEI or clinical signs are suggestive of vascular injury, the person may undergo surgery or receive further imaging including CT angiography or conventional arteriography. In addition to vascular management, people must be evaluated for bone, soft tissue, and nerve injury. Plain films can be used for fractures alongside CTs for soft tissue assessment. Fractures must be debrided and stabilized, nerves repaired when possible, and soft tissue debrided and covered. This process can often require multiple procedures over time depending on the severity of injury. Epidemiology
In 2015, about a million gunshot wounds occurred from interpersonal violence. Firearms, globally in 2016, resulted in 251,000 deaths up from 209,000 in 1990. | This theory is based on high incidence of dead parasites or ova within stone in autopsy findings. Diagnosis
The diagnosis can be suspected by imaging, with typical characteristics centering around appearance of the liver, typically with CT, ultrasound or MRI. Traits that raise suspicion for the infection include intra- and extra- hepatic dilatation and strictures with intraductal pigmented stones, usually in the absence of gallstones and with regions of segmental liver atrophy, particularly the lateral aspect of the left hepatic lobe. There is also reduced arborization of peripheral ducts. Approximately 5% of chronic infections go on to develop cholangiocarcinoma.Pathogenic bacteria responsible for the infection include E. coli, Klebsiella, Pseudomonas, and Proteus species. Anaerobes are a less frequent cause, and a culture positive for multiple strains can be common. When related to Clonorchis sinensis, definitive diagnosis is by identification of eggs by microscopic demonstration in faeces or in duodenal aspirate, but other sophisticated methods have been developed, such as ELISA, which has become the most important clinical technique. Diagnosis by detecting DNAs from eggs in faeces are also developed using PCR, real-time PCR, and LAMP, which are highly sensitive and specific. Treatment
The treatment of RPC involves management of sepsis during episodes of cholangitis with antibiotics, abscess drainage, and blood pressure support. With resistant infection, a surgical hepatectomy or hepaticocutaneousjejunostomy can be performed. Lifelong surveillance for malignancy is also usually necessary. See also
Cholangitis
Cholecystitis
Clonorchiasis
Clonorchis sinensis
Hepaticojejunostomy
Cirrhosis
References
== External links == | 0-1
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Eflornithine should only be used during pregnancy if the potential benefit outweighs the potential risk to the fetus. However, since African trypanosomiasis has a high mortality rate if left untreated, treatment with eflornithine may justify any potential risk to the fetus. Side effects
Eflornithine is not genotoxic; no tumour-inducing effects have been observed in carcinogenicity studies, including one photocarcinogenicity study. No teratogenic effects have been detected. Topical
The topical form of elflornithine is sold under the brand name Vaniqa. The most frequently reported side effect is acne (7–14%). Other side effects commonly (> 1%) reported are skin problems, such as skin reactions from in-growing hair, hair loss, burning, stinging or tingling sensations, dry skin, itching, redness or rash. Intravenous
The intravenous dosage form of eflornithine is sold under the brand name Ornidyl. Most side effects related to systemic use through injection are transient and reversible by discontinuing the drug or decreasing the dose. Hematologic abnormalities occur frequently, ranging from 10 to 55%. These abnormalities are dose-related and are usually reversible. Thrombocytopenia is thought to be due to a production defect rather than to peripheral destruction. Seizures were seen in approximately 8% of patients, but may be related to the disease state rather than the drug. Reversible hearing loss has occurred in 30–70% of patients receiving long-term therapy (more than 4–8 weeks of therapy or a total dose of >300 grams); high-frequency hearing is lost first, followed by middle- and low-frequency hearing. Because treatment for African trypanosomiasis is short-term, patients are unlikely to experience hearing loss. | Similarly, the dose should be reduced by half in those taking strong CYP2D6 inhibitors. Vortioxetine can be discontinued abruptly without tapering, but it is recommended that at doses of 15 to 20 mg/day it be tapered first to 10 mg/day one week prior to full discontinuation if possible. Available forms
Vortioxetine is available in the form of 5, 10, and 20 mg immediate-release, film-coated oral tablets. Contraindications
Vortioxetine is contraindicated in those with hypersensitivity to vortioxetine or to any other components of vortioxetine tablets. It is also contraindicated in those taking monoamine oxidase inhibitors (MAOIs) due to the possibility of serotonin syndrome. Adverse effects
The most common side effects reported with vortioxetine are nausea, vomiting, constipation, and sexual dysfunction, among others. With the exceptions of nausea and sexual dysfunction, these side effects were reported by less than or equal to 10% of study participants given vortioxetine. Significant percentages of placebo-treated participants also report these side effects. Discontinuation of treatment due to adverse effects in clinical trials was 8% with vortioxetine versus 3% with placebo.Sexual dysfunction, such as decreased libido, abnormal orgasm, delayed ejaculation, and erectile dysfunction, are well-known side effects of SSRIs and serotonin–norepinephrine reuptake inhibitors (SNRIs). In clinical trials, sexual dysfunction occurred more often with vortioxetine than with placebo and appeared to be dose-dependent. The specific incidences of treatment-emergent sexual dysfunction as measured with the Arizona Sexual Experience Scale (ASEX) were 14 to 20% for placebo and 16 to 34% for vortioxetine over a dosage range of 5 to 20 mg/day. | 0-1
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More severe disease is likely to occur in people who are immunosuppressed.More than 50 infants with congenital LCMV infection have been reported worldwide. The probability that a woman will become infected after being exposed to rodents, the frequency with which LCMV crosses the placenta, and the likelihood of clinical signs among these infants are still poorly understood. In one study, antibodies to LCMV were detected in 0.8% of normal infants, 2.7% of infants with neurological signs and 30% of infants with hydrocephalus. In Argentina, no congenital LCMV infections were reported among 288 healthy mothers and their infants. However, one study found that two of 95 children in a home for people with severe mental disabilities had been infected with this virus. The prognosis for severely affected infants appears to be poor. In one series, 35% of infants diagnosed with congenital infections had died by the age of 21 months.Transplant-acquired lymphocytic choriomeningitis proves to have a very high morbidity and mortality rate. In the three clusters reported in the U.S. from 2005 to 2010, nine of the ten infected recipients died. One donor had been infected from a recently acquired pet hamster while the sources of the virus in the other cases were unknown. Epidemiology
LCMV has been isolated from fleas, ticks, cockroaches, Culicoides and Aedes mosquitoes. Ticks, lice and mosquitoes have been shown to transmit this virus mechanically in the laboratory. The presence of LCMV in laboratories may cause serious long-term repercussions to worker safety. | Estazolam, sold under the brand name Prosom among others, is a tranquilizer medication of the triazolobenzodiazepine (TBZD) class, which are benzodiazepines (BZDs) fused with a triazole ring . It possesses anxiolytic, anticonvulsant, hypnotic, sedative and skeletal muscle relaxant properties. Estazolam is an intermediate-acting oral benzodiazepine. It is used for short-term treatment of insomnia. It was patented in 1968 and came into medical use in 1975. Medical uses
Estazolam is prescribed for the short-term treatment of certain sleep disorders. It is an effective hypnotic drug showing efficacy in increasing the time spent asleep as well as reducing awakenings during the night. Combination with non-pharmacological options for sleep management results in long-term improvements in sleep quality after discontinuation of short-term estazolam therapy. Estazolam is also sometimes used as a preoperative sleep aid. It was found to be superior to triazolam in side effect profile in preoperative patients in a trial. Estazolam also has anxiolytic properties and due to its long half life can be an effective short-term treatment for insomnia associated with anxiety. Side effects
A hang-over effect commonly occurs with next day impairments of mental and physical performance. Other side effects of estazolam include somnolence, dizziness, hypokinesia, and abnormal coordination.In September 2020, the U.S. Food and Drug Administration (FDA) required the boxed warning be updated for all benzodiazepine medicines to describe the risks of abuse, misuse, addiction, physical dependence, and withdrawal reactions consistently across all the medicines in the class. | 0-1
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Acute zonal occult outer retinopathy (AZOOR) is an inflammatory retinopathy in the category of white dot syndromes typified by acute loss of one or more zones of outer retinal function associated with photopsia, minimal funduscopic changes and abnormal electroretinography findings.This retinal disease was first described by Donald Gass in 1992. Relatively little is known about the condition. Risk factors
Caucasian females in their mid-thirties appear to be most susceptible but the disease may affect anyone regardless of age, sex or race. Pathophysiology
The disease mechanism is unknown but it is believed that it may be caused by a virus, or an auto immune response. References
== External links == | Carac may refer to
a trade name of the drug Fluorouracil
a sweet pie specialty of Swiss origin, see Carac (pastry) | 0-1
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2 oz or 60 grams) of fresh mushrooms treated with ultraviolet light have increased vitamin D content to levels up to 80 micrograms or 3200 IU if exposed to just five minutes of UV light after being harvested.Button mushrooms with enhanced vitamin D2 content produced this way functions similarly to a vitamin D2 supplement; both effectively improves vitamin D status. Vitamin D2 from UV-irradiated yeast baked into bread or mushrooms is bioavailable and increases blood levels of 25(OH)D.
Names
Viosterol, the name given to early preparations of irradiated ergosterol, is essentially synonymous with ergocalciferol. However, currently, Viosterol is also the brand name for cholecalciferol (vitamin D3) in some countries.Ergocalciferol is manufactured and marketed under various names, including Deltalin (Eli Lilly and Company), Drisdol (Sanofi-Synthelabo) and Calcidol (Patrin Pharma). References
External links
"Ergocalciferol". Drug Information Portal. U.S. National Library of Medicine. NIST Chemistry WebBook page for ergocalciferol | 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 | 0-1
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Medical uses
Oxymetazoline is available over-the-counter as a topical decongestant in the form of oxymetazoline hydrochloride in nasal sprays such as Otrivin, Afrin, Operil, Dristan, Dimetapp, Oxyspray, Facimin, Nasivin, Nostrilla, Utabon, Sudafed OM, Vicks Sinex, Zicam, SinuFrin, Drixoral
and Mucinex Full Force.In the United States, oxymetazoline 1% cream is approved by the Food and Drug Administration for topical treatment of persistent facial erythema (redness) associated with rosacea in adults.Due to its vasoconstricting properties, oxymetazoline is also used to treat nose bleeds and eye redness due to minor irritation (marketed as Visine L.R. in the form of eye drops). In July 2020, oxymetazoline received approval by the FDA for the treatment of acquired drooping eyelid. Side effects
Rebound congestion
Rebound congestion, or rhinitis medicamentosa, may occur. A 2006 review of the pathology of rhinitis medicamentosa concluded that use of oxymetazoline for more than three days may result in rhinitis medicamentosa and recommended limiting use to three days. Australian regulatory submission
In a submission to the Therapeutic Goods Administration, a Novartis representative concluded, "The justification was not based on evidence." Citing an existing extensive body of evidence and noting a range of recommended periods from five to ten days, Novartis recommended the established five day period for its use for self-medication without medical consultation as it coincides with the typical duration of the common cold. Use in pregnancy
The Food and Drug Administration places oxymetazoline in category C, indicating risk to the fetus cannot be ruled out. | Oxymetazoline, sold under the brand name Afrin among others, is a topical decongestant and vasoconstrictor medication. It is available over-the-counter as a nasal spray to treat nasal congestion and nosebleeds, as eyedrops to treat eye redness due to minor irritation, and (in the United States) as a prescription topical cream to treat persistent facial redness due to rosacea in adults. Its effects begin within minutes and last for up to 6 hours. Intranasal use for longer than three days may cause congestion to recur or worsen, resulting in physical dependence. Oxymetazoline is a derivative of imidazole. It was developed from xylometazoline at E. Merck Darmstadt by Wolfgang Fruhstorfer and Helmut Müller-Calgan in 1961. A direct sympathomimetic, oxymetazoline binds to and activates α1 adrenergic receptors and α2 adrenergic receptors, most notably. One study classified it in the following order: α(2A) > α(1A) ≥ α(2B) > α(1D) ≥ α(2C) >> α(1B), but this is not universally agreed upon. There is little consistency across the (relatively large) number of in-vitro studies with respect to binding affinity/selectivity. | 11
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VATS may also be used to achieve chemical pleurodesis; this involves insufflation of talc, which activates an inflammatory reaction that causes the lung to adhere to the chest wall.If a chest tube is already in place, various agents may be instilled through the tube to achieve chemical pleurodesis, such as talc, tetracycline, minocycline or doxycycline. Results of chemical pleurodesis tend to be worse than when using surgical approaches, but talc pleurodesis has been found to have few negative long-term consequences in younger people. Aftercare
If pneumothorax occurs in a smoker, this is considered an opportunity to emphasize the markedly increased risk of recurrence in those who continue to smoke, and the many benefits of smoking cessation. It may be advisable for someone to remain off work for up to a week after a spontaneous pneumothorax. If the person normally performs heavy manual labor, several weeks may be required. Those who have undergone pleurodesis may need two to three weeks off work to recover.Air travel is discouraged for up to seven days after complete resolution of a pneumothorax if recurrence does not occur. Underwater diving is considered unsafe after an episode of pneumothorax unless a preventive procedure has been performed. Professional guidelines suggest that pleurectomy be performed on both lungs and that lung function tests and CT scan normalize before diving is resumed. Aircraft pilots may also require assessment for surgery. Neonatal period
For newborn infants with pneumothorax, different management strategies have been suggested including careful observation, thoracentesis (needle aspiration), or insertion of a chest tube. | Arterial supply to the intestines is provided by the superior and inferior mesenteric arteries (SMA and IMA respectively), both of which are direct branches of the aorta.The superior mesenteric artery supplies:
Small bowel
Ascending and proximal two-thirds of the transverse colonThe inferior mesenteric artery supplies:
Distal one-third of the transverse colon
Descending colon
Sigmoid colonOf note, the splenic flexure, or the junction between the transverse and descending colon, is supplied by the most distal portions of both the inferior mesenteric artery and superior mesenteric artery, and is thus referred to medically as a watershed area, or an area especially vulnerable to ischemia during periods of systemic hypoperfusion, such as in shock.Acute abdomen of the ischemic variety is usually due to:
A thromboembolism from the left side of the heart, such as may be generated during atrial fibrillation, occluding the SMA. Nonocclusive ischemia, such as that seen in hypotension secondary to heart failure, may also contribute, but usually results in a mucosal or mural infarct, as contrasted with the typically transmural infarct seen in thromboembolus of the SMA. Primary mesenteric vein thromboses may also cause ischemic acute abdomen, usually precipitated by hypercoagulable states such as polycythemia vera.Clinically, patients present with diffuse abdominal pain, bowel distention, and bloody diarrhea. On physical exam, bowel sounds will be absent. Laboratory tests reveal a neutrophilic leukocytosis, sometimes with a left shift, and increased serum amylase. Abdominal radiography will show many air-fluid levels, as well as widespread edema. Acute ischemic abdomen is a surgical emergency. | 0-1
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Another review indicated that, based upon the longest follow-up studies conducted to date, lifetime stimulant therapy that begins during childhood is continuously effective for controlling ADHD symptoms and reduces the risk of developing a substance use disorder as an adult.Current models of ADHD suggest that it is associated with functional impairments in some of the brains neurotransmitter systems; these functional impairments involve impaired dopamine neurotransmission in the mesocorticolimbic projection and norepinephrine neurotransmission in the noradrenergic projections from the locus coeruleus to the prefrontal cortex. Psychostimulants like methylphenidate and amphetamine are effective in treating ADHD because they increase neurotransmitter activity in these systems. Approximately 80% of those who use these stimulants see improvements in ADHD symptoms. Children with ADHD who use stimulant medications generally have better relationships with peers and family members, perform better in school, are less distractible and impulsive, and have longer attention spans. The Cochrane reviews on the treatment of ADHD in children, adolescents, and adults with pharmaceutical amphetamines stated that short-term studies have demonstrated that these drugs decrease the severity of symptoms, but they have higher discontinuation rates than non-stimulant medications due to their adverse side effects. A Cochrane review on the treatment of ADHD in children with tic disorders such as Tourette syndrome indicated that stimulants in general do not make tics worse, but high doses of dextroamphetamine could exacerbate tics in some individuals. Available forms
Adderall is available as immediate-release (IR) tablets or two different extended-release (XR) formulations. The extended-release capsules are generally used in the morning. | Gastrointestinal side effects may include abdominal pain, constipation, diarrhea, and nausea. Other potential physical side effects include appetite loss, blurred vision, dry mouth, excessive grinding of the teeth, nosebleed, profuse sweating, rhinitis medicamentosa (drug-induced nasal congestion), reduced seizure threshold, tics (a type of movement disorder), and weight loss. Dangerous physical side effects are rare at typical pharmaceutical doses.Amphetamine stimulates the medullary respiratory centers, producing faster and deeper breaths. In a normal person at therapeutic doses, this effect is usually not noticeable, but when respiration is already compromised, it may be evident. Amphetamine also induces contraction in the urinary bladder sphincter, the muscle which controls urination, which can result in difficulty urinating. This effect can be useful in treating bed wetting and loss of bladder control. The effects of amphetamine on the gastrointestinal tract are unpredictable. If intestinal activity is high, amphetamine may reduce gastrointestinal motility (the rate at which content moves through the digestive system); however, amphetamine may increase motility when the smooth muscle of the tract is relaxed. Amphetamine also has a slight analgesic effect and can enhance the pain relieving effects of opioids.USFDA-commissioned studies from 2011 indicate that in children, young adults, and adults there is no association between serious adverse cardiovascular events (sudden death, heart attack, and stroke) and the medical use of amphetamine or other ADHD stimulants. However, amphetamine pharmaceuticals are contraindicated in individuals with cardiovascular disease. | 11
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The Austrian physician Franz Joseph Gall presented the science of phrenology in the early 19th century through his work The Anatomy and Physiology of the Nervous System in General, and of the Brain in Particular.Hippocrates described trigonocephaly as follows: Mens heads are by no means all like to one another, nor are the sutures of the head of all men constructed in the same form. Thus, whoever has a prominence in the anterior part of the head (by prominence is meant the round protuberant part of the bone which projects beyond the rest of it), in him the sutures of the head take the form of the Greek letter tau, τ.Hermann Welcker coined the term trigonocephaly in 1862. He described a child with a V-shaped skull and a cleft lip. Popular culture
Via a photo shown on a Facebook page, the mother of a child previously diagnosed with this condition recognised the symptoms and reported them to the family involved, resulting in an immediate diagnosis that medical professionals had overlooked in all earlier consultations. References
== External links == | Peroxisomal disorders represent a class of medical conditions caused by defects in peroxisome functions. This may be due to defects in single enzymes important for peroxisome function or in peroxins, proteins encoded by PEX genes that are critical for normal peroxisome assembly and biogenesis. Peroxisome biogenesis disorders
Peroxisome biogenesis disorders (PBDs) include the Zellweger syndrome spectrum (PBD-ZSD) and rhizomelic chondrodysplasia punctata type 1 (RCDP1). PBD-ZSD represents a continuum of disorders including infantile Refsum disease, neonatal adrenoleukodystrophy, and Zellweger syndrome. Collectively, PBDs are autosomal recessive developmental brain disorders that also result in skeletal and craniofacial dysmorphism, liver dysfunction, progressive sensorineural hearing loss, and retinopathy.PBD-ZSD is most commonly caused by mutations in the PEX1, PEX6, PEX10, PEX12, and PEX26 genes. This results in the over-accumulation of very long chain fatty acids and branched chain fatty acids, such as phytanic acid. In addition, PBD-ZSD patients show deficient levels of plasmalogens, ether-phospholipids necessary for normal brain and lung function.RCDP1 is caused by mutations in the PEX7 gene, which encodes the PTS2 receptor. RCDP1 patients can develop large tissue stores of branched chain fatty acids, such as phytanic acid, and show reduced levels of plasmalogens. Enzyme and transporter defects
Peroxisomal disorders also include:
References
External links
Peroxisomal+disorders at the US National Library of Medicine Medical Subject Headings (MeSH) | 0-1
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After recovery long term stiffness or limited range of motion may occur in some patients. Visible or limited scarring may also occur for patients. References
External links
Textbook of Hallux Valgus and Forefoot Surgery, links to complete text in PDF files | Inhalant use, especially glue-sniffing, is widely associated with the late-1970s punk youth subculture in the UK and North America. Raymond Cochrane and Douglas Carroll claim that when glue sniffing became widespread in the late 1970s, it was "adopted by punks because public [negative] perceptions of sniffing fitted in with their self-image" as rebels against societal values. While punks at first used inhalants "experimentally and as a cheap high, adult disgust and hostility [to the practice] encouraged punks to use glue sniffing as a way of shocking society." As well, using inhalants was a way of expressing their anti-corporatist DIY (do it yourself) credo; by using inexpensive household products as inhalants, punks did not have to purchase industrially manufactured liquor or beer. One history of the punk subculture argues that "substance abuse was often referred to in the music and did become synonymous with the genre, glue-sniffing especially" because the youths "faith in the future had died and that the youth just didnt care anymore" due to the "awareness of the threat of nuclear war and a pervasive sense of doom." In a BBC interview with a person who was a punk in the late 1970s, they said that "there was a real fear of imminent nuclear war—people were sniffing glue knowing that it could kill them, but they didnt care because they believed that very soon everybody would be dead anyway." A number of 1970s punk rock and 1980s hardcore punk songs refer to inhalant use. | 0-1
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This condition is differentiated from malignant glaucoma by the presence of a deep and clear anterior chamber and a lack of aqueous misdirection. Also, the corneal appearance is not as hazy. A reduction in visual acuity can occur followed neuroretinal breakdown. Associated factors include inflammation, drugs, trauma and intraocular surgery, including cataract surgery and vitrectomy procedures. Gede Pardianto (2005) reported on four patients who had toxic glaucoma. One of them underwent phacoemulsification with small particle nucleus drops. Some cases can be resolved with some medication, vitrectomy procedures or trabeculectomy. Valving procedures can give some relief, but further research is required. Absolute glaucoma
Absolute glaucoma (H44.5) is the end stage of all types of glaucoma. The eye has no vision, absence of pupillary light reflex and pupillary response, and has a stony appearance. Severe pain is present in the eye. The treatment of absolute glaucoma is a destructive procedure like cyclocryoapplication, cyclophotocoagulation, or injection of 99% alcohol. Types
Glaucoma is an umbrella term for eye conditions that damage the optic nerve and that can lead to a loss of vision. The main cause of damage to the optic nerve is intraocular pressure (IOP), excessive fluid pressure within the eye, which can be caused by factors such as blockage of drainage ducts and narrowing or closure of the angle between the iris and cornea. Glaucoma is primarily categorized as either open-angle or closed-angle (or angle-closure). In open-angle glaucoma, the iris meets the cornea normally, allowing the fluid from inside the eye to drain, thus relieving the internal pressure. | The only signs are gradually progressive visual field loss and optic nerve changes (increased cup-to-disc ratio on fundoscopic examination). About 10% of people with closed angles present with acute angle closure characterized by sudden ocular pain, seeing halos around lights, red eye, very high intraocular pressure (>30 mmHg (4.0 kPa)), nausea and vomiting, suddenly decreased vision, and a fixed, mid-dilated pupil. It is also associated with an oval pupil in some cases. Acute angle closure is an emergency. Opaque specks may occur in the lens in glaucoma, known as glaukomflecken. Causes
Ocular hypertension (increased pressure within the eye) is the most important risk factor for glaucoma, but only about 50% of people with primary open-angle glaucoma actually have elevated ocular pressure. Ocular hypertension—an intraocular pressure above the traditional threshold of 21 mmHg (2.8 kPa) or even above 24 mmHg (3.2 kPa)—is not necessarily a pathological condition, but it increases the risk of developing glaucoma. One study found a conversion rate of 18% within five years, meaning fewer than one in five people with elevated intraocular pressure will develop glaucomatous visual field loss over that period of time. It is a matter of debate whether every person with an elevated intraocular pressure should receive glaucoma therapy; currently, most ophthalmologists favor treatment of those with additional risk factors.Open-angle glaucoma accounts for 90% of glaucoma cases in the United States. Closed-angle glaucoma accounts for fewer than 10% of glaucoma cases in the United States, but as many as half of glaucoma cases in other nations (particularly East Asian countries). | 11
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In 2016, it was the 223rd most commonly prescribed medication in the United States, with more than two million prescriptions. Medical uses
Birth control
At low doses, levonorgestrel is used in monophasic and triphasic formulations of combined oral contraceptive pills, with available monophasic doses ranging from 100 to 250 µg, and triphasic doses of 50 µg/75 µg/125 µg. It is combined with the estrogen ethinylestradiol in these formulations.At very low daily dose of 30 µg, levonorgestrel is used in some progestogen-only pill formulations.Levonorgestrel is the active ingredient in a number of intrauterine devices including Mirena and Skyla. It is also the active ingredient in the birth control implants Norplant and Jadelle.One of the more common forms of contraception that contains only levonorgestrel is an IUD. One IUD, the Mirena, is a small hollow cylinder containing levonorgestrel and polydimethylsiloxane and covered with a release rate controlling membrane. Emergency birth control
Levonorgestrel is used in emergency contraceptive pills (ECPs), both in a combined Yuzpe regimen which includes estrogen, and as a levonorgestrel-only method. The levonorgestrel-only method uses levonorgestrel 1.5 mg (as a single dose or as two 0.75 mg doses 12 hours apart) taken within three days of unprotected sex. With one study indicating that beginning as late as 120 hours (5 days) after intercourse could be effective. However, taking more than one dose of emergency contraception does not increase the chance of pregnancy not happening. Planned Parenthood asserts "Taking the morning-after pill (also known as emergency contraception) multiple times doesnt change its effectiveness, and wont cause any long-term side effects." | Orofaciodigital syndrome or oral-facial-digital syndrome is a group of at least 13 related conditions that affect the development of the mouth, facial features, and digits in between 1 in 50,000 to 250,000 newborns with the majority of cases being type I (Papillon-League-Psaume syndrome). Type
The different types are:s
Type I, Papillon-League-Psaume syndrome
Type II, Mohr syndrome
Type III, Sugarman syndrome
Type IV, Baraitser-Burn syndrome
Type V, Thurston syndrome
Type VI, Varadi-Papp syndrome
Type VII, Whelan syndrome
Type VIII, Oral-facial-digital syndrome, Edwards type (not to be confused with Edwards syndrome)
Type IX, OFD syndrome with retinal abnormalities
Type X, OFD with fibular aplasia
Type XI, Gabrielli syndrome
References
== External links == | 0-1
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Protein restriction
Vegetarian diets and, for younger children, breastfeeding are common ways to limit protein intake without endangering tryptophan transport to the brain. Tryptophan
Formulas such as XLys, XTrp Analog, XLys, XTrp Maxamaid, XLys, XTrp Maxamum or Glutarex 1 are designed to provide amino acids other than lysine and tryptophan, to help prevent protein malnutrition. The entry of tryptophan into the brain is crucial in the proper synthesis of the neurotransmitter serotonin in the brain. One way to acutely cause depression, bulimia or anxiety in humans, in order to assess an individuals vulnerability to those disorders, is to supplement with a formula with all or most amino acids except tryptophan. Acute tryptophan depletion is a diagnostic procedure, not a treatment for GA1. The protein synthesis elicited by the amino acids leads circulating amino acids, including tryptophan, to be incorporated into proteins. Tryptophan is thus lowered in the brain as a result of the protein synthesis enhancement, causing circulating tryptophan to drop more than other amino acids. A relative excess of other large neutral amino acids may also compete with tryptophan for transport across the blood–brain barrier through the large neutral amino acid transporter 1. The consequence is acute tryptophan depletion in the brain and a consequent decrease in serotonin synthesis. 5-Hydroxytryptophan, a precursor of serotonin that is not metabolized to glutaryl-CoA, glutaric acid and secondary metabolites, could be used as an adjunct to selective tryptophan restriction, although it has risks. | Several systemic illnesses have been associated with plastic bronchitis:
Cardiac: constrictive pericarditis, congenital heart disease
Pulmonary: asthma, allergic bronchopulmonary aspergillosis, aspergillosis, bronchiectasis, cystic fibrosis, tuberculosis, pneumonia, and bronchocentric granulomatosis
Disorders of lymphatic drainage: lymphangiectasia, lymphangiomatosis
Miscellaneous: acute chest syndrome/sickle cell disease, amyloidosis, rheumatoid arthritis, membranous colitis, inhaled irritants, neoplastic (lymphoma)The most common form of plastic bronchitis follows cardiac surgery for congenital heart disease, especially the Fontan procedure. Systemic blood flow is diverted to pulmonary flow, elevating pressures in the pulmonary venous system, and promoting leaks of proteinaceous and lipid-rich fluids from the lymphatics into the bronchial tree. Diagnosis
The diagnosis of plastic bronchitis is confirmed by recovery of casts that have been coughed up or visualized during a bronchoscopy. There is no specific cytologic, pathologic or laboratory test that is diagnostic for casts due to lymphatic PB. Imaging
Simple chest X-rays may reveal collapse due to airway obstruction. The contralateral lung may be hyperinflated. Casts can be visualized within the major airways using computerized axial tomography scans.Heavy T2-weighted MRI, and, as appropriate, intranodal lymphangiogram and/or dynamic contrast-enhanced MR lymphangiography may be useful for identifying pathological lymphatic tissue or lymphatic flow. Management
Acute therapy for PB is often focused on removal or facilitated expectoration of the casts. This is followed by short and long term efforts to identify and remediate the underlying condition resulting in the excessive airway leakage or inflammation that is causing the casts to form.PB can present as a life threatening emergency when the casts obstruct the major airways resulting in acute respiratory distress. | 0-1
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However, these criteria were primarily established for use in scientific research, including selection for randomized controlled trials, which require higher confidence levels. As a result, many people with SLE may not meet the full ACR criteria. Criteria
The American College of Rheumatology (ACR) established eleven criteria in 1982, which were revised in 1997 as a classificatory instrument to operationalise the definition of SLE in clinical trials. They were not intended to be used to diagnose individuals and do not do well in that capacity. For the purpose of identifying people for clinical studies, a person has SLE if any 4 out of 11 symptoms are present simultaneously or serially on two separate occasions. Malar rash (rash on cheeks); sensitivity = 57%; specificity = 96%. Discoid rash (red, scaly patches on skin that cause scarring); sensitivity = 18%; specificity = 99%. Serositis: Pleurisy (inflammation of the membrane around the lungs) or pericarditis (inflammation of the membrane around the heart); sensitivity = 56%; specificity = 86% (pleural is more sensitive; cardiac is more specific). Oral ulcers (includes oral or nasopharyngeal ulcers); sensitivity = 27%; specificity = 96%. Arthritis: nonerosive arthritis of two or more peripheral joints, with tenderness, swelling, or effusion; sensitivity = 86%; specificity = 37%. Photosensitivity (exposure to ultraviolet light causes rash, or other symptoms of SLE flareups); sensitivity = 43%; specificity = 96%. Blood—hematologic disorder—hemolytic anemia (low red blood cell count), leukopenia (white blood cell count<4000/µl), lymphopenia (<1500/µl), or low platelet count (<100000/µl) in the absence of offending drug; sensitivity = 59%; specificity = 89%. | In addition, differences in GnRH signalling have also been shown to contribute to the onset of SLE. While females are more likely to relapse than males, the intensity of these relapses is the same for both sexes.In addition to hormonal mechanisms, specific genetic influences found on the X chromosome may also contribute to the development of SLE. Studies indicate that the X chromosome can determine the levels of sex hormones. A study has shown an association between Klinefelter syndrome and SLE. XXY males with SLE have an abnormal X–Y translocation resulting in the partial triplication of the PAR1 gene region. Changing rate of disease
The rate of SLE in the United States increased from 1.0 in 1955 to 7.6 in 1974. Whether the increase is due to better diagnosis or an increased frequency of the disease is unknown. History
The history of SLE can be divided into three periods: classical, neoclassical, and modern. In each period, research and documentation advanced the understanding and diagnosis of SLE, leading to its classification as an autoimmune disease in 1851, and to the various diagnostic options and treatments now available to people with SLE. The advances made by medical science in the diagnosis and treatment of SLE have dramatically improved the life expectancy of a person diagnosed with SLE. Etymology
There are several explanations ventured for the term lupus erythematosus. Lupus is Latin for "wolf", and "erythro" is derived from ερυθρός, Greek for "red". All explanations originate with the reddish, butterfly-shaped malar rash that the disease classically exhibits across the nose and cheeks. | 11
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Patients are monitored with EEG leads, pulse oximetry, temperature and pressure sensors to detect nasal and oral airflow, respiratory impedance plethysmography or similar resistance belts around the chest and abdomen to detect motion, an ECG lead, and EMG sensors to detect muscle contraction in the chin, chest, and legs. A hypopnea can be based on one of two criteria. It can either be a reduction in airflow of at least 30% for more than 10 seconds associated with at least 4% oxygen desaturation or a reduction in airflow of at least 30% for more than 10 seconds associated with at least 3% oxygen desaturation or an arousal from sleep on EEG.An "event" can be either an apnea, characterized by complete cessation of airflow for at least 10 seconds, or a hypopnea in which airflow decreases by 50 percent for 10 seconds or decreases by 30 percent if there is an associated decrease in the oxygen saturation or an arousal from sleep. To grade the severity of sleep apnea, the number of events per hour is reported as the apnea-hypopnea index (AHI). An AHI of less than 5 is considered normal. An AHI of 5–15 is mild; 15–30 is moderate, and more than 30 events per hour characterizes severe sleep apnea. Home oximetry
In patients who are at high likelihood of having OSA, a randomized controlled trial found that home oximetry (a non-invasive method of monitoring blood oxygenation) may be adequate and easier to obtain than formal polysomnography. | Neurocognitive and behavioral consequences
Nocturnal sleep fragmentation has been linked to neurocognitive impairments, therefore, the identification of SDB such as OSA is crucial in children, those impairments having the possibility to be reversible with the appropriate treatment for the sleep disorder. The neurocognitive and behavioral dysfunctions commonly present in children with OSA include the following: hyperactivity, impulsivity, aggressive behaviors, low social and communication abilities and reduced adaptive skills. Children with OSA commonly show cognitive deficits, resulting in attention and concentration difficulties, as well as lower academic performance and IQ. Poor academic performances have been linked to OSA and suggested to result from cortical and sympathetic arousals and hypoxemia which affects memory consolidation. A study with Indian children affected by OSA has shown poor school grades, including mathematics, science, language and physical education. This study allowed to see the overall impact of OSA on learning abilities associated with language or numeracy skills, and physical development. It has been suggested that the deficits in academic performance related to OSA could be mediated through reduced executive functions or language skills, those domains contributing highly to learning abilities and behavior. The deficits in school performance can nevertheless be improved if adenotonsillectomy is performed on children to treat the OSA. It is thus crucial to identify the OSA for children with school difficulties; many cases remaining unnoticed.As studies have shown that learning skills and behaviors can be improved if the OSA is treated, the neurocognitive and behavioral deficits are thus at least partly reversible. | 11
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Treatment
Treatment may consist of topical applications of steroid based creams and the use of compression stockings or intermittent pneumatic compression pumps, to help force the underlying buildup of fluids back out of the lower leg.Compression therapy should consist of moderate pressures and works best for ambulating patients. Ultimately, treating the underlying venous reflux is necessary to treat Stasis dermatitis. Invasive surgical procedures like saphenofemoral junction ligation with stripping were the norm for treatment in the past. However, less invasive methods are now more widely used. These newer methods include endovenous thermal ablation, ambulatory phlebotomy, and ultrasound foam sclerotherapy. Complications
If stasis dermatitis goes untreated, the patient is at risk of developing venous ulcers and Acroangiodermatitis. See also
Sinus pericranii
List of cutaneous conditions
References
== External links == | However, the clinical preparations prepared from such insulins differ from endogenous human insulin in several important respects; an example is the absence of C-peptide which has in recent years been shown to have systemic effects itself. Novo Nordisk has also developed a genetically engineered insulin independently using a yeast process.According to a survey that the International Diabetes Federation conducted in 2002 on the access to and availability of insulin in its member countries, approximately 70% of the insulin that is currently sold in the world is recombinant, biosynthetic human insulin. A majority of insulin used clinically today is produced this way, although clinical experience has provided conflicting evidence on whether these insulins are any less likely to produce an allergic reaction. Adverse reactions have been reported; these include loss of warning signs that patients may slip into a coma through hypoglycemia, convulsions, memory lapse and loss of concentration. However, the International Diabetes Federations position statement from 2005 is very clear in stating that "there is NO overwhelming evidence to prefer one species of insulin over another" and "[modern, highly purified] animal insulins remain a perfectly acceptable alternative. "Since January 2006, all insulins distributed in the U.S. and some other countries are synthetic "human" insulins or their analogues. | 0-1
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Excess methyllithium is then added to create methyl ketones which when reduced with lithium aluminum hydride gives the amine group.The synthesis pictured to the left is a synthesis of rimantadine as synthesized in Europe
History
Rimantadine was discovered in 1963 and patented in 1965 in the US by William W. Prichard in Du Pont & Co., Wilmington, Delaware (patent on new chemical compound U.S. Patent 3,352,912, 1965 and on the first method of synthesis U.S. Patent 3,592,934, 1967). Prichards methods of synthesis of rimantadine from the corresponding ketone oxime were based on its reduction with lithium aluminum hydride. See also
Adapromine
Bromantane
Memantine
Tromantadine
Synonyms
1-(1-Adamantyl)ethanamine, 1-(Adamantan-1-yl)ethanamine, 1-(adamantan-1-yl)ethan-1-aminem, alpha-Methyl-1-adamantanemethylamine, alpha-Methyladamantanemethylamine, Rimantadine [INN:BAN], Rimantadinum [INN-Latin], 1-(1-Adamantyl)ethylamin, Remantadine, Rimantadina [INN-Spanish], 1-Adamantan-1-yl-ethylamine, RIMANTADIN, HSDB 7438, CHEMBL959, BRN 2715740, 1-Adamantanemethylamine, .alpha.-methyl-, .alpha.-Methyladamantanemethylamine, 1-(1-adamantyl)-ethylamine, 1-(tricyclo[3.3.1.1~3,7~]dec-1-yl)ethanamine, Riamantadine, Rimantadina, Rimantadinum, Tricyclo(3.3.1.13,7)decane-1-methanamine, alpha-methyl-, [1-(1-adamantyl)ethyl]amine hydrochloride, Tricyclo(3.3.1.1(sup 3,7))decane-1-methanamine, alpha-methyl-, 1-ADAMANTANEMETHYLAMINE, alpha-METHYL-, 1-Rimantadine, 887336-05-2, Tricyclo[3.3.1.13,7]decane-1-methanamine, a-methyl-, Rimant, 1-(1-adamantyl)ethylamine, Rimantadine (INN), Enamine_005755, NCGC00159491-02, Rimant & .alpha. | IFN, Rimantadine (Flumadine), Rimantidine & .alpha.IFN, 1-Adamantan-1-ylethylamine, rimantidin, Rimantadin A, (R)-1-(Adamantan-1-yl)ethan-1-amine, 1-adamantanylethylamine, Maybridge1_002066, SCHEMBL2981, 1-tricyclo[3.3.1.1~3,7~]dec-1-ylethanamine, Oprea1_602732, SCHEMBL2619249, CHEMBL1201272, DTXSID2023561, SCHEMBL20409367, CHEBI:94440, CTK6A4437, HMS1410F13, HMS2090L19, HMS3604N13, HMS3655J05, 1-Adamantanemethylamine, ?-methyl-, ALBB-013870, BCP12269, HY-B0338, ZX-AN012619, ANW-72018, BBL013215, BDBM50216627, MFCD00869344, s1964, STK177253, (alpha-methyl-1-adamantyl)methylamine, AKOS000264537, AKOS006238592, AKOS016038537, .alpha.-Methyl-1-adamantanemethylamine, AM84461, API0024288, BBV-156986, CCG-236078, CS-2380, DB00478, FCH3207896, MCULE-9027470290, IDI1_007990, NCGC00159491-03, NCGC00159491-05, AK-58175, AS-68744, CC-34261, LS-15019, OR315791, SBI-0206810.P001, AB0012750, AX8049536, DB-042207, FT-0630403, H6325, ST45025920, SW220023-1, EN300-33990, C07236, D08483, Q421711-[(3R,5S,7s)-adamantan-1-yl]ethan-1-amine, AB00638368-09, AB00959689-03, AB01506092_02, AB01506092_03, 392R284, C-06592, BRD-A84282119-003-01-2, Z56757137, 1-(Tricyclo[3.3.1.1>3,7>]dec-1-yl)ethanamine (HCl), Tricyclo(3.3.1.1^3,7)decane-1-methanamine, .alpha.-methyl-, 1-(1-Adamantyl)ethylamine Hydrochloride;Rimantadine hydrochloride, Tricyclo(3.3.1.1(sup 3,7))decane-1-methanamine, .alpha.-methyl-, Tricyclo[3,3,1,1(3,7)]decane-1-methanamine, .alpha.-methyl-, Tricyclo(3.3.1.1^3,7)decane-1-methanamine, .alpha.-methyl- & IFN.alpha
References
External links
U.S. FDA press release announcing rimantadines approval
U.S. Center for Drug Evaluation and Research rimantadine description
U.S. NIH rimantadine description
U.S. CDC flu anti-viral treatment information | 11
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For example, one association is with mutations in the XBP1 gene, which is involved in the unfolded protein response pathway of the endoplasmic reticulum. The gene variants of NOD2/CARD15 seem to be related with small-bowel involvement. Other well documented genes which increase the risk of developing Crohns disease are ATG16L1, IL23R, IRGM, and SLC11A1. There is considerable overlap between susceptibility loci for IBD and mycobacterial infections. Genome-wide association studies have shown that Crohns disease is genetically linked to coeliac disease.Crohns has been linked to the gene LRRK2 with one variant potentially increasing the risk of developing the disease by 70%, while another lowers it by 25%. The gene is responsible for making a protein, which collects and eliminates waste product in cells, and is also associated with Parkinsons disease. Immune system
There was a prevailing view that Crohns disease is a primary T cell autoimmune disorder; however, a newer theory hypothesizes that Crohns results from an impaired innate immunity. The later hypothesis describes impaired cytokine secretion by macrophages, which contributes to impaired innate immunity and leads to a sustained microbial-induced inflammatory response in the colon, where the bacterial load is high. Another theory is that the inflammation of Crohns was caused by an overactive Th1 and Th17 cytokine response.In 2007, the ATG16L1 gene was implicated in Crohns disease, which may induce autophagy and hinder the bodys ability to attack invasive bacteria. | Other conditions that can present similarly include irritable bowel syndrome and Behçets disease.There is no known cure for Crohns disease. Treatment options are intended to help with symptoms, maintain remission, and prevent relapse. In those newly diagnosed, a corticosteroid may be used for a brief period of time to rapidly improve symptoms, alongside another medication such as either methotrexate or a thiopurine used to prevent recurrence. Stopping smoking is recommended in people with Crohns disease. One in five people with the disease is admitted to the hospital each year, and half of those with the disease will require surgery for the disease at some point over a ten-year period. While surgery should be used as little as possible, it is necessary to address some abscesses, certain bowel obstructions, and cancers. Checking for bowel cancer via colonoscopy is recommended every few years, starting eight years after the disease has begun.Crohns disease affects about 3.2 per 1,000 people in Europe, North America, and the UK. It is less common in Asia and Africa. It has historically been more common in the developed world. Rates have, however, been increasing, particularly in the developing world, since the 1970s. Inflammatory bowel disease resulted in 47,400 deaths in 2015, and those with Crohns disease have a slightly reduced life expectancy. It tends to start in young adulthood, though it can occur at any age. Males and females are equally affected. | 11
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Murray Valley encephalitis virus (MVEV) is a zoonotic flavivirus endemic to northern Australia and Papua New Guinea. It is the causal agent of Murray Valley encephalitis (MVE; previously known as Australian encephalitis or Australian X disease). In humans, it can cause permanent neurological disease or death. MVEV is related to Kunjin virus, which has a similar ecology, but a lower morbidity rate. Although the arbovirus is endemic to Northern Australia, it has occasionally spread to the southern states during times of heavy rainfall during the summer monsoon season via seasonal flooding of the Murray-Darling River system. These outbreaks can be "...decades apart, with no or very few cases identified in between". Vector
MVEV is a mosquito-borne virus that is maintained in a bird-mosquito-bird cycle. Water birds from the order Ciconiiformes, including herons and cormorants, provide the natural reservoir for MVEV. The major mosquito vector is Culex annulirostris. Human infection occurs only through bites from infected mosquitoes; the virus cannot be transmitted from person to person. History
The first epidemics of MVE occurred in 1917 and 1918 in Southeastern Australia following years of high rainfall. The virus was isolated from human samples in 1951 during an epidemic in the Murray Valley, Australia.Epidemics usually occur due to either infected birds or mosquitoes migrating from endemic areas to non-endemic areas. The New South Wales government has placed sentinel flocks of chickens near known bird breeding sites as an early warning system. These flocks are tested for MVE during the mosquito breeding season. Presentation
The majority of MVEV infections are sub-clinical, i.e. | do not produce disease symptoms, although some people may experience a mild form of the disease with symptoms such as fever, headaches, nausea and vomiting and only a very small number of these cases go on to develop MVE. In fact, serological surveys which measure the level of anti-MVEV antibodies within the population estimate that only one in 800–1000 of all infections result in clinical disease.The incubation period following exposure to the virus is around 1 to 4 weeks. Following infection, a person has lifelong immunity to the virus. When a patient appears to show MVE symptoms and has been in an MVE-endemic area during the wet season, when outbreaks usually occur, MVE infection must be confirmed by laboratory diagnosis, usually by detection of a significant rise of MVE-specific antibodies in the patients serum. Of those who contract MVE, one-quarter die from the disease. Clone
The scientific study of the genetics of MVEV has been facilitated by the construction and manipulation of an infectious cDNA clone of the virus. Mutations in the envelope gene have been linked to the attenuation of disease in mouse models of infection. References
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Other regions include the anterior region of the thalamus (accounting for amnesic symptoms), the medial dorsal thalamus, the basal forebrain, the median and dorsal raphe nuclei, and the cerebellum.One as-yet-unreplicated study has associated susceptibility to this syndrome with a hereditary deficiency of transketolase, an enzyme that requires thiamine as a coenzyme. Post-gastrectomy
The fact that gastrointestinal surgery can lead to the development of WKS was demonstrated in a study that was completed on three patients who recently undergone a gastrectomy. These patients had developed WKS but were not alcoholics and had never suffered from dietary deprivation. WKS developed between 2 and 20 years after the surgery. There were small dietary changes that contributed to the development of WKS but overall the lack of absorption of thiamine from the gastrointestinal tract was the cause. Therefore, it must be ensured that patients who have undergone gastrectomy have a proper education on dietary habits, and carefully monitor their thiamine intake. Additionally, an early diagnosis of WKS, should it develop, is very important. Alcohol–thiamine interactions
Strong evidence suggests that ethanol interferes directly with thiamine uptake in the gastrointestinal tract. Ethanol also disrupts thiamine storage in the liver and the transformation of thiamine into its active form. The role of alcohol consumption in the development of WKS has been experimentally confirmed through studies in which rats were subjected to alcohol exposure and lower levels of thiamine through a low-thiamine diet. | In 1947, 52 cases of WKS were documented in a prisoner of war hospital in Singapore where the prisoners diets included less than 1 mg of thiamine per day. Such cases provide an opportunity to gain an understanding of what effects this syndrome has on cognition. In this particular case, cognitive symptoms included insomnia, anxiety, difficulties in concentration, loss of memory for the immediate past, and gradual degeneration of mental state; consisting of confusion, confabulation, and hallucinations. In other cases of WKS, cognitive effects such as severely disrupted speech, giddiness, and heavy-headedness have been documented. In addition to this, it has been noted that some patients displayed an inability to focus, and the inability of others to catch patients attention.In a study conducted in 2003 by Brand et al. on the cognitive effects of WKS, the researchers used a neuropsychological test battery which included tests of intelligence, speed of information processing, memory, executive function and cognitive estimation. They found that subjects with WKS showed impairments in all aspects of this test battery but most noticeably, on the cognitive estimation tasks. This task required subjects to estimate a physical quality such as size, weight, quantity or time (e.g. What is the average length of a shower? ), of a particular item. Patients with WKS performed worse than normal control participants on all of the tasks in this category. The patients found estimations involving time to be the most difficult, whereas quantity was the easiest estimation to make. | 11
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Variability in testing and data collection methods makes comparisons of prevalence and progression difficult.The prevalence of myopia has been reported as high as 70–90% in some Asian countries, 30–40% in Europe and the United States, and 10–20% in Africa. Myopia is about twice as common in Jewish people than in people of non-Jewish ethnicity. Myopia is less common in African people and associated diaspora. In Americans between the ages of 12 and 54, myopia has been found to affect African Americans less than Caucasians. Asia
In some parts of Asia, myopia is very common. Singapore is believed to have the highest prevalence of myopia in the world; up to 80% of people there have myopia, but the accurate figure is unknown. Chinas myopia rate is 31%: 400 million of its 1.3 billion people are myopic. The prevalence of myopia in high school in China is 77%, and in college is more than 80%. In some areas, such as China and Malaysia, up to 41% of the adult population is myopic to 1.00 dpt, and up to 80% to 0.5 dpt. A study of Jordanian adults aged 17 to 40 found over half (54%) were myopic. Some research suggests the prevalence of myopia in Indian children is less than 15%. Europe
In first-year undergraduate students in the United Kingdom 50% of British whites and 53% of British Asians were myopic. A recent review found 27% of Western Europeans aged 40 or over have at least −1.00 diopters of myopia and 5% have at least −5.00 diopters. | Dependence and withdrawal
Drug tolerance develops rapidly in amphetamine abuse (i.e., recreational amphetamine use), so periods of extended abuse require increasingly larger doses of the drug in order to achieve the same effect. According to a Cochrane review on withdrawal in individuals who compulsively use amphetamine and methamphetamine, "when chronic heavy users abruptly discontinue amphetamine use, many report a time-limited withdrawal syndrome that occurs within 24 hours of their last dose." This review noted that withdrawal symptoms in chronic, high-dose users are frequent, occurring in roughly 88% of cases, and persist for 3–4 weeks with a marked "crash" phase occurring during the first week. Amphetamine withdrawal symptoms can include anxiety, drug craving, depressed mood, fatigue, increased appetite, increased movement or decreased movement, lack of motivation, sleeplessness or sleepiness, and lucid dreams. The review indicated that the severity of withdrawal symptoms is positively correlated with the age of the individual and the extent of their dependence. Mild withdrawal symptoms from the discontinuation of amphetamine treatment at therapeutic doses can be avoided by tapering the dose. Overdose
An amphetamine overdose can lead to many different symptoms, but is rarely fatal with appropriate care. The severity of overdose symptoms increases with dosage and decreases with drug tolerance to amphetamine. Tolerant individuals have been known to take as much as 5 grams of amphetamine in a day, which is roughly 100 times the maximum daily therapeutic dose. Symptoms of a moderate and extremely large overdose are listed below; fatal amphetamine poisoning usually also involves convulsions and coma. | 0-1
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Obstruction may refer to:
Places
Obstruction Island, in Washington state
Obstruction Islands, east of New Guinea
Medicine
Obstructive jaundice
Obstructive sleep apnea
Airway obstruction, a respiratory problem
Recurrent airway obstruction
Bowel obstruction, a blockage of the intestines. Gastric outlet obstruction
Distal intestinal obstruction syndrome
Congenital lacrimal duct obstruction
Bladder outlet obstruction
Politics and law
Obstruction of justice, the crime of interfering with law enforcement
Obstructionism, the practice of deliberately delaying or preventing a process or change, especially in politics
Emergency Workers (Obstruction) Act 2006
Science and mathematics
Obstruction set in forbidden graph characterizations, in the study of graph minors in graph theory
Obstruction theory, in mathematics
Propagation path obstruction
Single Vegetative Obstruction Model
Sports
Obstruction (baseball), when a fielder illegally hinders a baserunner
Obstructing the field
See also
The Five Obstructions, a 2003 film
USS Obstructor, an American minelayer ship used in World War II | Therefore, the mutation in the α4 subunit could lead to reduced GABA release, causing hyperexcitability. Pathophysiology
CHRNA4
The first mutation associated with ADNFLE is a serine to phenylalanine transition at position 248 (S248F), located in the second transmembrane spanning region of the gene encoding a nicotinic acetylcholine receptor α4 subunit. Using the numbering based on the human CHRNA4 protein, this mutation is called S280F. Receptors containing this mutant subunit are functional, but desensitize at a much faster pace compared to wild-type only receptors. These mutant containing receptors also recover from desensitization at a much slower rate than wild-type only receptors. These mutant receptors also have a decreased single channel conductance than wild-type and have a lower affinity for acetylcholine. Also importantly, this mutation along with the others in CHRNA4 produce receptors less sensitive to calcium.The second discovered ADNFLE mutation was also in CHRNA4. This mutation, L259_I260insL, is caused by the insertion of three nucleotides (GCT) between a stretch of leucine amino acids and an isoleucine. As with the S248F mutation, the L259_I260insL mutation is located in the second transmembrane spanning region. Electrophysiological experiments have shown that this mutant is tenfold more sensitive to acetylcholine than wild-type. Calcium permeability, however is notably decreased in mutant compared to wild-type containing receptors. Furthermore, this mutant shows slowed desensitization compared to both wild-type and S248F mutant receptors.Also located in the second transmembrane spanning region, the S252L mutation has also been associated with ADNFLE. | 0-1
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The interposition of a Teflon pad between the trochlear nerve and a compressing artery and vein at the nerves exit from the midbrain led to a remission lasting for a follow-up of 22 months. References
== External links == | Hereditary sclerosing poikiloderma is an autosomal dominant conditions with skin changes consisting of generalized poikiloderma appearing in childhood. : 576
See also
Mandibuloacral dysplasia
Poikiloderma
Skin lesion
References
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Alternatively, functioning may be affected by the stress of having to hide a condition in work or school, etc., by adverse effects of medications or other substances, or by mismatches between illness-related variations and demands for regularity.It is also the case that, while often being characterized in purely negative terms, some mental traits or states labeled as disorders can also involve above-average creativity, non-conformity, goal-striving, meticulousness, or empathy. In addition, the public perception of the level of disability associated with mental disorders can change.Nevertheless, internationally, people report equal or greater disability from commonly occurring mental conditions than from commonly occurring physical conditions, particularly in their social roles and personal relationships. The proportion with access to professional help for mental disorders is far lower, however, even among those assessed as having a severely disabling condition. Disability in this context may or may not involve such things as:
Basic activities of daily living. Including looking after the self (health care, grooming, dressing, shopping, cooking etc.) or looking after accommodation (chores, DIY tasks, etc.) Interpersonal relationships. Including communication skills, ability to form relationships and sustain them, ability to leave the home or mix in crowds or particular settings
Occupational functioning. | The main factors associated with an increased incidence of benzodiazepine dependence include:
Dose
Duration
Concomitant use of antidepressantsBenzodiazepine dependence should be suspected also in individuals having substance use disorders including alcohol, and should be suspected in individuals obtaining their own supplies of benzodiazepines. Benzodiazepine dependence is almost certain in individuals who are members of a tranquilizer self-help group.Research has found that about 40 percent of people with a diagnosis of benzodiazepine dependence are not aware that they are dependent on benzodiazepines, whereas about 11 percent of people judged not to be dependent believe that they are. When assessing a person for benzodiazepine dependence, asking specific questions rather than questions based on concepts is recommended by experts as the best approach of getting a more accurate diagnosis. For example, asking persons if they "think about the medication at times of the day other than when they take the drug" would provide a more meaningful answer than asking "do you think you are psychologically dependent?". The Benzodiazepine Dependence Self Report Questionnaire is one questionnaire used to assess and diagnose benzodiazepine dependence. Definition
Benzodiazepine dependence is the condition resulting from repeated use of benzodiazepine drugs. It can include both a physical dependence as well as a psychological dependence and is typified by a withdrawal syndrome upon a fall in blood plasma levels of benzodiazepines, e.g., during dose reduction or abrupt withdrawal. | 0-1
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The first influential writer to propose such an idea explicitly was Julien Offray de La Mettrie, in his book Man a Machine (Lhomme machine). His arguments, however, were very abstract. The most influential modern physical theories of consciousness are based on psychology and neuroscience. Theories proposed by neuroscientists such as Gerald Edelman and Antonio Damasio, and by philosophers such as Daniel Dennett, seek to explain consciousness in terms of neural events occurring within the brain. Many other neuroscientists, such as Christof Koch, have explored the neural basis of consciousness without attempting to frame all-encompassing global theories. At the same time, computer scientists working in the field of artificial intelligence have pursued the goal of creating digital computer programs that can simulate or embody consciousness.A few theoretical physicists have argued that classical physics is intrinsically incapable of explaining the holistic aspects of consciousness, but that quantum theory may provide the missing ingredients. Several theorists have therefore proposed quantum mind (QM) theories of consciousness. Notable theories falling into this category include the holonomic brain theory of Karl Pribram and David Bohm, and the Orch-OR theory formulated by Stuart Hameroff and Roger Penrose. Some of these QM theories offer descriptions of phenomenal consciousness, as well as QM interpretations of access consciousness. None of the quantum mechanical theories have been confirmed by experiment. Recent publications by G. Guerreshi, J. Cia, S. Popescu, and H. Briegel could falsify proposals such as those of Hameroff, which rely on quantum entanglement in protein. | Chromoblastomycosis is a long-term fungal infection of the skin and subcutaneous tissue (a chronic subcutaneous mycosis).It can be caused by many different types of fungi which become implanted under the skin, often by thorns or splinters. Chromoblastomycosis spreads very slowly.It is rarely fatal and usually has a good prognosis, but it can be very difficult to cure. The several treatment options include medication and surgery.The infection occurs most commonly in tropical or subtropical climates, often in rural areas. Symptoms and signs
The initial trauma causing the infection is often forgotten or not noticed. The infection builds at the site over a period of years, and a small red papule (skin elevation) appears. The lesion is usually not painful, with few, if any symptoms. Patients rarely seek medical care at this point.Several complications may occur. Usually, the infection slowly spreads to the surrounding tissue while still remaining localized to the area around the original wound. However, sometimes the fungi may spread through the blood vessels or lymph vessels, producing metastatic lesions at distant sites. Another possibility is secondary infection with bacteria. This may lead to lymph stasis (obstruction of the lymph vessels) and elephantiasis. The nodules may become ulcerated, or multiple nodules may grow and coalesce, affecting a large area of a limb. Cause
Chromoblastomycosis is believed to originate in minor trauma to the skin, usually from vegetative material such as thorns or splinters; this trauma implants fungi in the subcutaneous tissue. | 0-1
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This study also concluded there were no gender differences in prevalence and that OCPD was not a predicter of disability. History
In 1908, Sigmund Freud named what is now known as obsessive–compulsive or anankastic personality disorder "anal retentive character". He identified the main strands of the personality type as a preoccupation with orderliness, parsimony (frugality), and obstinacy (rigidity and stubbornness). The concept fits his theory of psychosexual development. Freud believed that the anal retentive character faced difficulties regulating the control of defecation, leading to repercussions by the parents, and it is the latter that would cause the anal retentive character.Aubrey Lewis, in his 1936 book Problems of Obsessional Illness, suggests that anal-erotic characteristics are found in patients without obsessive thoughts, and proposed two types of obsessional personality, one melancholy and stubborn, the other uncertain and indecisive.In the book Contributions to the theory of the anal character, Karl Abraham noted that the core feature of the anal character is being perfectionistic, and he believed that these traits will help an individual in becoming industrious and productive, whilst hindering their social and interpersonal functioning, such as working with others.OCPD was included in the first edition of the Diagnostic and Statistical Manual of Mental Disorders in 1952 by the American Psychiatric Association under the name "compulsive personality". It was defined as a chronic and excessive preoccupation with adherence to rules and standards of conscience. | Almost immediately thereafter, at the suggestion of Miguel Couto, then professor of the Faculdade de Medicina do Rio de Janeiro, the disease was widely referred to as "Chagas disease". Chagas discovery brought him national and international renown, but in highlighting the inadequacies of the Brazilian governments response to the disease, Chagas attracted criticism to himself and to the disease that bore his name, stifling research on his discovery and likely frustrating his nomination for the Nobel Prize in 1921.In the 1930s, Salvador Mazza rekindled Chagas disease research, describing over a thousand cases in Argentinas Chaco Province. In Argentina, the disease is known as mal de Chagas-Mazza in his honor. Serological tests for Chagas disease were introduced in the 1940s, demonstrating that infection with T. cruzi was widespread across Latin America. This, combined with successes eliminating the malaria vector through insecticide use, spurred the creation of public health campaigns focused on treating houses with insecticides to eradicate triatomine bugs. The 1950s saw the discovery that treating blood with crystal violet could eradicate the parasite, leading to its widespread use in transfusion screening programs in Latin America. Large-scale control programs began to take form in the 1960s, first in São Paulo, then various locations in Argentina, then national-level programs across Latin America. These programs received a major boost in the 1980s with the introduction of pyrethroid insecticides, which did not leave stains or odors after application and were longer-lasting and more cost-effective. | 0-1
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Retrieved 2008-10-02. "TWINS Guide to the First Year" (PDF). TWINS Magazine. Fort Collins, Colorado. 2008. Archived from the original (PDF) on 2008-10-30. Retrieved 2008-10-06. Samson, Jennifer. "Facts About Multiples: An Encyclopedia of Multiple Birth Records". Archived from the original on 2009-10-15. Retrieved 2008-10-18. Taylor, Ally. "Twin Zygosity Test for Dichorionic Diamniotic (Di/Di) Twins! Zygosity Reveal". Retrieved 2018-03-30. Am J Med Genet C Semin Med Genet. 2009 May 15;151C(2):136-41. Not really identical: epigenetic differences in monozygotic twins and implications for twin studies in psychiatry. Haque FN, Gottesman II, Wong AH. Twin brothers promoted as Majors General together. Seneviratne brothers, who are twins and joined the Army on a same day, were promoted to the rank of Major General, again on the same day. == External links == | This relatively common dental procedure may be done with soft-tissue lasers, such as the CO2 laser.A frenotomy can be performed as a standalone procedure or as part of another surgery. The procedure is typically quick and is performed under local anesthesia. First, the area under the tongue is numbed with an injection. Once the patient is numb, a small incision is made in the tissue and the tongue is freed from its tether. The incision is then closed with dissolvable sutures. Recovery from a frenotomy is typically quick and most patients experience little to no pain or discomfort.According to Lalakea and Messner, surgery can be considered for patients of any age with a tight frenulum, as well as a history of speech, feeding, or mechanical/social difficulties. Adults with ankyloglossia may elect the procedure. Some of those who have done so report post-operative pain.Horton et al., have a classical belief that people with ankyloglossia can compensate in their speech for a limited tongue range of motion. For example, if the tip of the tongue is restricted for making sounds such as /n, t, d, l/, the tongue can compensate through dentalization; this is when the tongue tip moves forward and up. When producing /r/, the elevation of the mandible can compensate for restriction of tongue movement. Also, compensations can be made for /s/ and /z/ by using the dorsum of the tongue for contact against the palate rugae. Thus, Horton et al. | 0-1
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Other common causes of infectious enteritis include bacteria such as Shigella and E. coli, as well as viruses such as adenovirus, astrovirus and calicivirus. Other less common pathogens include Bacillus cereus, Clostridium perfringens, Clostridium difficile and Staphylococcus aureus.Campylobacter jejuni is one of the most common sources of infectious enteritis, and the most common bacterial pathogen found in 2 year old and smaller children with diarrhoea. It has been linked to consumption of contaminated water and food, most commonly poultry and milk. The disease tends to be less severe in developing countries, due to the constant exposure which people have with the antigen in the environment, leading to early development of antibodies.Rotavirus is responsible for infecting 140 million people and causing 1 million deaths each year, mostly in children younger than 5 years. This makes it the most common cause of severe childhood diarrhoea and diarrhea-related deaths in the world. It selectively targets mature enterocytes in the small intestine, causing malabsorption, as well as inducing secretion of water. It has also been observed to cause villus ischemia, and increase intestinal motility. The net result of these changes is induced diarrhoea. Enteritis necroticans is an often fatal illness, caused by β-toxin of Clostridium perfringens. This causes inflammation and segments of necrosis throughout the gastrointestinal tract. It is most common in developing countries, however has also been documented in post-World War II Germany. | Studies have shown the efficacy of antibiotics in reducing the duration of the symptoms of infectious enteritis of bacterial origin, however antibiotic treatments are usually not required due to the self-limiting duration of infectious enteritis. Etymology
The word enteritis () uses combining forms of entero- and -itis, both New Latin from Greek, respectively from ἑντερον (enteron, small intestine) and -ιτις (-itis, inflammation). See also
Enteropathy
Staphylococcal enteritis
References
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Nephrogenic diabetes insipidus, also known as renal diabetes insipidus, is a form of diabetes insipidus primarily due to pathology of the kidney. This is in contrast to central or neurogenic diabetes insipidus, which is caused by insufficient levels of antidiuretic hormone (also called vasopressin). Nephrogenic diabetes insipidus is caused by an improper response of the kidney to antidiuretic hormone, leading to a decrease in the ability of the kidney to concentrate the urine by removing free water. Signs and symptoms
The clinical manifestation is similar to neurogenic diabetes insipidus, presenting with polydipsia (excessive thirst) and polyuria (excretion of a large amount of dilute urine). Dehydration is common, and incontinence can occur secondary to chronic bladder distension. On investigation, there will be an increased plasma osmolarity and decreased urine osmolarity. As pituitary function is normal, antidiuretic hormone levels are likely to be abnormal or raised. Polyuria will continue as long as the patient is able to drink. If the patient is unable to drink and is still unable to concentrate the urine, then hypernatremia will ensue with its neurologic symptoms. Causes
Acquired
Nephrogenic diabetes insipidus is most common in its acquired forms, meaning that the defect was not present at birth. These acquired forms have numerous potential causes. The most obvious cause is a kidney or systemic disorder, including amyloidosis, polycystic kidney disease, electrolyte imbalance, or some other kidney defect.The major causes of acquired nephrogenic diabetes insipidus that produce clinical symptoms (e.g., polyuria) in the adult are lithium toxicity and high blood calcium. | This, however, is not a diagnostic finding, as it depends on patient hydration.Desmopressin can also be used; if the patient is able to concentrate urine following administration of desmopressin, then the cause of the diabetes insipidus is neurogenic diabetes insipidus; if no response occurs to desmopressin, then the cause is likely to be nephrogenic. Treatment
Persons with nephrogenic diabetes insipidus will need to consume enough fluids to equal the amount of urine produced. Any underlying cause such as high blood calcium must be corrected to treat nephrogenic diabetes insipidus. The first line of treatment is hydrochlorothiazide and amiloride. Patients may also consider a low-salt and low-protein diet.Thiazide diuretics are used in treatment because diabetes insipidus causes the excretion of more sodium than water, while maintaining the corticomedullary gradient (not maintained when using loop diuretics). The maintained corticomedullary gradient allows more absorption of water in the collecting duct. This improves the blood osmolarity and prevents hypernatremia.High serum osmolarity stimulates polydipsia in an attempt to dilute the serum back to normal and provide free water for excreting the excess serum solutes. However, since the patient is unable to concentrate urine to excrete the excess solutes, the resulting urine fails to decrease serum osmolarity and the cycle repeats itself, hence polyuria. Etymology
The name of the disease comes from:
diabetes: from Latin: diabetes, from Ancient Greek: διαβήτης diabḗtēs "a passer-through; siphon", from Greek διαβαίνειν diabaínein "to pass through", from δια- dia- "through" + βαίνειν baínein "to go". | 11
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In the (low seismicity) United Kingdom, for example, it has been calculated that the average recurrences are:
an earthquake of 3.7–4.6 every year, an earthquake of 4.7–5.5 every 10 years, and an earthquake of 5.6 or larger every 100 years. This is an example of the Gutenberg–Richter law. The number of seismic stations has increased from about 350 in 1931 to many thousands today. As a result, many more earthquakes are reported than in the past, but this is because of the vast improvement in instrumentation, rather than an increase in the number of earthquakes. The United States Geological Survey (USGS) estimates that, since 1900, there have been an average of 18 major earthquakes (magnitude 7.0–7.9) and one great earthquake (magnitude 8.0 or greater) per year, and that this average has been relatively stable. In recent years, the number of major earthquakes per year has decreased, though this is probably a statistical fluctuation rather than a systematic trend. More detailed statistics on the size and frequency of earthquakes is available from the United States Geological Survey. A recent increase in the number of major earthquakes has been noted, which could be explained by a cyclical pattern of periods of intense tectonic activity, interspersed with longer periods of low intensity. | 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. | 11
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Gallstones within the ampulla of Vater can obstruct the exocrine system of the pancreas and can result in pancreatitis. Signs and symptoms
Gallstones, regardless of size or number, are often asymptomatic. These "silent stones" do not require treatment and can remain asymptomatic even years after they form.A characteristic symptom of a gallstone attack is the presence of colic-like pain in the upper-right side of the abdomen, often accompanied by nausea and vomiting. Pain from symptomatic gallstones may range from mild to severe and can steadily increase over a period lasting from 30 minutes to several hours. Other symptoms may include fever, as well as referred pain between the shoulder blades or below the right shoulder. If one or more gallstones block the bile ducts and cause bilirubin to leak into the bloodstream and surrounding tissue, jaundice and itching may also occur. In this case, liver enzyme levels are likely to be raised.Often, gallbladder attacks occur after eating a heavy meal. Attacks are most common in the evening or at night. Other complications
In rare cases, gallstones that cause severe inflammation can erode through the gallbladder into adherent bowel, potentially causing an obstruction termed gallstone ileus.Other complications can include ascending cholangitis, which occurs when a bacterial infection causes purulent inflammation in the biliary tree and liver, and acute pancreatitis caused by blockage of the bile ducts that prevents active enzymes from being secreted into the bowel, instead damaging the pancreas. Rarely, gallbladder cancer may occur as a complication. | The gene mutation is inherited as an autosomal recessive trait. This means both parents have to pass a defective copy of the ALMS1 gene in order for their child to have the syndrome, even though the parents may not show signs or symptoms of the condition.The ALMS1 gene contains instructions to encode a specific protein known as ALMS1. The protein then is involved in ciliary function, cell cycle control and intracellular transport. In addition, the protein is expressed in all organ tissues of the body. It has a role in the proper function, maintenance and formation of cilia, which are found in all types of cells in the body. At least 239 disease-causing mutations in ALMS1 have been described as of 2015. Most of these mutations have led to the production of a dysfunctional version of the ALSM1 protein which are present in tissues, but at low levels. Diagnosis
It is possible to clinically detect Alström syndrome in infancy, but more frequently, it is detected much later, as doctors tend to detect symptoms as separate problems. Currently, Alström syndrome is often diagnosed clinically, since genetic testing is costly and only available on a limited basis.A physical examination would be needed to properly diagnose the patient. Certain physical characteristics can determine if the patient has some type of genetic disorder. Usually, a geneticist would perform the physical examination by measuring the distance around the head, distance between the eyes and the length of arms and legs. | 0-1
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Around 90% of individuals with PCD have ultrastructural defects affecting protein(s) in the outer and/or inner dynein arms, which give cilia their motility, with roughly 38% of these defects caused by mutations on two genes, DNAI1 and DNAH5, both of which code for proteins found in the ciliary outer dynein arm.There is an international effort to identify genes that code for inner dynein arm proteins or proteins from other ciliary structures (radial spokes, central apparatus, etc.) associated with PCD. The role of DNAH5 in heterotaxy syndromes and left-right asymmetry is also under investigation. At least 32 genes have been implicated in this condition. Another gene associated with this condition is GAS2L2. Pathophysiology
This condition is genetically inherited. Structures that make up the cilia, including inner and/or outer dynein arms, central apparatus, radial spokes, etc. are missing or dysfunctional and thus the axoneme structure lacks the ability to move. Axonemes are the elongated structures that make up cilia and flagella. Additionally, there may be chemical defects that interfere with ciliary function in the presence of adequate structure. Whatever the underlying cause, dysfunction of the cilia begins during and impacts the embryologic phase of development. Specialised monocilia known as nodal cilia are at the heart of this problem. They lack the central-pair microtubules of ordinary motile cilia and so rotate clockwise rather than beat; in the primitive node at the anterior end of the primitive streak in the embryo, these are angled posteriorly such that they describe a D-shape rather than a circle. | Primary ciliary dyskinesia (PCD) is a rare, autosomal recessive genetic ciliopathy, that causes defects in the action of cilia lining the upper and lower respiratory tract, sinuses, Eustachian tube, middle ear, Fallopian tube, and flagella of sperm cells. The alternative name of "immotile ciliary syndrome" is no longer favored as the cilia do have movement, but are merely inefficient or unsynchronized. When accompanied by situs inversus the condition is known as Kartagener syndrome.Respiratory epithelial motile cilia, which resemble microscopic "hairs" (although structurally and biologically unrelated to hair), are complex organelles that beat synchronously in the respiratory tract, moving mucus toward the throat. Normally, cilia beat 7 to 22 times per second, and any impairment can result in poor mucociliary clearance, with subsequent upper and lower respiratory infection. Cilia also are involved in other biological processes (such as nitric oxide production), currently the subject of dozens of research efforts. Signs and symptoms
The main consequence of impaired ciliary function is reduced or absent mucus clearance from the lungs, and susceptibility to chronic recurrent respiratory infections, including sinusitis, bronchitis, pneumonia, and otitis media. Progressive damage to the respiratory system is common, including progressive bronchiectasis beginning in early childhood, and sinus disease (sometimes becoming severe in adults). However, diagnosis is often missed early in life despite the characteristic signs and symptoms. In males, immotility of sperm can lead to infertility, although conception remains possible through the use of in vitro fertilization, there also are reported cases where sperm were able to move. | 11
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Impact testing results showed that the stiffness and the damping resistance of a test subject’s tissue are correlated with the mass, velocity, and size of the striking object. Such properties may be useful for forensics investigation when contusions were induced. When a solid object impacts a human soft tissue, the energy of the impact will be absorbed by the tissues to reduce the effect of the impact or the pain level; subjects with more soft tissue thickness tended to absorb the impacts with less aversion. Soft tissues have the potential to undergo large deformations and still return to the initial configuration when unloaded, i.e. they are hyperelastic materials, and their stress-strain curve is nonlinear. The soft tissues are also viscoelastic, incompressible and usually anisotropic. Some viscoelastic properties observable in soft tissues are: relaxation, creep and hysteresis. In order to describe the mechanical response of soft tissues, several methods have been used. These methods include: hyperelastic macroscopic models based on strain energy, mathematical fits where nonlinear constitutive equations are used, and structurally based models where the response of a linear elastic material is modified by its geometric characteristics. Pseudoelasticity
Even though soft tissues have viscoelastic properties, i.e. stress as function of strain rate, it can be approximated by a hyperelastic model after precondition to a load pattern. After some cycles of loading and unloading the material, the mechanical response becomes independent of strain rate. | In patients with comorbid substance use disorder and BP-II, episodes have a longer duration and treatment compliance decreases. Preliminary studies suggest that comorbid substance use is also linked to increased risk of suicidality. Diagnosis
BP-II is diagnosed according to the criteria established in the American Psychiatric Associations Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). In addition, alternative diagnostic criteria is established in the World Health Organizations International Classification of Diseases-10th Revision (ICD-10). The diagnostic criteria are established from self-reported experiences from patients or their family members, the psychiatric assessment, and the mental status examination. In addition, Screening instruments like the Mood Disorders Questionnaire are helpful tools in determining a patients status on the bipolar spectrum. In addition, certain features have been shown to increase the chances that depressed patients have a bipolar disorder, including atypical symptoms of depression like hypersomnia and hyperphagia, a family history of bipolar disorder, medication-induced hypomania, recurrent or psychotic depression, antidepressant refractory depression, and early or postpartum depression. DSM-5 criteria
According to the DSM-5, a patient diagnosed with BP-II will have experienced at least one hypomanic episode, at least one major depressive episodes, and no manic episode. Furthermore, the occurrence of the mood episodes are not better explained by schizoaffective disorder, schizophrenia, delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorder. | 0-1
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Gastroesophageal varices may refer to:
Esophageal varices, dilated sub-mucosal veins in esophagus
Gastric varices, dilated submucosal veins in the stomach | Alopecia totalis is the loss of all hair on the head and face. Its causes are unclear, but believed to be autoimmune. Research suggests there may be a genetic component linked to developing alopecia totalis; the presence of DRB1*0401 and DQB1*0301, both of which are Human Leukocyte Antigens (HLA), were found to be associated with long-standing alopecia totalis. Treatment
Methotrexate and corticosteroids are proposed treatments.Scalp cooling has specifically been used to prevent alopecia in docetaxel chemotherapy, although it has been found prophylactic in other regimens as well. Treatment effects may take time to resolve, with one study showing breast cancer survivors wearing wigs up to 2 years after chemotherapy. See also
Alopecia areata
Alopecia universalis
References
== External links == | 0-1
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It is typically used after other antinausea drugs have failed.There appears to be a low risk of harm to the baby with use during pregnancy, though there may be an increase in heart problems among the babies.Ondansetron is in pregnancy category B in the US. It is not known if ondansetron is excreted in breast milk. Cyclic vomiting syndrome
Ondansetron is one of several antiemetic drugs used during the vomiting phase of cyclic vomiting syndrome. Gastroenteritis
Trials in emergency department settings support the use of ondansetron to reduce vomiting associated with gastroenteritis and dehydration. A retrospective review found it was used commonly for this purpose, being administered in over 58% of cases. Its use reduced hospital admissions, but was also associated with higher rates of return visits to the emergency department. Furthermore, people who had initially received ondansetron were more likely to be admitted on the return visit than people who had not received the drug. However, this effect may simply be due to the agent being used more frequently in people who present with more severe illness. Its use was not found to mask serious diagnoses. Special populations
Children
Ondansetron has rarely been studied in people under 4 years of age. As such, little data is available to guide dosage recommendations. Elderly
It is not necessary to adjust the dosage for people under 75 years of age. The use of ondansetron has not been studied in people older than 75 years of age, and it is not known if dosage should be adjusted for this group. | Bimatoprost, sold under the brand name Lumigan among others, is a medication used to treat high pressure inside the eye including glaucoma. Specifically it is used for open angle glaucoma when other agents are not sufficient. It may also be used to increase the size of the eyelashes. It is used as an eye drop and effects generally occur within four hours.Common side effects include red eyes, dry eyes, change in color of the eyes, blurry vision, and cataracts. Use during pregnancy or breastfeeding is generally not recommended. It is a prostaglandin analog and works by increasing the outflow of aqueous fluid from the eyes.Bimatoprost was approved for medical use in the United States in 2001. It is available as a generic medication. In 2018, it was the 274th most commonly prescribed medication in the United States, with more than 2 million prescriptions. Uses
Medical
Bimatoprost is used for the treatment of open-angle glaucoma and ocular hypertension in adults, either alone or in combination with a beta blocker, typically timolol.Studies have shown bimatoprost to be more effective than timolol in reduction of intraocular pressure (IOP) and at least as effective as the prostaglandin analogs latanoprost and travoprost in reducing IOP. Cosmetic
Bimatoprost may be used to treat small or underdeveloped eyelashes. The medical term for this is treatment of hypotrichosis; however, the U.S. Food and Drug Administration (FDA) approval is for purely cosmetic purposes (see Prostaglandin F receptor#Clinical significance). Side effects
Side effects are similar to other prostaglandin analogs applied to the eye. | 0-1
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The results of an x-ray examination of pulmonary geotrichosis presents smooth, dense patchy infiltrations and some cavities. Bronchial geotrichosis shows peribronchial thickening with fine mottling may be present on middle or basilar pulmonary fields. Bronchial geotrichosis usually present itself as non-specific diffuse peribronchical infiltration. Treatment
Geotrichosis generally has a good prognosis and patients generally have successful recovery. However, there is not a standard treatment for geotrichosis. There are several types of antimicrobial or antifungal compounds that can be used for geotrichosis treatment. Another method of treatment involves symptomatic care, bed rest, iodine therapy, aerosol nystatin and amphotericin B. Azole drugs including isoconazole and clotrimazole are used for geotrichosis treatment. Associated treatment for pulmonary geotrichosis includes the use of potassium iodide, sulfonamides or colistin. The associated asthma can be treated with desensitization and prednisolone. Amphotericin B, clotrimazole and S-fluorocytosine have become more susceptible to G. candidum. Antimycotic resistance can appear due to repeated treatment. References
== External links == | Additional images
References
External links
Genetests/NCBI/NIH/UW entries on Hyperphosphatemic Familial Tumoral Calcinosis | 0-1
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Depersonalization can consist of a detachment within the self, regarding ones mind or body, or being a detached observer of oneself. Subjects feel they have changed and that the world has become vague, dreamlike, less real, lacking in significance or being outside reality while looking in. It can be described as feeling like one is on “autopilot” and that the persons sense of individuality or selfhood has been hindered or suppressed.Chronic depersonalization refers to depersonalization/derealization disorder, which is classified by the DSM-5 as a dissociative disorder, based on the findings that depersonalization and derealization are prevalent in other dissociative disorders including dissociative identity disorder.Though degrees of depersonalization and derealization can happen to anyone who is subject to temporary anxiety or stress, chronic depersonalization is more related to individuals who have experienced a severe trauma or prolonged stress/anxiety. Depersonalization-derealization is the single most important symptom in the spectrum of dissociative disorders, including dissociative identity disorder and "dissociative disorder not otherwise specified" (DD-NOS). It is also a prominent symptom in some other non-dissociative disorders, such as anxiety disorders, clinical depression, bipolar disorder, schizophrenia, schizoid personality disorder, hypothyroidism or endocrine disorders, schizotypal personality disorder, borderline personality disorder, obsessive–compulsive disorder, migraines, and sleep deprivation; it can also be a symptom of some types of neurological seizure. In social psychology, and in particular self-categorization theory, the term depersonalization has a different meaning and refers to "the stereotypical perception of the self as an example of some defining social category". | Description
Individuals who experience depersonalization feel divorced from their own personal self by sensing their body sensations, feelings, emotions, behaviors etc. as not belonging to the same person or identity. Often a person who has experienced depersonalization claims that things seem unreal or hazy. Also, a recognition of a self breaks down (hence the name). Depersonalization can result in very high anxiety levels, which further increase these perceptions.Depersonalization is a subjective experience of unreality in ones self, while derealization is unreality of the outside world. Although most authors currently regard depersonalization (personal/self) and derealization (reality/surroundings) as independent constructs, many do not want to separate derealization from depersonalization. Prevalence
Depersonalization is a symptom of anxiety disorders, such as panic disorder. It can also accompany sleep deprivation (often occurring when experiencing jet lag), migraine,
epilepsy (especially temporal lobe epilepsy,complex-partial seizure, both as part of the aura and during the seizure),
obsessive-compulsive disorder, severe stress or trauma, anxiety, the use of recreational drugs
—especially cannabis, hallucinogens, ketamine, and MDMA, certain types of meditation, deep hypnosis, extended mirror or crystal gazing, sensory deprivation, and mild-to-moderate head injury with little or full loss of consciousness (less likely if unconscious for more than 30 minutes). Interoceptive exposure is a non-pharmacological method that can be used to induce depersonalization.In the general population, transient depersonalization/derealization are common, having a lifetime prevalence between 26 and 74%. A random community-based survey of 1,000 adults in the US rural south found a 1-year depersonalization prevalence rate at 19%. | 11
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Early diagnosis and treatment are imperative in helping reduce joint damage and other symptoms, which will help reduce levels of permanent damage leading to long term disability. Non-pharmacological treatments
The optimal approach to treating a child with JIA typically involves a team of medical professionals, which may include (but is not limited to) paediatric rheumatologists, paediatric rheumatology nurses, general paediatricians, general practitioners, adult rheumatologists, physical therapists (PTs), occupational therapists (OTs), podiatrists, psychologists, social workers, pharmacists, ophthalmologists and orthopaedic surgeons. The multi-disciplinary team (MDT) work in conjunction with the child and their parents, the local health service and medical team, the childs school and teachers, community leaders and sports coaches to best support the child and their family.Together, the team help children to participate as fully and independently as possible in their daily activities by maximising quality of life, maximising function and minimising disruption to the life of the child or young person. The multidisciplinary team work together to provide the child and their family with support and education about JIA, strategies to promote age-appropriate self-sufficiency and help the child to adapt and adjust to any challenges they face. There are many ways to make daily tasks easier or more manageable. One of the key ways the multidisciplinary team helps children with JIA is to involve them, and their families, in the decision-making process regarding their treatment and rehabilitation. In young children with JIA, symptoms may result in either delay or regression in developmental milestones such as walking, running or climbing. Upper limb function may also be affected. | These terms were replaced in 1997 with the release of the revised ILAR (International League of Associations for Rheumatology) classification criteria.There is currently an international movement underway to further revise the classification criteria for JIA, although this is in a preliminary phase.MeSH uses "juvenile arthritis" as the primary entry, and uses "idiopathic", "chronic" and "rheumatoid" in alternate entries. Society
Some famous people with this condition are:
Antoni Gaudi, architect
Clark Middleton, actor
Claire Cottrill, singer-songwriter
Rosemary Sutcliff, author
References
External links
Arthritis Australia, Juvenile Idiopathic Arthritis
JIA@NRAS (UK)
JIA - NIH Medline Plus. | 11
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It may also result in reoccurrence of the condition that is being treated. Rarely tardive dyskinesia can occur when the medication is stopped. Overdose
Symptoms
Symptoms are usually due to side effects. Most often encountered are:
Anticholinergic side effects (dry mouth, constipation, paralytic ileus, difficulties in urinating, decreased perspiration)
Coma in severe cases, accompanied by respiratory depression and massive hypotension, shock
Hypotension or hypertension
Rarely, serious ventricular arrhythmia (torsades de pointes), with or without prolonged QT-time
Sedation
Severe extrapyramidal side effects with muscle rigidity and tremors, akathisia, etc. Treatment
Treatment is mostly symptomatic and involves intensive care with stabilization of vital functions. In early detected cases of oral overdose, induction of emesis, gastric lavage, and the use of activated charcoal can be tried. In the case of a severe overdose, antidotes such as bromocriptine or ropinirole may be used to treat the extrapyramidal effects caused by haloperidol, acting as dopamine receptor agonists. ECG and vital signs should be monitored especially for QT prolongation and severe arrhythmias should be treated with antiarrhythmic measures. Prognosis
An overdose of haloperidol can be fatal, but in general the prognosis after overdose is good, provided the person has survived the initial phase. Pharmacology
Haloperidol is a typical butyrophenone type antipsychotic that exhibits high affinity dopamine D2 receptor antagonism and slow receptor dissociation kinetics. It has effects similar to the phenothiazines. The drug binds preferentially to D2 and α1 receptors at low dose (ED50 = 0.13 and 0.42 mg/kg, respectively), and 5-HT2 receptors at a higher dose (ED50 = 2.6 mg/kg). | Adjunctive treatment of alcohol and opioid withdrawal
Agitation and confusion associated with cerebral sclerosis
Alcohol-induced psychosis
Hallucinations in alcohol withdrawal
Hyperactive delirium (to control the agitation component of delirium)
Hyperactivity, aggression
Otherwise uncontrollable, severe behavioral disorders in children and adolescents
Schizophrenia
Therapeutic trial in personality disorders, such as borderline personality disorder
Treatment of intractable hiccups
Treatment of neurological disorders, such as tic disorders such as Tourette syndrome, and chorea
Treatment of severe nausea and emesis in postoperative and palliative care, especially for palliating adverse effects of radiation therapy and chemotherapy in oncology. Also used as a first line antiemetic for acute Cannabis Hyperemesis Syndrome.Haloperidol was considered indispensable for treating psychiatric emergency situations, although the newer atypical drugs have gained a greater role in a number of situations as outlined in a series of consensus reviews published between 2001 and 2005.In a 2013 comparison of 15 antipsychotics in schizophrenia, haloperidol demonstrated standard effectiveness. It was 13–16% more effective than ziprasidone, chlorpromazine, and asenapine, approximately as effective as quetiapine and aripiprazole, and 10% less effective than paliperidone. A 2013 systematic review compared haloperidol to placebo in schizophrenia:
Pregnancy and lactation
Data from animal experiments indicate haloperidol is not teratogenic, but is embryotoxic in high doses. In humans, no controlled studies exist. Reports in pregnant women revealed possible damage to the fetus, although most of the women were exposed to multiple drugs during pregnancy. In addition, reports indicate neonates exposed to antipsychotic drugs are at risk for extrapyramidal and/or withdrawal symptoms following delivery, such as agitation, hypertonia, hypotonia, tremor, somnolence, respiratory distress, and feeding disorder. | 11
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Familial amyloid polyneuropathy, also called transthyretin-related hereditary amyloidosis, transthyretin amyloidosis abbreviated also as ATTR (hereditary form), or Corino de Andrades disease, is an autosomal dominant neurodegenerative disease. It is a form of amyloidosis, and was first identified and described by Portuguese neurologist Mário Corino da Costa Andrade, in 1952. FAP is distinct from senile systemic amyloidosis (SSA), which is not inherited, and which was determined to be the primary cause of death for 70% of supercentenarians who have been autopsied. FAP can be ameliorated by liver transplantation. Presentation
Usually manifesting itself between 20 and 40 years of age, it is characterized by pain, paresthesia, muscular weakness and autonomic dysfunction. In its terminal state, the kidneys and the heart are affected. FAP is characterized by the systemic deposition of amyloidogenic variants of the transthyretin protein, especially in the peripheral nervous system, causing a progressive sensory and motor polyneuropathy. Cause
FAP is caused by a mutation of the TTR gene, located on human chromosome 18q12.1-11.2. A replacement of valine by methionine at position 30 (TTR V30M) is the mutation most commonly found in FAP. The transthyretin protein is a tetramer. The tetramer has to dissociate into misfolded monomers to aggregate into a variety of structures including amyloid fibrils. Because most patients are heterozygotes, they deposit both mutant and wild type TTR subnits.FAP is inherited in an autosomal dominant manner. | This means that the defective gene responsible for the disorder is located on an autosome (chromosome 18 is an autosome), and only one copy of the defective gene is sufficient to cause the disorder, when inherited from a parent who has the disorder. Diagnosis
Clinical suspicion for FAP is raised on the basis of a family history of neuropathy and physical exam showing signs of neuropathy. Diagnosis can be made using genetic testing to identify mutations in the TTR gene, but may include other corroborative investigation. Nerve conduction testing typically shows an axonal polyneuropathy, with sensory involvement greater than motor. Superimposed mononeuropathies may also be evident, such as a median mononeuropathy at the wrist (carpal tunnel syndrome). Electromyography (EMG) may show evidence of chronic denervation and reinnervation. Autonomic testing, including quantitative sweat testing, can reveal involvement of the autonomic nervous system. Occasionally, biopsy of skin, nerve, or muscle may be performed, which can show signs of denervation and amyloid deposition with response to anti-TTR antibodies. Additional testing should be performed to identify involvement of the heart or kidneys.Sudomotor function through electrochemical skin conductance may provide a measure of subclinical autonomic involvement. Treatments
The medication tafamidis has been approved for the treatment of transthyretin familial amyloid polyneuropathy in Europe. Studies have found that it delays neurological problems when started early. The US Food and Drug Administrations Peripheral and Central Nervous System Drugs Advisory Committee rejected the drug in June 2012, in a 13-4 vote. | 11
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They remain fully contained within a prostate acinus (the berry-shaped termination of a gland, where the secretion is produced) or duct. The latter can be demonstrated with special staining techniques (immunohistochemistry for cytokeratins) to identify the basal cells forming the supporting layer of the acinus. In prostate cancer, the abnormal cells spread beyond the boundaries of the acinus and form clusters without basal cells. In HGPIN, the basal cell layer is disrupted but present. PIN is primarily found in the peripheral zone of the prostate (75-80%), rarely in the transition zone (10-15%) and very rarely in the central zone (5%), a distribution that parallels the zonal distribution for prostate carcinoma.Because it is thought to be a premalignant state, PIN is often considered the prostate equivalent of what is called carcinoma in situ (localized cancer) in other organs. However, PIN differs from carcinoma in situ in that it may remain unchanged or even spontaneously regress.Several architectural variants of PIN have been described, and many cases have multiple patterns. The main ones are tufting, micropapillary, cribriform, and flat. Although these different appearances may cause confusion with other conditions, they have not been found to be of clinical importance. Rarer types are signet-ring-cell, small-cell-neuroendocrine, mucinous, foamy, inverted, and with squamous differentiation. | Hydrocortisone sodium succinate is a synthetic glucocorticoid corticosteroid and a corticosteroid ester. == References == | 0-1
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A premature ventricular contraction (PVC) is a common event where the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node. PVCs may cause no symptoms or may be perceived as a "skipped beat" or felt as palpitations in the chest. PVCs do not usually pose any danger.The electrical events of the heart detected by the electrocardiogram (ECG) allow a PVC to be easily distinguished from a normal heart beat. However, very frequent PVCs can be symptomatic of an underlying heart condition (such as arrhythmogenic right ventricular cardiomyopathy). Furthermore, very frequent (over 20% of all heartbeats) PVCs are considered a risk factor for arrhythmia-induced cardiomyopathy, in which the heart muscle becomes less effective and symptoms of heart failure may develop. Ultrasound of the heart is therefore recommended in people with frequent PVCs. If PVCs are frequent or troublesome, medication (beta blockers or certain calcium channel blockers) may be used. Very frequent PVCs in people with dilated cardiomyopathy may be treated with radiofrequency ablation. Signs and symptoms
Although there are many possible symptoms associated with PVCs, PVCs may also have no symptoms at all. PVCs may be perceived as a skipped heart beat, a strong beat, palpitations, or lightheadedness. They may also cause chest pain, a faint feeling, fatigue, or hyperventilation after exercise. Symptoms may be more pronounced at times of stress. | If symptoms are infrequent, other forms of continuous heart beat recording may be used, such as a 24 or 48-hour Holter monitor or even 14- to 30-day recorders if the symptoms are very occasional. The advantage of these monitors is that they allow a quantification of the amount of abnormal beats ("burden") and ensure that there are no heart arrhythmias present that might require attention, such as ventricular tachycardia. If symptoms are associated with exercise, a supervised cardiac stress test may be required to reproduce the abnormality. Specifically, if this shows exercise-induced ventricular tachycardia this would require specific treatment. If PVCs are suppressed by exercise, this is an encouraging finding.On electrocardiography (ECG or Holter) premature ventricular contractions have a specific appearance of the QRS complexes and T waves, which are different from normal readings. By definition, a PVC occurs earlier than the regular normally conducted beat. Subsequently, the time between the PVC and the next normal beat is longer as the result of a compensatory pause. PVCs can be distinguished from premature atrial contractions because the compensatory pause is longer following premature ventricular contractions, in addition to a difference in QRS appearance.In some people, PVCs occur in a predictable pattern. Two PVCs in a row are called doublets and three PVCs in a rows are triplets. Depending whether there are one, two, or three normal (sinus) beats between each PVC, the rhythm is called bigeminy, trigeminy, or quadrigeminy. If 3 or more consecutive PVCs occur in a row it may be called ventricular tachycardia. | 11
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It independently prevents the head of the humerus from slipping inferiorly. The supraspinatus works in cooperation with the deltoid muscle to perform abduction, including when the arm is in an adducted position. Beyond 15 degrees the deltoid muscle becomes increasingly more effective at abducting the arm and becomes the main propagator of this action. Clinical significance
The supraspinatus forms part of the rotator cuff and is one of its most frequently damaged components, whether from acute injury or gradual degeneration. Bad posture and age are leading risk factors, with a high prevalence of unsymptomatic partial and full tears, as well as symptomatic syndromes with chronic pain. Connected pathologies include acromial impingement, frozen shoulder, and poor sleep, especially on the side. Both ultrasound and MRI are now effective methods of diagnosis. Tear
DiagnosisAntero-posterior projectional radiography of the shoulder may demonstrate a high-riding humeral head, with an acromiohumeral distance of less than 7 mm. RepairOne study has indicated that arthroscopic surgery for full-thickness supraspinatus tears is effective for improving shoulder functionality.A comparative effectiveness review of nonoperative and operative treatments for rotator cuff tears was performed at the University of Alberta Evidence-based Practice Center in 2010. The review identified one study which reported that, "Patients receiving early surgery had superior function compared with the delayed surgical group". The review noted that the level of significance of the study was not reported, and the review chose not to include it as one of their conclusions. | The supraspinatus (plural supraspinati) is a relatively small muscle of the upper back that runs from the supraspinous fossa superior portion of the scapula (shoulder blade) to the greater tubercle of the humerus. It is one of the four rotator cuff muscles and also abducts the arm at the shoulder. The spine of the scapula separates the supraspinatus muscle from the infraspinatus muscle, which originates below the spine. Structure
The supraspinatus muscle arises from the supraspinous fossa, a shallow depression in the body of the scapula above its spine. The supraspinatus muscle tendon passes laterally beneath the cover of the acromion. Research in 1996 showed that the postero-lateral origin was more lateral than classically described.The supraspinatus tendon is inserted into the superior facet of the greater tubercle of the humerus. The distal attachments of the three rotator cuff muscles that insert into the greater tubercle of the humerus can be abbreviated as SIT when viewed from superior to inferior (for supraspinatus, infraspinatus, and teres minor), or SITS when the subscapularis muscle, which attaches to the lesser tubercle of the humerus, is included. Nerve supply
The suprascapular nerve (C5) innervates the supraspinatus muscle as well as the infraspinatus muscle. It comes from the upper trunk of the brachial plexus. This nerve can be damaged along its course in fractures of the overlying clavicle, which can reduce the persons ability to initiate the abduction. Function
The supraspinatus muscle performs abduction of the arm, and pulls the head of the humerus medially towards the glenoid cavity. | 11
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There is no clinically significant activity against Gram-negative bacteria.Two trials, DISCOVER 1 and DISCOVER 2, demonstrated noninferiority of dalbavancin compared to vancomycin/linezolid in the treatment of ABSSSI. Patients were randomly assigned to receive two doses of dalbavancin on days 1 and 8, or to receive intravenous vancomycin for at least 3 days with the option of switching to oral linezolid to complete 10 to 14 days of therapy. Investigators assessed the cessation of spread of infection-related erythema and the absence of fever at 48 to 72 hours as the primary endpoint and found that once-weekly dalbavancin was as effective as twice-daily intravenous vancomycin followed by oral linezolid. This once-weekly dosing regimen may offer an advantageous treatment option compared to daily or twice-daily dosing. Contraindications
Hypersensitivity to dalbavancin can occur, causing issues such as skin reactions or anaphylaxis. Caution is advised for patients with known hypersensitivity to other glycopeptides. There is currently no data on cross-reactivity between dalbavancin and vancomycin. Side effects
The most common adverse reactions encountered in Phase II and Phase III trials were nausea (5.5%), headache (4.7%), and diarrhea (4.4%), as well as rash (2.7%) and itchiness (2.1%). Other less frequent but serious adverse reactions included hematologic disorders, hepatotoxicity, Clostridium difficile colitis, bronchospasm, infusion-related reactions including Red Man Syndrome, and anaphylactic shock. In trials, dalbavancin was associated with higher rates of hemorrhagic events compared to comparator groups and should be a precaution in patients undergoing surgery or taking anticoagulants. | It is a once-weekly, two-dose antibiotic, the rights to which Actavis acquired when it bought Durata Therapeutics in 2014.The U.S. Food and Drug Administration (FDA) approved dalbavancin in May 2014, for the treatment of acute bacterial skin and skin structure infections (ABSSSIs) caused by certain susceptible bacteria such as Staphylococcus aureus including methicillin-susceptible and methicillin-resistant strains of Streptococcus pyogenes, in intravenous dosage form. Medical uses
Dalbavancin is an antibiotic used to treat acute bacterial skin and skin structure infections (ABSSSI) in adults caused by susceptible Gram-positive organisms, including methicillin-resistant Staphylococcus aureus (MRSA). MRSA infections have become problematic in the community and in healthcare settings due to resistance to many available antibiotics. Because dalbavancin has demonstrated efficacy against MRSA and other microorganisms to treat serious or life-threatening infections, it was the first drug approved as a Qualified Infectious Disease Product under the Generating Antibiotic Incentives Now (GAIN) act, which is part of the FDA Safety and Innovation Act.It has strong activity against many Gram-positive bacteria, including methicillin-sensitive and methicillin-resistant Staphylococcus aureus, Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus anginosus, Streptococcus intermedius, and Streptococcus constellatus. Based on MIC data and other studies, dalbavancin is more potent and bactericidal and therefore requires lower concentrations than vancomycin against these organisms. Dalbavancin also shows in vitro activity against vancomycin-susceptible Enterococcus faecium and Enterococcus faecalis. Other Gram-positive organisms belonging to the Bacillus spp., Listeria spp., and Corynebacterium spp. may show in vitro susceptibility, and dalbavancin may exhibit activity against enterococci expressing the VanB or VanC phenotype of acquired resistance against vancomycin. | 11
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Crime
A travel advisory published by the US Overseas Security Advisory Council (OSAC) in 2012 stated: One common and particularly dangerous method that criminals use in order to rob a victim is through the use of drugs. The most common [in Colombia] has been scopolamine. Unofficial estimates put the number of annual scopolamine incidents in Colombia at approximately 50,000. Scopolamine can render a victim unconscious for 24 hours or more. In large doses, it can cause respiratory failure and death. It is most often administered in liquid or powder form in foods and beverages. The majority of these incidents occur in night clubs and bars, and usually men, perceived to be wealthy, are targeted by young, attractive women. It is recommended that, to avoid becoming a victim of scopolamine, a person should never accept food or beverages offered by strangers or new acquaintances, nor leave food or beverages unattended in their presence. Victims of scopolamine or other drugs should seek immediate medical attention. Between 1998 and 2004, 13% of emergency-room admissions for "poisoning with criminal intentions" in a clinic of Bogotá, Colombia, have been attributed to scopolamine, and 44% to benzodiazepines. Most commonly, the person has been poisoned by a robber who gave the victim a scopolamine-laced beverage, in the hope that the victim would become unconscious or unable to effectively resist the robbery.Beside robberies, it is also allegedly involved in express kidnappings and sexual assault. | The name "scopolamine" is derived from one type of nightshade known as Scopolia, while the name "hyoscine" is derived from another type known as Hyoscyamus niger. It is on the World Health Organizations List of Essential Medicines. Medical uses
Scopolamine has a number of uses in medicine where it is used in low doses to treat:
Postoperative nausea and vomiting. Motion sickness, including sea sickness, leading to its use by scuba divers (where it is often applied as a transdermal patch behind the ear)
Gastrointestinal spasms
Renal or biliary spasms
Aid in gastrointestinal radiology and endoscopy
Irritable bowel syndrome
Clozapine-induced drooling
Bowel colic
Eye inflammationIt is sometimes used as a premedication, (especially to reduce respiratory tract secretions) in surgery, most commonly by injection. Breastfeeding
Scopolamine enters breast milk by secretion. Although no human studies exist to document the safety of scopolamine while nursing, the manufacturer recommends that caution be taken if scopolamine is administered to a breastfeeding woman. Elderly
The likelihood of experiencing adverse effects from scopolamine is increased in the elderly relative to younger people. This phenomenon is especially true for older people who are also on several other medications. Scopolamine use should be avoided in this age group because of these potent anticholinergic adverse effects, which have also been linked to an increased risk for dementia. | 11
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Another procedure is posterior colporrhaphy, which involves suturing of vaginal tissue. Surgery may also involve insertion of a supporting mesh (that is, a patch). There are also surgical techniques directed at repairing or strengthening the rectovaginal septum, rather than simple excision or plication of vaginal skin which provides no support. Both gynecologists and colorectal surgeons can address this problem. Potential complications of surgical correction of a rectocele include bleeding, infection, dyspareunia (pain during intercourse), as well as recurrence or even worsening of the rectocele symptoms. The use of synthetic or biologic grafts has been questioned. References
External links
Rectocele details, description, video (in Russia) | Perifolliculitis is the presence of inflammatory cells in the skin around the hair follicles. It is often found accompanying folliculitis, or inflammation of the hair follicle itself. It can have infectious or non-infectious causes. == References == | 0-1
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Increases in expression of such genes as Pax-2, as well as inhibition of Pax-6, from the notochord have been implicated in normal differentiation of cephalic midline structures. Inappropriate expression of any of these genes may result in mild to severe forms of holoprosencephaly. Other candidate genes have been located, including the SHH (holoprosencephaly type 3 a.k.a. HPE3), TGIF, ZIC2, SIX3 and BOC genes.Although many children with holoprosencephaly have normal chromosomes, specific chromosomal abnormalities have been identified in some patients (trisomy of chromosome 13, also known as Patau syndrome). There is evidence that in some families, HPE is inherited (autosomal dominant as well as autosomal or X-linked recessive inheritance). Features consistent with familial transmission of the disease (e.g., a single central maxillary incisor) should be carefully assessed in parents and family members. Non-genetic factors
Numerous possible risk factors have been identified, including gestational diabetes, transplacental infections (the "TORCH complex"), first trimester bleeding, and a history of miscarriage. As well, the disorder is found twice as often in female babies. However, there appears to be no correlation between HPE and maternal age.There is evidence of a correlation between HPE and the use of various drugs classified as being potentially unsafe for pregnant and lactating mothers. These include insulin, birth control pills, aspirin, lithium, thorazine, retinoic acid, and anticonvulsants. There is also a correlation between alcohol consumption and HPE, along with nicotine, the toxins in cigarettes and toxins in cigarette smoke when used during pregnancy. Prognosis
HPE is not a condition in which the brain deteriorates over time. | Lobar
Can present with decreased distance between eyes, a flat nasal bridge, closely spaced nostrils, mental and locomotion delays may be present. Syntelencephaly or middle interhemispheric variant of holoprosencephaly (MIHV)
Mild phenotypic presentation which can present with flat nasal bridge, metopic prominence, shallow philtrum, and possible mental and locomotion delays. "Microform"
Mild phenotypic presentation with reduced distance between eyes, sharp nasal bridge, single maxillary central incisor. Diagnosis
Holoprosencephaly is typically diagnosed during fetal development when there are abnormalities found on fetal brain imaging, however it can also be diagnosed after birth. The Protocol for diagnosis includes neuroimaging (Ultrasound or fetal MRI prior to birth or Ultrasound, MRI or CT post birth), syndrome evaluation, cytogenetics, molecular testing, and genetic counseling.There are four classifications of holoprosencephaly as well as a “microform". These classifications can be distinguished by their anatomical differences. | 11
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Two different methods for the direct application of indigo dye were developed in England in the 18th century and remained in use well into the 19th century. One of these, known as china blue, involved iron(II) sulfate. After printing an insoluble form of indigo onto the fabric, the indigo was reduced to leuco-indigo in a sequence of baths of ferrous sulfate (with reoxidation to indigo in air between immersions). The china blue process could make sharp designs, but it could not produce the dark hues of other methods. In the second half of the 1850s ferrous sulfate was used as a photographic developer for collodion process images. Hydrates
Iron(II) sulfate can be found in various states of hydration, and several of these forms exist in nature. FeSO4·H2O (mineral: szomolnokite, relatively rare)
FeSO4·4H2O (mineral: rozenite, white, relatively common, may be dehydratation product of melanterite)
FeSO4·5H2O (mineral: siderotil, relatively rare)
FeSO4·6H2O (mineral: ferrohexahydrite, relatively rare)
FeSO4·7H2O (mineral: melanterite, blue-green, relatively common)
The tetrahydrate is stabilized when the temperature of aqueous solutions reaches 56.6 °C (133.9 °F). At 64.8 °C (148.6 °F) these solutions form both the tetrahydrate and monohydrate.Mineral forms are found in oxidation zones of iron-bearing ore beds, e.g. pyrite, marcasite, chalcopyrite, etc. They are also found in related environments, like coal fire sites. Many rapidly dehydrate and sometimes oxidize. Numerous other, more complex (either basic, hydrated, and/or containing additional cations) Fe(II)-bearing sulfates exist in such environments, with copiapite being a common example. | Pathophysiology
Regardless of the underlying cause of purpura fulminans, the mechanism of disease is similar with deficiency in protein C concentration or decrease in protein C activity which promotes blood clotting (thrombosis).In cases of severe sepsis, there is widespread activation of the acute systemic inflammatory response, including activation of the coagulation and complement pathways, as well as endothelial dysfunction. Activated protein C helps regulate the systemic inflammatory response. During sepsis, signalling by the inflammatory cytokines, interleukin-1 and tumour necrosis factor, mediate altered protein transcription in the systemic inflammatory response, resulting in decreased synthesis of the regulatory proteins antithrombin, protein C and protein S, with increased synthesis of prothrombotic proteins Factor VIII, von Willebrand factor, and fibrinogen. Activated protein C binds to endothelial protein C receptor and subsequently cleaves the endothelial cell protease activated receptor-1, not only altering coagulation profiles but down-regulating pro-inflammatory and pro-apoptotic mediators, up-regulation of anti-inflammatory and anti-apoptotic pathways and stabilization of the endothelial cell barrier functions.Systemic coagulation activation may lead to depletion of circulating coagulation factors and platelets, which subsequently lead to bleeding. In early purpura fulminans, lesion progression correlates with the histological appearance of blockage of small skin blood vessels with blood clots causing capillary dilation and congestion with red blood cells. | 0-1
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Definitive diagnosis requires testing for the PML/RARA fusion gene. This may be done by polymerase chain reaction (PCR), fluorescence in situ hybridization, or conventional cytogenetics of peripheral blood or bone marrow. This mutation involves a translocation of the long arm of chromosomes 15 and 17. On rare occasions, a cryptic translocation may occur which cannot be detected by cytogenetic testing; on these occasions PCR testing is essential to confirm the diagnosis. Treatment
Initial treatment
APL is unique among leukemias due to its sensitivity to all-trans retinoic acid (ATRA; tretinoin), the acid form of vitamin A. Treatment with ATRA dissociates the NCOR-HDACL complex from RAR and allows DNA transcription and differentiation of the immature leukemic promyelocytes into mature granulocytes by targeting the oncogenic transcription factor and its aberrant action. Unlike other chemotherapies, ATRA does not directly kill the malignant cells. ATRA induces the terminal differentiation of the leukemic promyelocytes, after which these differentiated malignant cells undergo spontaneous apoptosis on their own. ATRA alone is capable of inducing remission but it is short-lived in the absence of concurrent "traditional" chemotherapy. As of 2013 the standard of treatment for concurrent chemotherapy has become arsenic trioxide, which combined with ATRA is referred to ATRA-ATO; before 2013 the standard of treatment was anthracycline (e.g. daunorubicin, doxorubicin, idarubicin or mitoxantrone)-based chemotherapy. Both chemotherapies result in a clinical remission in approximately 90% of patients with arsenic trioxide having a more favorable side effect profile.ATRA therapy is associated with the unique side effect of differentiation syndrome. | Lancet series on stillbirth 2016 | 0-1
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Lymph nodes act as a filtering system outside the lung, collecting cancer cells that are beginning to migrate out of the lung. Distant: the cancer has spread (or metastasized) to other parts of the body (aka: extensive stage SCLC).At the time of diagnosis, 60–70% of people already have metastases.Small-cell carcinoma is an undifferentiated neoplasm composed of primitive-appearing cells. As the name implies, the cells in small-cell carcinomas are smaller than normal cells, and barely have room for any cytoplasm. Some researchers identify this as a failure in the mechanism that controls the size of the cells. Treatment
Small-cell lung cancer is most commonly treated with a combination of two drugs, which is more effective than one drug alone. Chemotherapy
Cisplatin and etoposide,
Carboplatin and etoposide. Cisplatin-resistance
The drug paclitaxel may be useful in the treatment of cisplatin-resistant cancer. About 68.1% of cisplatin-resistant cells
appear to be sensitive to paclitaxel and 66.7% of paclitaxel-resistant cells to
cisplatin. The mechanism for this activity is unknown. Paclitaxel-based chemotherapy showed modest activity in SCLC patients refractory to both etoposide- and camptothecin-based chemotherapy. The newer agent lurbinectedin is active in relapsed SCLC and was approved for medical use in the United States in June 2020. Immunotherapy
In 2018, the FDA approved two immunotherapies for small cell lung cancer:
1. Nivolumab (Opdivo), and
2. Atezolizumab (Tecentriq)
Funding controversy
Tecentriq treatment costs on average $13,200 per month, depending on the dosage schedule. | Despite updated data showing 30% more people with extensive stage small cell lung cancer are alive at 24 months compared to those who received chemotherapy alone, Canadian regulator had rejected to fund Tecentriq for extensive stage small-cell lung cancer "as too costly" followed by United Kingdom also citing "drug’s cost-effectiveness." Radiation therapy
Chest radiation helps SCLC patients live longer by killing cancer cells and helping prevention of cancer recurrence. Another type of radiation, prophylactic cranial radiation, prevents central nervous system recurrence and can improve survival in patients with good performance status who have had a complete response or a very good partial response to chemoradiation in LD or chemotherapy in ED. In case of relapse
If small cell lung cancer comes back after treatment, the following combination of drugs may be used as a salvage therapy:
Cyclophosphamide (Cytoxan, Procytox),
Doxorubicin (Adriamycin) and
Vincristine (Oncovin)
Paclitaxel (Taxol)
Irinotecan (Camptosar) Current guidelines recommend that patients who relapse > 6 months from initial therapy should be retreated with the original chemotherapy regimen. For patients who relapse in < 6 months, single-agent chemotherapy either topotecan second-line therapy, or paclitaxel can be used. Novel agents
Several newer agents, including temozolomide and bendamustine, have activity in relapsed SCLC. | 11
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In 2001, Aventis, in association with Médecins Sans Frontières and the World Health Organization, signed a long-term agreement to manufacture and donate the drug.In addition to sleeping sickness, previous names have included negro lethargy, maladie du sommeil (Fr), Schlafkrankheit (Ger), African lethargy, and Congo trypanosomiasis. The British-led Sleeping Sickness Commission collecting tsetse flies, Uganda and Nyasaland, 1908-1913
Research
The genome of the parasite has been sequenced and several proteins have been identified as potential targets for drug treatment. Analysis of the genome also revealed the reason why generating a vaccine for this disease has been so difficult. T. brucei has over 800 genes that make proteins the parasite "mixes and matches" to evade immune system detection.Using a genetically modified form of a bacterium that occurs naturally in the gut of the vectors is being studied as a method of controlling the disease.Recent findings indicate that the parasite is unable to survive in the bloodstream without its flagellum. This insight gives researchers a new angle with which to attack the parasite.Trypanosomiasis vaccines are undergoing research. Additionally, the Drugs for Neglected Diseases Initiative has contributed to the African sleeping sickness research by developing a compound called fexinidazole. This project was originally started in April 2007 and enrolled 749 people in the DRC and Central African Republic. The results showed efficacy and safety in both stages of the disease, both in adults and children ≥ 6 years old and weighing ≥ 20 kg. The European Medicines Agency approved it for first and second stage disease outside of Europe in November 2018. | A saddle sore in humans is a skin ailment on the buttocks due to, or exacerbated by, horse riding or cycling on a bicycle saddle. It often develops in three stages: skin abrasion, folliculitis (which looks like a small, reddish acne), and finally abscess. Because it most commonly starts with skin abrasion, it is desirable to reduce the factors which lead to skin abrasion. Some of these factors include:
Reducing the friction. In equestrian activities, friction is reduced with a proper riding position and using properly fitting clothing and equipment. In cycling, friction from bobbing or swinging motion while pedaling is reduced by setting the appropriate saddle height. Angle and fore/aft position can also play a role, and different cyclists have different needs and preferences in relation to this. Selecting an appropriate size and design of horse riding saddle or bicycle saddle. Wearing proper clothing. In bicycling, this includes cycling shorts, with chamois padding. For equestrian activity, long, closely fitted pants such as equestrian breeches or jodhpurs minimize chafing. For western riding, closely fitted jeans with no heavy inner seam, sometimes combined with chaps, are preferred. Padded cycling shorts worn under riding pants helps some equestrians, and extra padding, particularly sheepskin, on the seat of the saddle may help in more difficult situations such as long-distance endurance riding. Using petroleum jelly, chamois cream or lubricating gel to further reduce friction.If left untreated over an extended period of time, saddle sores may need to be drained by a physician. | 0-1
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This effect can also be produced by prolonged ingestion of liquorice (which can be of potent strength in liquorice candy), by causing inhibition of the 11β-hydroxysteroid dehydrogenase enzyme and likewise leading to secondary apparent mineralocorticoid excess syndrome. Frequently, if liquorice is the cause of the high blood pressure, a low blood level of potassium will also be present. Cortisol induced hypertension cannot be completely explained by the activity of Cortisol on Aldosterone receptors. Experiments show that treatment with Spironolactone (an inhibitor of the aldosterone receptor), does not prevent hypertension with excess cortisol. It seems that inhibition of nitric oxide synthesis may also play a role in cortisol induced hypertension.Yet another related disorder causing hypertension is glucocorticoid remediable aldosteronism, which is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient, causing of primary hyperaldosteronism, the Gene mutated will result in an aldosterone synthase that is ACTH-sensitive, which is normally not. GRA appears to be the most common monogenic form of human hypertension.Compare these effects to those seen in Conns disease, an adrenocortical tumor which causes excess release of aldosterone, that leads to hypertension.Another adrenal related cause is Cushings syndrome which is a disorder caused by high levels of cortisol. Cortisol is a hormone secreted by the cortex of the adrenal glands. Cushings syndrome can be caused by taking glucocorticoid drugs, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH). | Antibiotic resistance is a growing problem with increasing rates of multiple drug-resistant tuberculosis (MDR-TB).In 2018, one quarter of the worlds population was thought to have a latent infection of TB. New infections occur in about 1% of the population each year. In 2020, an estimated 10 million people developed active TB, resulting in 1.5 million deaths, making it the second leading cause of death from an infectious disease after COVID-19. As of 2018, most TB cases occurred in the regions of South-East Asia (44%), Africa (24%), and the Western Pacific (18%), with more than 50% of cases being diagnosed in seven countries: India (27%), China (9%), Indonesia (8%), the Philippines (6%), Pakistan (6%), Nigeria (4%), and Bangladesh (4%). By 2021 the number of new cases each year was decreasing by around 2% annually. About 80% of people in many Asian and African countries test positive while 5–10% of people in the United States population test positive via the tuberculin test. Tuberculosis has been present in humans since ancient times. Signs and symptoms
Tuberculosis may infect any part of the body, but most commonly occurs in the lungs (known as pulmonary tuberculosis). Extrapulmonary TB occurs when tuberculosis develops outside of the lungs, although extrapulmonary TB may coexist with pulmonary TB.General signs and symptoms include fever, chills, night sweats, loss of appetite, weight loss, and fatigue. Significant nail clubbing may also occur. Pulmonary
If a tuberculosis infection does become active, it most commonly involves the lungs (in about 90% of cases). | 0-1
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Extra-pulmonary infection is due to migration of the young worms away from the normal route to the lungs. In such case, any other part of the body can be infected. Cutaneous paragonimiasis is common in children and is generally indicated by skin nodules that move from one place to another. Cerebral paragonimias is most severe extra-pulmonary symptoms that affect the brain and leads to seizure, headache, visual disturbance, and motor and sensory disturbances.The acute phase (invasion and migration) may be marked by diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities, and eosinophilia. During the chronic phase, pulmonary manifestations include cough, expectoration of discolored sputum containing clumps of eggs, hemoptysis, and chest radiographic abnormalities. Extrapulmonary locations of the adult worms result in more severe manifestations, especially when the brain is involved. Diagnosis is based on microscopic demonstration of eggs in stool or sputum, but these are not present until 2 to 3 months after infection. (Eggs are also occasionally encountered in effusion fluid or biopsy material.) Concentration techniques may be necessary in patients with light infections. Biopsy may allow diagnostic confirmation and species identification when an adult or developing fluke is recovered.Diagnosis is done by microscopic examination of sputum and stool samples, and presence of the eggs is a confirmation. However, eggs are not always to be found. In such case, serological tests based on antibody detection using ELISA is a better method. A more arduous method like immunoblotting is also used. | Saccharopinuria (an excess of saccharopine in the urine), also called saccharopinemia, saccharopine dehydrogenase deficiency or alpha-aminoadipic semialdehyde synthase deficiency, is a variant form of hyperlysinemia. It is caused by a partial deficiency of the enzyme saccharopine dehydrogenase, which plays a secondary role in the lysine metabolic pathway. Inheritance is thought to be autosomal recessive, but this cannot be established as individuals affected by saccharopinuria typically have only a 40% reduction in functional enzyme. See also
Hyperlysinemia
References
External links
Saccharopinuria; Alpha-aminoadipic semialdehyde synthase deficiency at NIHs Office of Rare Diseases | 0-1
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The main concern about smoking and breastfeeding is that infants may have smoking-induced reductions to the milk iodine content. Smoking can adversely affect the lactation process by decreasing milk production and altering the milk composition. Smoking reduces daily milk output by roughly 250–300 mL. Not only will this be problematic on a daily basis for not producing enough milk, it will also cause the mother to wean her baby early. The altered milk composition also caused infants to exhibit daily behaviors such as colic and crying which can promote early weaning, again something that is not beneficial to the infant.Also, the nicotine obtained from smoking travels through a woman into her breast milk, thus giving nicotine to her child.Heavy use of cigarettes by the mother (more than 20 per day) has been shown to reduce the mothers milk supply and cause vomiting, diarrhoea, rapid heart rate, and restlessness in breastfed infants. Sudden Infant Death Syndrome (SIDS) is more common in babies exposed to a smoky environment. Breastfeeding mothers who smoke are counseled not to do so during or immediately before feeding their child, and are encouraged to seek advice to help them reduce their nicotine intake or quit. Other substance abuse
With respect to alcohol, the American Academy of Pediatrics states that when breastfeeding, "moderation is definitely advised" and recommends waiting for 2 hours after drinking before nursing or pumping. | Nevertheless, Marsh I is considered compatible with celiac disease and the most frequent cause of these findings, especially in people positive for HLA DQ2 and/or DQ8 haplotypes, is celiac disease, with a prevalence of 16-43%.In people with duodenal lymphocytosis – following guidelines from the European Society of Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) – a high count of celiac disease cells (or CD/CD3 ratio) in immunohistochemical assessment of biopsies, or the presence of IgA anti-TG2 and/or anti-endomysial intestinal deposits, might be specific markers for celiac disease. Catassi and Fasano proposed in 2010 that in patients without celiac disease antibodies, either lymphocytic infiltration associated with IgA subepithelial deposits or a histological response to a gluten-free diet, could support a diagnosis of celiac disease. Wheat allergy
The clinical presentation may be sufficient in most cases to distinguish a wheat allergy from other entities. It is excluded when there are normal levels of serum IgE antibodies to gluten proteins and wheat fractions, and no skin reaction to prick tests for wheat allergy. Nevertheless, these tests are not always completely reliable.If an allergic reaction can not be clearly identified, the diagnosis should be confirmed by food provocation tests, ideally performed in a double-blinded and placebo-controlled manner. Delayed allergic reactions may occur with these type of tests, which have to be negative over time, but there are no international consensus statements on diagnosing delayed wheat/food-related symptoms. Usually, reactions that appear between two hours and five days after the oral challenge are considered delayed. | 0-1
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In psychology, impulsivity (or impulsiveness) is a tendency to act on a whim, displaying behavior characterized by little or no forethought, reflection, or consideration of the consequences. Impulsive actions are typically "poorly conceived, prematurely expressed, unduly risky, or inappropriate to the situation that often result in undesirable consequences," which imperil long-term goals and strategies for success. Impulsivity can be classified as a multifactorial construct. A functional variety of impulsivity has also been suggested, which involves action without much forethought in appropriate situations that can and does result in desirable consequences. "When such actions have positive outcomes, they tend not to be seen as signs of impulsivity, but as indicators of boldness, quickness, spontaneity, courageousness, or unconventionality" Thus, the construct of impulsivity includes at least two independent components: first, acting without an appropriate amount of deliberation, which may or may not be functional; and second, choosing short-term gains over long-term ones.Impulsivity is both a facet of personality and a major component of various disorders, including FASD, ADHD, substance use disorders, bipolar disorder, antisocial personality disorder, and borderline personality disorder. Abnormal patterns of impulsivity have also been noted instances of acquired brain injury and neurodegenerative diseases. Neurobiological findings suggest that there are specific brain regions involved in impulsive behavior, although different brain networks may contribute to different manifestations of impulsivity, and that genetics may play a role.Many actions contain both impulsive and compulsive features, but impulsivity and compulsivity are functionally distinct. | While the majority of these cases are associated with appendiceal carcinomas, other conditions may also be found, including disseminated peritoneal adenomucinosis (DPAM), peritoneal carcinomas, several mucinous tumors (mucinous adenocarcinoma, mucinous cystadenoma, and mucinous cystadenocarcinoma), as well as other disease states. Other primary sites that have been reported include colon, rectum, stomach, gallbladder, bile ducts, small intestine, urinary bladder, lung, breast, fallopian tubes, and the pancreas. Diagnosis
This disease is often discovered during surgery for other conditions, e.g., hernia repair, following which an experienced pathologist can confirm the diagnosis. Advanced stages may present as tumors palpable on the abdomen or distention of the belly ("jelly belly" is sometimes used as a slang term for the condition). Due to the rarity of this disease, it is important to obtain an accurate diagnosis so that appropriate treatment may be obtained from a Gastro intestinal cancer surgeon. Diagnostic tests may include CT scans, examination of tissue samples obtained through laparoscopy, and the evaluation of tumor markers. In most cases a colonoscopy is unsuitable as a diagnostic tool because in most cases appendix cancer invades the abdominal cavity but not the colon (however, spread inside the colon is occasionally reported). PET scans may be used to evaluate high-grade mucinous adenocarcinoma, but this test is not reliable for detecting low-grade tumors because those do not take up the dye which shows up on scans. New MRI procedures are being developed for disease monitoring, but standard MRIs are not typically used as a diagnostic tool. Diagnosis is confirmed through pathology. | 0-1
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Late gadolinium enhancement shows increased signal of the midwall at the inferolateral wall of the base of the left ventricle, usually in the non-hypertrophic ventricle. T1-weighted imaging can show low T1 signal due to sphingolipid storage in the heart even without ventricular hypertrophy in 40% of the those affected by the disease. Thus, MRI is a useful way of diagnosing the disease early. T2 signal is increased in inflammation and oedema. Treatment
The treatments available for Fabry disease can be divided into therapies that aim to correct the underlying problem of decreased activity of the alpha galactosidase A enzyme and thereby reduce the risk of organ damage, and therapies to improve symptoms and life expectancy once organ damage has already occurred. Therapies targeting enzyme activity
Enzyme replacement therapy is designed to provide the enzyme the patient is missing as a result of a genetic malfunction. This treatment is not a cure, but can partially prevent disease progression, and potentially reverse some symptoms. As of March 2022, two medical drugs based on enzyme replacement therapy are available for Fabry disease:
Agalsidase alfa, sold under the brand name Replagal by the company Takeda (since its acquisition of the company Shire), is a recombinant form of alpha-galactosidase A It received approval in the EU in 2001. FDA approval was applied for the United States. However, Shire withdrew their application for approval in the United States in 2012, citing that the agency will require additional clinical trials before approval. As of March 2022, Replagal has not received FDA approval. | Skin
Angiokeratomas (tiny, painless papules that can appear on any region of the body, but are predominant on the thighs, around the navel, buttocks, lower abdomen, and groin) are common.Anhidrosis (lack of sweating) is a common symptom, and less commonly hyperhidrosis (excessive sweating).Additionally, patients can exhibit Raynauds disease-like symptoms with neuropathy (in particular, burning extremity pain).Ocular involvement may be present showing cornea verticillata (also known as vortex keratopathy), i.e. clouding of the corneas. Keratopathy may be the presenting feature in asymptomatic patients, and must be differentiated from other causes of vortex keratopathy (e.g. drug deposition in the cornea). This clouding does not affect vision.Other ocular findings can include conjunctival and retinal vascular abnormalities and anterior/posterior spoke-like cataract. Visual reduction from these manifestations is uncommon. Other manifestations
Fatigue, neuropathy (in particular, burning extremity pain, red hands and feet on and off), cerebrovascular effects leading to an increased risk of stroke - early strokes, mostly vertebrobasilar system tinnitus (ringing in the ears), vertigo, nausea, inability to gain weight, chemical imbalances, and diarrhea are other common symptoms. Causes
Fabry disease is caused by a DNA sequence (gene) that is not functioning as it should. A person who inherits this gene does not have enough of a functioning enzyme known as alpha-galactosidase A. The lack of alpha-galactosidase leads to Fabry disease. A deficiency of alpha galactosidase A (a-GAL A, encoded by GLA) due to mutation causes a glycolipid known as globotriaosylceramide (abbreviated as Gb3, GL-3, or ceramide trihexoside) to accumulate within the blood vessels, other tissues, and organs. | 11
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Therefore, current guidelines for patients on mechanical ventilation in intensive care recommends keeping oxygen concentration less than 60%. Likewise, divers who undergo treatment of decompression sickness are at increased risk of oxygen toxicity as treatment entails exposure to long periods of oxygen breathing under hyperbaric conditions, in addition to any oxygen exposure during the dive. Ocular toxicity
Prolonged exposure to high inspired fractions of oxygen causes damage to the retina. Damage to the developing eye of infants exposed to high oxygen fraction at normal pressure has a different mechanism and effect from the eye damage experienced by adult divers under hyperbaric conditions. Hyperoxia may be a contributing factor for the disorder called retrolental fibroplasia or retinopathy of prematurity (ROP) in infants. In preterm infants, the retina is often not fully vascularised. Retinopathy of prematurity occurs when the development of the retinal vasculature is arrested and then proceeds abnormally. Associated with the growth of these new vessels is fibrous tissue (scar tissue) that may contract to cause retinal detachment. Supplemental oxygen exposure, while a risk factor, is not the main risk factor for development of this disease. Restricting supplemental oxygen use does not necessarily reduce the rate of retinopathy of prematurity, and may raise the risk of hypoxia-related systemic complications.Hyperoxic myopia has occurred in closed circuit oxygen rebreather divers with prolonged exposures. It also occurs frequently in those undergoing repeated hyperbaric oxygen therapy. | Central nervous system toxicity may be referred to as the "Paul Bert effect".Pulmonary oxygen toxicity was first described by J. Lorrain Smith in 1899 when he noted central nervous system toxicity and discovered in experiments in mice and birds that 0.43 bar (43 kPa) had no effect but 0.75 bar (75 kPa) of oxygen was a pulmonary irritant. Pulmonary toxicity may be referred to as the "Lorrain Smith effect". The first recorded human exposure was undertaken in 1910 by Bornstein when two men breathed oxygen at 2.8 bar (280 kPa) for 30 minutes, while he went on to 48 minutes with no symptoms. In 1912, Bornstein developed cramps in his hands and legs while breathing oxygen at 2.8 bar (280 kPa) for 51 minutes. Smith then went on to show that intermittent exposure to a breathing gas with less oxygen permitted the lungs to recover and delayed the onset of pulmonary toxicity.Albert R. Behnke et al. in 1935 were the first to observe visual field contraction (tunnel vision) on dives between 1.0 bar (100 kPa) and 4.1 bar (410 kPa). During World War II, Donald and Yarbrough et al. performed over 2,000 experiments on oxygen toxicity to support the initial use of closed circuit oxygen rebreathers. Naval divers in the early years of oxygen rebreather diving developed a mythology about a monster called "Oxygen Pete", who lurked in the bottom of the Admiralty Experimental Diving Unit "wet pot" (a water-filled hyperbaric chamber) to catch unwary divers. | 11
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Avoiding rabeprazole during breastfeeding confers to lowest possible risk. Geriatrics
Advanced age does not appear to clinically impact rabeprazoles metabolism. However, elevations in the maximum plasma concentration and the total drug exposure (area under the curve, AUC) have occurred. Japanese ancestry
In a study on rabeprazoles pharmacokinetics, the AUC was elevated by approximately 50–60% in men of Japanese ancestry compared to men in the United States. See the pharmacogenetics section below for a pharmacogenetic explanation of these findings. Kidney or liver problems
In people that have kidney or liver problems, these problems do not appear to affect rabeprazoles metabolism in a clinically meaningful way. This includes individuals on dialysis for kidney problems. Severe liver problems like cirrhosis of the liver do affect rabeprazoles elimination half-life, but not to a degree of dangerous accumulation. In a review of patients taking rabeprazole while having end-stage kidney disease and mild-to-moderate severity, chronic compensated cirrhosis of the liver, the alteration in rabeprazoles metabolism was not clinically meaningful. Contraindications
Rabeprazole is contraindicated in the following populations and situations:
people with a known hypersensitivity to rabeprazole, substituted benzimidazoles (which are chemically similar to rabeprazole, like omeprazole), or any other component of the capsule formulation (e.g. certain dyes)
concurrent use of rilpivirine, a medication used to treat HIV infection
Hypersensitivity
Syndrome
An allergy to a PPI like rabeprazole may take the form of type I hypersensitivity or delayed hypersensitivity reactions. A selective (pattern C—see below for a discussion of cross-reactivity patterns) type I hypersensitivity reaction to rabeprazole resulting in anaphylaxis has been reported, as well as several whole group hypersentivities. | Rare instances of rabeprazole-induced liver injury (also known as hepatotoxicity) have been reported. Characteristic proton-pump inhibitor hepatoxicity usually occurs within the first four weeks of starting the medication.Rabeprazole is associated with elevated serum gastrin levels, which are thought to be dependent upon the degree of CYP2C19 metabolism the drug undergoes. In comparison, rabeprazole is not as significantly metabolized by this enzyme compared to other medications in the same class, like omeprazole. Elevated serum gastrin may be associated with gastric cancer.Acid suppression via rabeprazole can decrease the absorption of vitamin B12 and magnesium, leading to deficiency.Very serious side effects have been reported in people taking rabeprazole, but these effects have not been "correlated directly" with the use of rabeprazole. These include Stevens–Johnson syndrome, serious hematological abnormalities, coma, and death. Other possible side effects, common to other PPIs medications in the same class, include bone fractures due to osteoporosis and serious infections with Clostridium difficile. Overdose
No signs and symptoms have been reported in overdoses of rabeprazole up to 80 mg, but case examples are limited. Notably, rabeprazole has been used in higher doses for the treatment of hypersecretory conditions like Zollinger-Ellison syndrome (up to 120 mg daily).Animal experiments with ultra-high doses of rabeprazole have demonstrated lethality through unknown mechanisms. The lethal overdose syndrome in animals is characterized by convulsion and coma. Interactions
Drug-drug interactions
Rabeprazole does not interfere with the plasma concentration of drugs that are also metabolized by the same enzymes (i.e. CYP2C19) that it is metabolized by. | 11
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Posterior urethral valve (PUV) disorder is an obstructive developmental anomaly in the urethra and genitourinary system of male newborns. A posterior urethral valve is an obstructing membrane in the posterior male urethra as a result of abnormal in utero development. It is the most common cause of bladder outlet obstruction in male newborns. The disorder varies in degree, with mild cases presenting late due to milder symptoms. More severe cases can have renal and respiratory failure from lung underdevelopment as result of low amniotic fluid volumes, requiring intensive care and close monitoring. It occurs in about one in 8,000 babies. Presentation
PUV can be diagnosed before birth, or even at birth when the ultrasound shows that the male baby has a hydronephrosis. Some babies may also have oligohydramnios due to the urinary obstruction. The later presentation can be a urinary tract infection, diurnal enuresis, or voiding pain. Complications
Incontinence
Urinary tract infection
Renal failure
Vesicoureteral reflux
Chronic kidney disease
Oligohydramnios
Diagnosis
Abdominal ultrasound is of some benefit, but not diagnostic. Features that suggest posterior urethral valves are bilateral hydronephrosis, a thickened bladder wall with thickened smooth muscle trabeculations, and bladder diverticula.Voiding cystourethrogram (VCUG) is more specific for the diagnosis. Normal plicae circularis are variable in appearance and often not seen on normal VCUGs. PUV on voiding cystourethrogram is characterized by an abrupt tapering of urethral caliber near the verumontanum, with the specific level depending on the developmental variant. Vesicoureteral reflux is also seen in over 50% of cases. Very often the posterior urethra maybe dilated thus making the abrupt narrowing more obvious. | Pityriasis lichenoides is a form of pityriasis. Types include:
Pityriasis lichenoides et varioliformis acuta
Pityriasis lichenoides chronica
References
External links
DermNet scaly/pityriasis-lichenoides | 0-1
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Because of this, measurements of these hormones are not considered to be reliable guides to a womans exact menopausal status.Menopause occurs because of the sharp decrease of estradiol and progesterone production by the ovaries. After menopause, estrogen continues to be produced mostly by aromatase in fat tissues and is produced in small amounts in many other tissues such as ovaries, bone, blood vessels, and the brain where it acts locally. The substantial fall in circulating estradiol levels at menopause impacts many tissues, from brain to skin. In contrast to the sudden fall in estradiol during menopause, the levels of total and free testosterone, as well as dehydroepiandrosterone sulfate (DHEAS) and androstenedione appear to decline more or less steadily with age. An effect of natural menopause on circulating androgen levels has not been observed. Thus specific tissue effects of natural menopause cannot be attributed to loss of androgenic hormone production.Hot flashes and other vasomotor and body symptoms accompanying the menopausal transition are associated with estrogen insufficiency and changes that occur in the brain, primarily the hypothalamus and involve complex interplay between the neurotransmitters kisspeptin, neurokinin 3B (NK3B) and dynorphin, which are found in ‘KNDy’ neurons in the infundibular nucleus.Long-term effects of menopause may include osteoporosis, vaginal atrophy as well as changed metabolic profile resulting in increased cardiac and metabolic disease (diabetes) risks. Ovarian aging
Decreased inhibin feedback after hysterectomy is hypothesized to contribute to increased ovarian stimulation and earlier menopause. Hastened ovarian aging has been observed after endometrial ablation. | Brolucizumab (sold, depending on part of the world, under trade names Beovu or Vsiqq), is a humanized single-chain antibody fragment for the treatment of neovascular (wet) age-related macular degeneration (AMD).The most common side effects are reduced visual acuity, cataract (clouding of the lens in the eye), conjunctival haemorrhage (bleeding at the front of the eye) and vitreous floaters (spots in the vision). The most serious side effects are blindness, endophthalmitis (an infection inside the eye), retinal artery occlusion (blockage of the artery in the retina) and retinal detachment (separation of the retina from the back of the eye).Brolucizumab was designed to attach to and block a substance called vascular endothelial growth factor A (VEGF-A). VEGF-A is a protein that makes blood vessels grow and leak fluid and blood, damaging the macula. By blocking VEGF-A, brolucizumab reduces the growth of the blood vessels and controls the leakage and swelling. History
This drug was developed by ESBATech (discovery to phase 2a), Alcon Laboratories (phase 2b), and Novartis (phase 3).Brolucizumab is U.S. Food and Drug Administration (FDA) approved in ophthalmology as Beovu.Brolucizumab successfully completed phase III development in wet age-related macular degeneration (AMD) meeting the primary efficacy endpoint of non-inferiority to aflibercept in mean change in best corrected visual acuity (BCVA) from baseline to week 48. | 0-1
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Diagnosis
DSM-5 diagnosis
The current DSM-5 criteria for Intermittent Explosive Disorder include:
Recurrent outbursts that demonstrate an inability to control impulses, including either of the following:
Verbal aggression (tantrums, verbal arguments, or fights) or physical aggression that occurs twice in a week-long period for at least three months and does not lead to the destruction of property or physical injury (Criterion A1)
Three outbursts that involve injury or destruction within a year-long period (Criterion A2)
Aggressive behavior is grossly disproportionate to the magnitude of the psychosocial stressors (Criterion B)
The outbursts are not premeditated and serve no premeditated purpose (Criterion C)
The outbursts cause distress or impairment of functioning or lead to financial or legal consequences (Criterion D)
The individual must be at least six years old (Criterion E)
The recurrent outbursts cannot be explained by another mental disorder and are not the result of another medical disorder or substance use (Criterion F)It is important to note that DSM-5 now includes two separate criteria for types of aggressive outbursts (A1 and A2) which have empirical support:
Criterion A1: Episodes of verbal and/or non-damaging, nondestructive, or non-injurious physical assault that occur, on average, twice weekly for three months. These could include temper tantrums, tirades, verbal arguments/fights, or assault without damage. This criterion includes high frequency/low-intensity outbursts. Criterion A2: More severe destructive/assaultive episodes which are more infrequent and occur, on average, three times within a twelve-month period. These could be destroying an object without regard to value, assaulting an animal or individual. This criterion includes high-intensity/low-frequency outbursts. | Among a clinical population, a 2005 study found the lifetime prevalence of IED to be 6.3%.Prevalence appears to be higher in men than in women.Of US subjects with IED, 67.8% had engaged in direct interpersonal aggression, 20.9% in threatened interpersonal aggression, and 11.4% in aggression against objects. Subjects reported engaging in 27.8 high-severity aggressive acts during their worst year, with 2–3 outbursts requiring medical attention. Across the lifespan, the mean value of property damage due to aggressive outbursts was $1603.A study in the March 2016 Journal of Clinical Psychiatry suggests a relationship between infection with the parasite Toxoplasma gondii and psychiatric aggression such as IED. History
In the first edition of the American Psychiatric Associations Diagnostic and Statistical Manual (DSM-I), a disorder of impulsive aggression was referred to as a passive-aggressive personality type (aggressive type). This construct was characterized by a "persistent reaction to frustration are "generally excitable, aggressive, and over-responsive to environmental pressures" with "gross outbursts of rage or of verbal or physical aggressiveness different from their usual behavior".In the third edition (DSM-III), this was for the first time codified as intermittent explosive disorder and assigned clinical disorder status under Axis I. However, some researchers saw the criteria as poorly operationalized. About 80% of individuals who would now be diagnosed with the disorder would have been excluded.In the DSM-IV, the criteria were improved but still lacked objective criteria for the intensity, frequency, and nature of aggressive acts to meet criteria for IED. | 11
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Two 1994 studies first confirmed a link between this type of Waardenburg syndrome and mutations in the MITF gene (now classed as type 2A), located on chromosome 3 at locus 3p14.1–p12.3.Type 2B was first established in 1994 when the same study which found mutations in MITF in patients with Waardenburg syndrome type 2 also found that some patients did not have any mutations in this region. A second 1994 study found a link to chromosome 1 in the locus 1p21–p13.3. This became known as type 2B of the condition (with the gene designated WS2B), however it has not been documented since, and the gene responsible remains unknown.Type 2C was established in 2001 when a study of an Italian family with Waardenburg syndrome type 2 features found that they were due to an unknown gene on chromosome 8 at locus 8q23 that had been broken by a chromosomal translocation. The study established a provisional name for the gene, WS2C. However, mutations in this region in Waardenburg syndrome patients have not been found since.Type 2D was established in 2002 when a study looking to find mutations in the human version of the SNAI2 gene, known to cause depigmentation in mice, found deletions of both copies of this gene in two unrelated individuals with Waardenburg syndrome type 2. | Type 2B is caused by an autosomal dominant mutation in an unknown gene on chromosome 1 in the locus range of 1p21–1p13.3. The gene has been provisionally termed WS2B. Type 2C is caused by an autosomal dominant mutation in an unknown gene on chromosome 8 in the locus of 8p23. The gene has been provisionally termed WS2C. Type 2D is caused by an autosomal recessive mutation in both copies of the gene SNAI2. The study that discovered this association found that SNAI2 is activated by MITF as part of neural crest development, and this explained why mutations in MITF cause Waardenburg syndrome, as it results in a lack of activation of SNAI2. Mutations in a single copy of SNAI2 have also been found to cause patches of hair depigmentation (piebaldism) without any other symptoms. Type 2E is caused by an autosomal dominant mutation in the gene SOX10. Rarely, a mutation in a gene other than those currently known may be responsible for a Waardenburg syndrome with features of type 2. This is usually initially classified as simply type 2 but may be given its own subtype once a gene or locus is identified and established. Type 3 is caused by a mutation in the gene PAX3, the same gene as in type 1. | 11
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Medical science and cryobiologists generally regards cryonics with skepticism. Life extension
Life extension refers to an increase in maximum or average lifespan, especially in humans, by slowing down or reversing the processes of aging through anti-aging measures. Despite the fact that aging is by far the most common cause of death worldwide, it is socially mostly ignored as such and seen as "necessary" and "inevitable" anyway, which is why little money is spent on research into anti-aging therapies, a phenomenon known as the pro-aging trance.Average lifespan is determined by vulnerability to accidents and age or lifestyle-related afflictions such as cancer, or cardiovascular disease. Extension of average lifespan can be achieved by good diet, exercise and avoidance of hazards such as smoking. Maximum lifespan is also determined by the rate of aging for a species inherent in its genes. Currently, the only widely recognized method of extending maximum lifespan is calorie restriction. Theoretically, extension of maximum lifespan can be achieved by reducing the rate of aging damage, by periodic replacement of damaged tissues, or by molecular repair or rejuvenation of deteriorated cells and tissues. A United States poll found that religious people and irreligious people, as well as men and women and people of different economic classes have similar rates of support for life extension, while Africans and Hispanics have higher rates of support than white people. 38 percent of the polled said they would desire to have their aging process cured. Researchers of life extension are a subclass of biogerontologists known as "biomedical gerontologists". | Philosopher Galen Strawson writes that the death that many people wish for is an instant, painless, unexperienced annihilation. In this unlikely scenario, the person dies without realizing it and without being able to fear it. One moment the person is walking, eating, or sleeping, and the next moment, the person is dead. Strawson reasons that this type of death would not take anything away from the person, as he believes that a person cannot have a legitimate claim to ownership in the future. Society and culture
In society, the nature of death and humanitys awareness of its own mortality has for millennia been a concern of the worlds religious traditions and of philosophical inquiry. This includes belief in resurrection or an afterlife (associated with Abrahamic religions), reincarnation or rebirth (associated with Dharmic religions), or that consciousness permanently ceases to exist, known as eternal oblivion (associated with Secular humanism).Commemoration ceremonies after death may include various mourning, funeral practices and ceremonies of honouring the deceased. The physical remains of a person, commonly known as a corpse or body, are usually interred whole or cremated, though among the worlds cultures there are a variety of other methods of mortuary disposal. In the English language, blessings directed towards a dead person include rest in peace (originally the Latin requiescat in pace), or its initialism RIP. Death is the center of many traditions and organizations; customs relating to death are a feature of every culture around the world. | 11
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In herpetic gingivostomatitis, lesions can be found in these locations, but they are almost always accompanied by ulcerations on the gums, lips, tongue or buccal mucosa and/or by hyperemia, hypertrophy or hemorrhage of the gums. Hand Foot and Mouth Disease: Similar to herpangina, hand foot and mouth disease occurs predominantly in children. It is caused by Coxsackie A and B virus, and lesions or blisters are found bilaterally on the hands, feet and mouth of the patient. Oral candidiasis: Also known as thrush, herpetic gingivostomatitis can often be differentiated from these microorganism/bacterial causing white plaques on the palate, buccal mucosa, tongue, oropharynx etc. Apthous stomatitis: They are commonly known as apthous ulcers, and are characterized by grey membranes and peripheral erythema. Lesions/ulcers for herpetic gingivostomatitis may also be found on the palate and keratinzied gingivae hence aphthous ulcers can be ruled out. Stevens–Johnson syndrome: Stevens–Johnson syndrome is characterized by early symptoms of malaise and fever, and shortly after that erythema, purpura and plaques on the skin, which often progresses to epidermal necrosis and sloughing in extreme cases. Infectious mononucleosis - Infectious Mononucleosis presents with a high fever and lymphadenopathy, which is may or may not be presented in the symptoms of herpetic gingivostomatitis. However, upon closer oral examination, ulceration, petechiae and occasional gingivostomatitis may be spotted. Behcets syndrome - It is an inflammatory disorder in which the presenting symptoms are recurrent aphthous ulcers, and severe cases may result in the patient having genital lesions, gastro-intestinal problems, and even arthritis. | Hidradenoma refers to a benign adnexal tumor of the apical sweat gland. These are 1–3 cm translucent blue cystic nodules. It usually presents as a single, small skin-colored lesion, and may be considered closely related to or a variant of poromas. Hidradenomas are often sub-classified based on subtle histologic differences, for example:
Eccrine acrospiroma
Clear-cell hidradenoma or acrospiroma
Nodular hidradenoma or acrospiroma
Solid-cystic hidradenomaDiscussion of sweat gland tumors can be difficult and confusing due to the complex classification and redundant terminology used to describe the same tumors. For example, acrospiroma and hidradenoma are synonymous, and sometimes the term acrospiroma is used to generally describe benign sweat gland tumors. In addition, a single lesion may contain a mixture of cell-types. There has also been a change in understanding about how tumors that were previously believed to strictly derive from specific sweat gland types may, in fact, derive from both eccrine or apocrine glands.Hidradenomas are by definition benign, with malignant transformation very rare. When tumors show malignant characteristics, they are known as hidradenocarcinoma. Surgical excision is usually curative and local recurrences are rare, although malignant tumors may metastasize. See also
Spiroma
List of cutaneous conditions
List of cutaneous neoplasms associated with systemic syndromes
References
== External links == | 0-1
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Population
Hyperglycemia is one of the main symptoms of diabetes and it has substantially affected the population making it an epidemic due to the populations increased calorie consumption. Healthcare providers are trying to work more closely with people allowing them more freedom with interventions that suit their lifestyle. As physical inactivity and calorie consumption increases it makes individuals more susceptible to developing hyperglycemia. Hyperglycemia is caused by type 1 diabetes and non-whites have a higher susceptibility for it. Etymology
The origin of the term is Greek: prefix ὑπέρ- hyper- "over-", γλυκός glycos "sweet wine, must", αἷμα haima "blood", -ία, -εια -ia suffix for abstract nouns of feminine gender. See also
Prediabetes
Reference ranges for blood tests
References
External links
Hyperglycemia in infants – from MedlinePlus | In severe cases of thiamine deficiency, a few of the positive symptoms (including neuropathic pain) may persist indefinitely. Even after the restoration of a balanced nutritional intake, those patients with severe or chronic polyneuropathy may experience lifelong residual symptoms. Epidemiology
In 2020 the NIH quoted an estimate that in the United States 25% to 66% of chronic alcohol users experience some form of neuropathy. The rate of incidence of alcoholic polyneuropathy involving sensory and motor polyneuropathy has been stated as from 10% to 50% of alcoholics depending on the subject selection and diagnostic criteria. If electrodiagnostic criteria are used, alcoholic polyneuropathy may be found in up to 90% of individuals being assessed.The distribution and severity of the disease depends on regional dietary habits, individual drinking habits, as well as an individuals genetics. Large studies have been conducted and show that alcoholic polyneuropathy severity and incidence correlates best with the total lifetime consumption of alcohol. Factors such as nutritional intake, age, or other medical conditions are correlate in lesser degrees. For unknown reasons, alcoholic polyneuropathy has a high incidence in women.Certain alcoholic beverages can also contain congeners that may also be bioactive; therefore, the consumption of varying alcohol beverages may result in different health consequences. An individuals nutritional intake also plays a role in the development of this disease. | 0-1
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Alcohol use was associated with an increased probability of later use of tobacco and illegal drugs such as cannabis. Availability
Alcohol is the most available, widely consumed, and widely misused recreational drug. Beer alone is the worlds most widely consumed alcoholic beverage; it is the third-most popular drink overall, after water and tea. It is thought by some to be the oldest fermented beverage. Gender difference
Based on combined data in the US from SAMHSAs 2004–2005 National Surveys on Drug Use & Health, the rate of past-year alcohol dependence or misuse among persons aged 12 or older varied by level of alcohol use: 44.7% of past month heavy drinkers, 18.5% binge drinkers, 3.8% past month non-binge drinkers, and 1.3% of those who did not drink alcohol in the past month met the criteria for alcohol dependence or misuse in the past year. Males had higher rates than females for all measures of drinking in the past month: any alcohol use (57.5% vs. 45%), binge drinking (30.8% vs. 15.1%), and heavy alcohol use (10.5% vs. 3.3%), and males were twice as likely as females to have met the criteria for alcohol dependence or misuse in the past year (10.5% vs. 5.1%). Genetic variation
There are genetic variations that affect the risk for alcoholism. Some of these variations are more common in individuals with ancestry from certain areas, for example Africa, East Asia, the Middle East and Europe. The variants with strongest effect are in genes that encode the main enzymes of alcohol metabolism, ADH1B and ALDH2. | DNA damage
Alcohol-induced DNA damage, when not properly repaired, may have a key role in the neurotoxicity induced by alcohol. Metabolic conversion of ethanol to acetaldehyde can occur in the brain and the neurotoxic effects of ethanol appear to be associated with acetaldehyde induced DNA damages including DNA adducts and crosslinks. In addition to acetaldehyde, alcohol metabolism produces potentially genotoxic reactive oxygen species, which have been demonstrated to cause oxidative DNA damage. Diagnosis
Definition
Misuse, problem use, abuse, and heavy use of alcohol refer to improper use of alcohol, which may cause physical, social, or moral harm to the drinker. The Dietary Guidelines for Americans defines "moderate use" as no more than two alcoholic beverages a day for men and no more than one alcoholic beverage a day for women. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines binge drinking as the amount of alcohol leading to a blood alcohol content (BAC) of 0.08, which, for most adults, would be reached by consuming five drinks for men or four for women over a two-hour period. According to the NIAAA, men may be at risk for alcohol-related problems if their alcohol consumption exceeds 14 standard drinks per week or 4 drinks per day, and women may be at risk if they have more than 7 standard drinks per week or 3 drinks per day. It defines a standard drink as one 12-ounce bottle of beer, one 5-ounce glass of wine, or 1.5 ounces of distilled spirits. | 11
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Although the majority of compounds screened were of synthetic origin, one chemist, Jonathan Hartwell, who was employed there from 1958 onwards, had experience with natural product derived compounds, and began a plant screening operation. After some years of informal arrangements, in July 1960, the NCI commissioned the United States Department of Agriculture (USDA) botanists to collect samples from about 1,000 plant species per year. On 21 August 1962, one of those botanists, Arthur S. Barclay, collected bark from a single Pacific yew tree in a forest north of the town of Packwood, Washington, as part of a four-month trip to collect material from over 200 different species. The material was then processed by a number of specialist CCNSC subcontractors, and one of the trees samples was found to be cytotoxic in a cellular assay on 22 May 1964.Accordingly, in late 1964 or early 1965, the fractionation and isolation laboratory run by Monroe E. Wall in Research Triangle Park, North Carolina, began work on fresh Taxus samples, isolating the active ingredient in September 1966 and announcing their findings at an April 1967 American Chemical Society meeting in Miami Beach. They named the pure compound taxol in June 1967. Wall and his colleague Wani published their results, including the chemical structure, in 1971.The NCI continued to commission work to collect more Taxus bark and to isolate increasing quantities of taxol. | In the U.S., it is a Schedule II Narcotic controlled substance with a DEA ACSCN of 9220 and 2013 annual aggregate manufacturing quota of 4.5 kilos. The salts in use are the tartrate (free base conversion ratio 0.58) and hydrobromide (0.76). See also
Cough syrup
Racemorphan; Dextrorphan;
Noscapine
Codeine; Pholcodine
Dextromethorphan; Dimemorfan
Butamirate
Pentoxyverine
Tipepidine
Cloperastine; Levocloperastine
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Mucositis is the painful inflammation and ulceration of the mucous membranes lining the digestive tract, usually as an adverse effect of chemotherapy and radiotherapy treatment for cancer. Mucositis can occur anywhere along the gastrointestinal (GI) tract, but oral mucositis refers to the particular inflammation and ulceration that occurs in the mouth. Oral mucositis is a common and often debilitating complication of cancer treatment.Oral and gastrointestinal (GI) mucositis affects almost all patients undergoing high-dose chemotherapy and hematopoietic stem cell transplantation (HSCT), 80% of patients with malignancies of the head and neck receiving radiotherapy, and a wide range of patients receiving chemotherapy. Alimentary tract mucositis increases mortality and morbidity and contributes to rising health care costs.For most cancer treatment, about 5–15% of patients get mucositis. However, with 5-fluorouracil (5-FU), up to 40% get mucositis, and 10–15% get grade 3–4 oral mucositis. Irinotecan is associated with severe GI mucositis in over 20% of patients. Seventy-five to eighty percent of bone marrow transplantation recipients experience mucositis, of which oral mucositis is the most common and most debilitating, especially when melphalan is used. In grade 3 oral mucositis, the patient is unable to eat solid food, and in grade 4, the patient is unable to consume liquids as well.Radiotherapy to the head and neck or to the pelvis or abdomen is associated with Grade 3 and Grade 4 oral or GI mucositis, respectively, often exceeding 50% of patients. Among patients undergoing head and neck radiotherapy, pain and decreased oral function may persist long after the conclusion of therapy. | Pai syndrome, also known as Median cleft of the upper lip-corpus callosum lipoma-midline facial cutaneous polyps syndrome, is a very rare genetic disorder which is characterized by nervous system, cutaneous, ocular, nasal and bucal anomalies with facial dysmorphisms. Signs and symptoms
List of common symptoms:
Depressed nasal bridge
Median cleft lip
Central nervous system lipomas. Nasal polyposis
Presence of skin tags
Subcutaneous noduleList of not-so-common symptoms:[2]
Oral frenulum abnormalities
Bifid uvula
Hypertelorism
TelecanthusList of uncommon symptoms:[2]
Missing/underdeveloped corpus callosum
Down-slanting parpebral fissures
Encephalocele
Coloboma
Nose defects
Frontal bossing
High palate
Causes
A specific, shared genetic cause hasnt been found. The closest thing to it was a case reported by Masuno et al. of a Japanese girl with symptoms of the disorder plus short stature and intellectual disabilities with a spontaneous reciprocal translocation. This translocation involved chromosome Xq28 and chromosome 16q11.2 (more specifically, 46,X,t(X;16)(q28;q11.2). Epidemiology
According to OMIM, 18 cases have been described in medical literature, but according to ORPHAnet, 67 cases have been described. == References == | 0-1
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With this method, the long saphenous vein is preserved. Cryosurgery- A cryoprobe is passed down the long saphenous vein following saphenofemoral ligation. Then the probe is cooled with NO2 or CO2 to −85o F. The vein freezes to the probe and can be retrogradely stripped after 5 seconds of freezing. It is a variant of Stripping. The only point of this technique is to avoid a distal incision to remove the stripper. Sclerotherapy
A commonly performed non-surgical treatment for varicose and "spider leg veins" is sclerotherapy, in which medicine called a sclerosant is injected into the veins to make them shrink. The medicines that are commonly used as sclerosants are polidocanol (POL branded Asclera in the United States, Aethoxysklerol in Australia), sodium tetradecyl sulphate (STS), Sclerodex (Canada), Hypertonic Saline, Glycerin and Chromated Glycerin. STS (branded Fibrovein in Australia) liquids can be mixed at varying concentrations of sclerosant and varying sclerosant/gas proportions, with air or CO2 or O2 to create foams. Foams may allow more veins to be treated per session with comparable efficacy. Their use in contrast to liquid sclerosant is still somewhat controversial and there is no clear evidence that foam are superior. Sclerotherapy has been used in the treatment of varicose veins for over 150 years. Sclerotherapy is often used for telangiectasias (spider veins) and varicose veins that persist or recur after vein stripping. | Chlorzoxazone (INN) is a centrally acting muscle relaxant used to treat muscle spasm and the resulting pain or discomfort. It can also be administered for acute pain in general and for tension headache (muscle contraction headache). It acts on the spinal cord by depressing reflexes. It is sold under the brand names Lorzone, Paraflex and Muscol and in combination form as Parafon Forte, a combination of chlorzoxazone and acetaminophen (paracetamol). Possible side effects include dizziness, lightheadedness, malaise, nausea, vomiting, and liver dysfunction. Used with acetaminophen it has added risk of hepatotoxicity,. Like metaxalone, its mechanism of action is still in question. It is believed that metaxalone works by altering serotonin levels and acting as a mild MAO inhibitor. The mechanism of action of chlorzoaxazone is thought to act on Gaba-A & B receptors and voltage-gated calcium channels to a degree. General central nervous system depression is the only currently accepted aspect to its medical benefits. Elucidation of the exact mechanism of action is ongoing but there is limited study due to the existence of more effective, safe muscle relaxants (ex. diazepam, cyclobenzaprine, tizanidine), greatly limiting the potential benefit of identifying novel compounds which share chlorzoxazones mechanism of action. See also
Zoxazolamine
References
Further reading
External links
"Chlorzoxazone". Drug Information Portal. U.S. National Library of Medicine. Chloroxazone Safety Data Sheet Archived 2019-07-12 at the Wayback Machine
D.F. Marsh, U.S. Patent 2,895,877 (1959) | 0-1
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While binge eaters are often believed to be lacking in self-control, the root of such behavior might instead be linked to rigid dieting practices. The relationship between strict dieting and binge eating is characterized by a vicious circle. Binge eating is more likely to occur after dieting, and vice versa. Several forms of dieting include delay in eating (e.g., not eating during the day), restriction of overall calorie intake (e.g., setting calorie limit to 1,000 calories per day), and avoidance of certain types of food (e.g., "forbidden" food, such as sugar, carbohydrates, etc.) Strict and extreme dieting differs from ordinary dieting. Some evidence suggests the effectiveness of moderate calorie restriction in decreasing binge eating episodes among overweight individuals with binge eating disorder, at least in the short-term. "In the U.S, it is estimated that 3.5% of young women and 30% to 40% of people who seek weight loss treatments, can be clinically diagnosed with binge eating disorder." Diagnosis
International Classification of Diseases
BED was first included in the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1994 simply as a feature of eating disorder. In 2013 it gained formal recognition as a psychiatric condition in the DSM-5.The 2017 update to the American version of the ICD-10 includes BED under F50.81. ICD-11 may contain a dedicated entry (6B62), defining BED as frequent, recurrent episodes of binge eating (once a week or more over a period of several months) which are not regularly followed by inappropriate compensatory behaviors aimed at preventing weight gain. | Cold turkey is the most effective treatment method, as it directly removes the cause of the condition, yet the time period between the discontinuation of the drug and the relief of symptoms may be too long and uncomfortable for some individuals (particularly when trying to go to sleep when they are unable to breathe through their nose). The use of over-the-counter (OTC) saline nasal sprays may help open the nose without causing RM if the spray does not contain a decongestant. Symptoms of congestion and runny nose can often be treated with corticosteroid nasal sprays under the supervision of a physician. For very severe cases, oral steroids or nasal surgery may be necessary. For RM caused by topical decongestants, there are anecdotal reports of persons having success by withdrawing treatment from one nostril at a time.A study has shown that the anti-infective agent benzalkonium chloride, which is frequently added to topical nasal sprays as a preservative, aggravates the condition by further increasing the rebound swelling. See also
Topical decongestant
References
Further reading
Bernstein, I.Leonard (January 2000). "Is the use of benzalkonium chloride as a preservative for nasal formulations a safety concern? A cautionary note based on compromised mucociliary transport". Journal of Allergy and Clinical Immunology. 105 (1): 39–44. doi:10.1016/S0091-6749(00)90175-1. PMID 10629450. Remsen, K. A.; Black, M. J. (19 April 1980). "Rhinitis medicamentosa". CMAJ. 122 (8): 881–884. PMC 1801634. PMID 6154514. Adams, H. Richard (2013). "Adrenergic Agonists and Antagonists". In Riviere, Jim E.; Papich, Mark G. (eds.). Veterinary Pharmacology and Therapeutics. pp. 125–56. ISBN 978-1-118-68590-7. | 0-1
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Main side effects are gastrointestinal disturbance in the first or second day of treatment (a course of treatment is 28 days) which does not affect the efficacy. Because it is available as an oral formulation, the expense and inconvenience of hospitalization is avoided, and outpatient distribution of the drug becomes an option, making miltefosine a drug of choice. However, there are some important disadvantages: 1) there is evidence of reduced efficacy after a decade of use 2) it is teratogenic and cannot be used in women of child-bearing age without anticonception during and for 4 months after treatment.Incomplete treatment has been cited as a major reason of death from visceral leishmaniasis.The nonprofit Institute for OneWorld Health has adopted the broad spectrum antibiotic paromomycin for use in treating VL; its antileishmanial properties were first identified in the 1980s. A treatment with paromomycin costs about US$15. The drug had originally been identified in the 1960s. The Indian government approved paromomycin for sale and use in August 2006. Prognosis
Protective immunity
Immunity to Leishmania is determined by the interplay of white blood cells, cytokines, immune complexes, and genetic and environmental factors. Protective immunity develops either after successful treatment of VL (cured) or after asymptomatic infections that resolve without development of VL (asymptomatic). Both types of immunity are characterized by cell-mediated immunity (CMI), including skin test positivity, proliferation, and interleukin 2 (IL-2), interferon gamma (IFN-γ), and interleukin 12 (IL-12) secretion by peripheral blood mononuclear cells (PBMC) in response to Leishmania antigens. | Several species of canines serve as reservoir hosts of L. infantum (chagasi).Contemporary life has made itself felt even here, however—not as "progress" but in the form of the many small wars of Africas post-colonial era. In the Sudan, where civil war has been continuous since 1983, the violence has been concentrated in the more populated south, and kala-azar was concentrated there too. But the wars have driven a steady stream of refugees out of the region, and these traveled either across the southern border or into the remoter western part of the country called the Upper Nile, where both war and the disease that went with it had not yet penetrated.These refugees, moving at foot-speed, carried the disease with them, and when it arrived it hit the Upper Nile with a force comparable to smallpox hitting the American Indians. The isolated people of the Upper Nile had no access to medicine or education about the new disease among them. Worse, their immune systems were defenseless against this new pathogen, foreign to them though it came only from another part of their own country. One village at the center of the epidemic, Duar, was left with four survivors out of a population of a thousand, and from the late eighties to the mid-nineties a total of 100,000 died from the sickness in that region alone. | 11
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Shunt nephritis is a rare disease of the kidney that can occur in patients being treated for hydrocephalus with a cerebral shunt. It usually results from an infected shunt that produces a long-standing blood infection, particularly by the bacterium Staphylococcus epidermidis. Kidney disease results from an immune response that deposits immune complexes in the kidney. The most common signs and symptoms of the condition are blood and protein in the urine, anemia, and high blood pressure. Diagnosis is based on these findings in the context of characteristic laboratory values. Treatment includes antibiotics and the prompt removal of the infected shunt. Over half of individuals with shunt nephritis recover completely; most of the remainder have some degree of persistent kidney disease. Presentation
The clinical presentation of shunt nephritis is variable, but the most common manifestations of shunt nephritis include blood in the urine, protein in the urine, anemia, and high blood pressure. Recurrent fever, enlarged liver and spleen, and a skin rash may also be present. Rarely, the major complaint may be arthritis. Pathophysiology
Shunt nephritis occurs when a shunt becomes infected with bacteria, most commonly Staphylococcus epidermidis. Bacteria from this infected shunt seed the bloodstream, leading to blood infection (bacteremia). In response to long-standing infection (months to years), the body mounts an immune response that results in deposition of immune complexes in the kidney, leading to nephritis. Diagnosis
Urinalysis typically demonstrates hematuria and proteinuria. Levels of the complement protein C3 are low, while levels of C-reactive protein and cryoglobulins may be modestly elevated. | Blood cultures and cerebrospinal fluid cultures demonstrate Staphylococcus epidermidis, a coagulase-negative species of Staphylococcus. Biopsy of the kidney frequently demonstrates membranoproliferative glomerulonephritis, with deposits of C3, IgM, and IgG. Treatment
Management is focused on removing the infectious source. The shunt is removed immediately and antibiotics are begun. The infected shunt, typically a ventriculoatrial shunt, may be replaced with a ventriculoperitoneal shunt. Prognosis
In one review, over half of individuals with shunt nephritis made a complete recovery. An additional 40% of individuals had persistent urine abnormalities or end-stage renal disease. Death occurred in 9%. Epidemiology
Shunt nephritis is a rare condition affecting males and females of all ages. It occurs in approximately 0.7-2.3% of patients with shunt infections. Approximately 12% of ventriculoatrial shunts become infected, with Staphylococcus epidermidis being the infectious agent in 75% of cases. History
Shunt nephritis was first described by Black in 1965. Early cases and most cases since then are associated with infections of shunts that connect the ventricular system of the brain to the atria of the heart (ventriculoatrial shunts). Less commonly, shunt nephritis has been reported to arise from infections of shunts connecting the ventricular system to the abdominal cavity (ventriculoperitoneal shunts). == References == | 11
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Smear may refer to:
A smear test, wherein a sample is smeared over a microscope slide to be studied for any pathology
A smear test usually refers to a pap test, that is, a cervical smear
Smear (card game)
Smear Lake, a lake in Wisconsin
Smear campaign, or smear job, an attack on the reputation of an individual or group making use of disinformation tactics
Smear Campaign (album), an album by Napalm Death
Pat Smear, the guitarist and actor
Smear (optics), motion that degrades sharpness, which is generally linear over the integration time
Colloquial name for a glissando, a glide from one musical pitch to anotherSmearing may refer to:
Smearing of an image taken by an astronomical interferometer:
Bandwidth smearing, a chromatic aberration;
Time smearing, a consequence of Earth rotation during the observation;
Smearing (climbing), a technique of rock climbing
Electron smearing, a tool for improving convergence in DFT calculations
See also
Smeared, the debut studio album by Canadian rock band Sloan | (1969), 67 147-151 - the paper which renamed Streptomyces mediterranei as Nocardia mediterranei. Lechevalier et al., Int. J. Syst. Bacteriol. (1986), 36, 29) - the paper which renamed Nocardia mediterranei as Amycolatopsis mediterranei. Bala S (2004). "Reclassification of "Amycolatopsis mediterranei" DSM 46095 as "Amycolatopsis rifamycinica" sp. nov". International Journal of Systematic and Evolutionary Microbiology. 54 (4): 1145–1149. doi:10.1099/ijs.0.02901-0. PMID 15280283. - the paper with the latest name change
External links
"Rifamycin". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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Placenta praevia is when the placenta attaches inside the uterus but in a position near or over the cervical opening. Symptoms include vaginal bleeding in the second half of pregnancy. The bleeding is bright red and tends not to be associated with pain. Complications may include placenta accreta, dangerously low blood pressure, or bleeding after delivery. Complications for the baby may include fetal growth restriction.Risk factors include pregnancy at an older age and smoking as well as prior cesarean section, labor induction, or termination of pregnancy. Diagnosis is by ultrasound. It is classified as a complication of pregnancy.For those who are less than 36 weeks pregnant with only a small amount of bleeding recommendations may include bed rest and avoiding sexual intercourse. For those after 36 weeks of pregnancy or with a significant amount of bleeding, cesarean section is generally recommended. In those less than 36 weeks pregnant, corticosteroids may be given to speed development of the babys lungs. Cases that occur in early pregnancy may resolve on their own.It affects approximately 0.5% of pregnancies. After four cesarean sections, however, it affects 10% of pregnancies. Rates of disease have increased over the late 20th century and early 21st century. The condition was first described in 1685 by Paul Portal. Signs and symptoms
Women with placenta previa often present with painless, bright red vaginal bleeding. This commonly occurs around 32 weeks of gestation, but can be as early as late mid-trimester. More than half of women affected by placenta praevia (51.6%) have bleeding before delivery. | Oxycodone/ibuprofen (INNs, trade name Combunox) is an oral combination drug formulation of the opioid analgesic oxycodone and the nonsteroidal anti-inflammatory drug (NSAID) ibuprofen that is used in the treatment of chronic and acute pain. This particular drug is supplied in a fixed dose combination tablet which contains Oxycodone Hydrochloride, USP 5 mg with Ibuprofen, USP 400 mg. Adverse effects
See also
Oxycodone/paracetamol
Oxycodone/aspirin
Hydrocodone/ibuprofen
References
External links
"Ibuprofen mixture with oxycodone". Drug Information Portal. U.S. National Library of Medicine. | 0-1
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This is done by using glycosidase enzymes from specific bacteria to strip the blood group antigens from red blood cells. The removal of A and B antigens still does not address the problem of the Rh blood group antigen on the blood cells of Rh positive individuals, and so blood from Rh negative donors must be used. The sort of blood is named "enzyme converted to O" (ECO) blood. Patient trials will be conducted before the method can be relied on in live situations. One such Phase II trial was done on B-to-O blood in 2002.Another approach to the blood antigen problem is the manufacture of artificial blood, which could act as a substitute in emergencies. Pseudoscience
During the 1930s, connecting blood groups to personality types became popular in Japan and other areas of the world. Studies of this association have yet to confirm its existence definitively.Other popular but unsupported ideas include the use of a blood type diet, claims that group A causes severe hangovers, group O is associated with perfect teeth, and those with blood group A2 have the highest IQs. Scientific evidence in support of these concepts is limited at best. See also
Secretor status – secretion of ABO antigens in body fluids
References
Further reading
Dean L (2005). "Chapter 5: The ABO blood group". Blood Groups and Red Cell Antigens. Retrieved 24 March 2007. Farr A (1 April 1979). "Blood group serology--the first four decades (1900–1939)". Med Hist. 23 (2): 215–26. doi:10.1017/s0025727300051383. PMC 1082436. PMID 381816. | Retinal tear accounts for 11.4–44% of vitreous hemorrhage cases. Posterior vitreous detachment
As one gets older, pockets of fluid can develop in the vitreous. When these pockets develop near the back of the eye, the vitreous can pull away from the retina and possibly tear it. Posterior vitreous detachment accounts for 3.7–11.7% of vitreous hemorrhage cases. Other causes
Less common causes of vitreous hemorrhage make up 6.4–18% of cases, and include:
Proliferative sickle cell retinopathy
Macroaneurysms
Age-related macular degeneration
Terson syndrome
Retinal neovascularization as a result of branch or central retinal vein occlusion
Other
Diagnosis
Vitreous hemorrhage is diagnosed by identifying symptoms, examining the eye, and performing tests to identify the cause. Some common tests include:
Examination of the eye with a microscope
Pupil dilation and examination
An ultrasound examination may be used if the doctor does not have a clear view of the back of the eye
Blood tests to check for specific causes such as diabetes
A CT scan to check for injury around the eye
Referral to a retinal specialist
Complications
Ghost cell glaucoma: Secondary open angle glaucoma caused by degenerated red blood cells. Treatments
The treatment method used depends on the cause of the hemorrhage. In most cases, the patient is advised to rest with the head elevated 30–45°, and sometimes to put patches over the eyes to limit movement prior to treatment in order to allow the blood to settle. The patient is also advised to avoid taking medications that cause blood thinning (such as aspirin or similar medications). The goal of the treatment is to fix the cause of the hemorrhage as quickly as possible. | 0-1
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Castleman disease (CD) describes a group of rare lymphoproliferative disorders that involve enlarged lymph nodes, and a broad range of inflammatory symptoms and laboratory abnormalities. Whether Castleman disease should be considered an autoimmune disease, cancer, or infectious disease is currently unknown. Castleman disease includes at least three distinct subtypes: unicentric Castleman disease (UCD), human herpesvirus 8 associated multicentric Castleman disease (HHV-8-associated MCD), and idiopathic multicentric Castleman disease (iMCD). These are differentiated by the number and location of affected lymph nodes and the presence of human herpesvirus 8, a known causative agent in a portion of cases. Correctly classifying the Castleman disease subtype is important, as the three subtypes vary significantly in symptoms, clinical findings, disease mechanism, treatment approach, and prognosis. All forms involve overproduction of cytokines and other inflammatory proteins by the bodys immune system as well as characteristic abnormal lymph node features that can be observed under the microscope. In the United States, approximately 4,300 to 5,200 new cases are diagnosed each year.Castleman disease is named after Benjamin Castleman, who first described the disease in 1956. The Castleman Disease Collaborative Network is the largest organization dedicated to accelerating research and treatment for Castleman disease as well as improving patient care. Classification
Castleman disease (CD) can involve one or more enlarged lymph nodes in a single region of the body (unicentric CD, UCD) or it can involve multiple enlarged lymph node regions (multi centric CD, MCD). | Multicentric Castleman disease (MCD)
In this form, patients have multiple regions of enlarged lymph nodes with characteristic microscopic features, flu-like symptoms, and organ dysfunction due to excessive cytokines or inflammatory proteins. MCD is further classified into three categories based on underlying cause: POEMS-associated MCD, HHV-8-associated MCD, and idiopathic MCD (iMCD). POEMS-associated MCD
A cancerous cell population found in patients with POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal plasma cell disorder, and skin changes) can cause MCD in a fraction of patients by producing cytokines that initiate a cytokine storm. In patients who have both POEMS-associated MCD, treatment should be directed at the POEMS syndrome. HHV-8-associated multicentric Castleman disease (HHV-8-MCD)
HHV-8-associated MCD patients have multiple regions of enlarged lymph nodes and episodic inflammatory symptoms due to uncontrolled infection with HHV-8. HHV-8-associated MCD is most commonly diagnosed in HIV infected or otherwise immunocompromised individuals that are not able to control HHV-8 infection. Thus, HHV-8-associated MCD patients may experience additional symptoms related to their HIV infection or other conditions. First-line treatment of HHV-8-associated MCD is rituximab, a drug used to eliminate a type of immune cell called the B lymphocyte. It is highly effective for HHV-8-associated MCD, but occasionally antivirals and/or cytotoxic chemotherapies are needed. Idiopathic multicentric Castleman disease (iMCD)
Idiopathic multicentric Castleman disease (iMCD), which is the most common form of MCD, occurs for an unknown cause. There is no evidence of POEMS syndrome, HHV-8, or any other cancer or infectious disease. | 11
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This was followed by the report in 1775 by British surgeon Percivall Pott that chimney sweeps carcinoma, a cancer of the scrotum, was a common disease among chimney sweeps. With the widespread use of the microscope in the 18th century, it was discovered that the cancer poison spread from the primary tumor through the lymph nodes to other sites ("metastasis"). This view of the disease was first formulated by the English surgeon Campbell De Morgan between 1871 and 1874. Society and culture
Although many diseases (such as heart failure) may have a worse prognosis than most cases of cancer, cancer is the subject of widespread fear and taboos. The euphemism of "a long illness" to describe cancers leading to death is still commonly used in obituaries, rather than naming the disease explicitly, reflecting an apparent stigma. Cancer is also euphemised as "the C-word"; Macmillan Cancer Support uses the term to try to lessen the fear around the disease. In Nigeria, one local name for cancer translates into English as "the disease that cannot be cured". | In 2015 the IARC reported that eating processed meat (e.g., bacon, ham, hot dogs, sausages) and, to a lesser degree, red meat was linked to some cancers.Dietary recommendations for cancer prevention typically include an emphasis on vegetables, fruit, whole grains and fish and an avoidance of processed and red meat (beef, pork, lamb), animal fats, pickled foods and refined carbohydrates. Medication
Medications can be used to prevent cancer in a few circumstances. In the general population, NSAIDs reduce the risk of colorectal cancer; however, due to cardiovascular and gastrointestinal side effects, they cause overall harm when used for prevention. Aspirin has been found to reduce the risk of death from cancer by about 7%. COX-2 inhibitors may decrease the rate of polyp formation in people with familial adenomatous polyposis; however, it is associated with the same adverse effects as NSAIDs. Daily use of tamoxifen or raloxifene reduce the risk of breast cancer in high-risk women. The benefit versus harm for 5-alpha-reductase inhibitor such as finasteride is not clear.Vitamin supplementation does not appear to be effective at preventing cancer. While low blood levels of vitamin D are correlated with increased cancer risk, whether this relationship is causal and vitamin D supplementation is protective is not determined. One 2014 review found that supplements had no significant effect on cancer risk. | 11
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In academic studies of color blindness, on the other hand, there is more interest in developing flexible tests to collect precise datasets, identify copunctal points, and measure just noticeable differences. Pseudoisochromatic plates
A pseudoisochromatic plate (from Greek pseudo, meaning "false", iso, meaning "same" and chromo, meaning "color") is the type of test exemplified by the Ishihara test, where a figure (usually one or more numerals) is embedded in the plate as a number of spots surrounded by spots of a slightly different color. The figure can be seen with normal color vision, but not with a particular color defect. The figure and background colors must be carefully chosen to appear isochromatic to a color deficient individual, but not an individual with normal color vision. Pseudoisochromatic Plates are used as screening tools because they are cheap, fast and simple, but they do not provide precise diagnosis of CVD, and are often followed with another test if a user fails the Ishihara test.The basic Ishihara test may not be useful in diagnosing young, preliterate children, who cant read the numerals, but larger editions contain plates that showcase a simple path to be traced with a finger, rather than numerals.One of the most common alternative color vision tests based on pseudoisochromatic plates is the HRR color test (developed by Hardy, Rand, and Rittler), which solves many of the criticisms of the Ishihara test. For example, it detects blue-yellow color blindness, is less susceptible to memorization and uses shapes, so it is accessible to the illiterate and young children. | Subgaleal hemorrhage, also known as subgaleal hematoma, is bleeding in the potential space between the skull periosteum and the scalp galea aponeurosis. Symptoms
The diagnosis is generally clinical, with a fluctuant boggy mass developing over the scalp (especially over the occiput) with superficial skin bruising. The swelling develops gradually 12–72 hours after delivery, although it may be noted immediately after delivery in severe cases. Subgaleal hematoma growth is insidious, as it spreads across the whole calvaria and may not be recognized for hours to days. If enough blood accumulates, a visible fluid wave may be seen. Patients may develop periorbital ecchymosis ("raccoon eyes").Patients with subgaleal hematoma may present with hemorrhagic shock given the volume of blood that can be lost into the potential space between the skull periosteum and the scalp galea aponeurosis, which has been found to be as high as 20-40% of the neonatal blood volume in some studies. The swelling may obscure the fontanel and cross cranial suture lines, distinguishing it from cephalohematoma, in which the bleed is confined by its subperiosteal location.Patients with subgaleal hemorrhage may also have significant hyperbilirubinemia due to resorption of hemolyzed blood. Laboratory studies may demonstrate reduced hemoglobin and hematocrit due to blood loss into the subgaleal space, and coagulation studies may reflect an underlying coagulopathy. Mortality has been reported to occur in 12-14% of cases, generally as a consequence of massive blood loss presenting with shock, often in the setting of uncorrected coagulopathy. | 0-1
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MORM syndrome is an autosomal recessive congenital disorder characterized by mental retardation, truncal obesity, retinal dystrophy, and micropenis". The disorder shares similar characteristics with Bardet–Biedl syndrome and Cohen syndrome, both of which are autosomal recessive genetic disorders. MORM syndrome can be distinguished from the above disorders because symptoms appear at a young age. The disorder is not dependent on sex of the offspring, both male and female offspring are equally likely to inherit the disorder. The syndrome is caused by a mutation in the INPP5E gene which can be located on chromosome 9 in humans. Further mapping resulted in the identification of a MORM syndrome locus on chromosome 9q34.3 between the genetic markers D9S158 and D9S905. Presentation
For individuals with MORM syndrome, symptoms do not appear until about one year of age. From conception to birth, individuals with MORM syndrome appear asymptotic, with no abnormal characteristics. Vision is negatively affected within the first year of life, particularly night vision. Individuals with MORM syndrome experience decreased visual acuity, meaning their ability to see distinct sharp lines decreases. Vision quality continues to deteriorate until age three. Any further reduction in vision acuity is not observed until the individual is between the ages thirty to forty. Delayed sentence processing and intellectual disability is associated with individuals with MORM syndrome, primarily observed at age four. Individuals continue to develop and grow until they are five to twelve years old. | During this age bracket, truncal obesity can develop, characterized by the buildup of fat around ones trunk or torso as opposed to the persons extremities. Males enter puberty at around age twelve and develop normally, except for their penis, which will remain at the prepubescent size, resulting in a micropenis. Both the life span and fertility of individuals with MORM syndrome is unclear . Genetic
MORM syndrome is associated with the gene INPP5E. INPP5E is a gene whose function is not well understood. It is hypothesized to play a role in primary cilia stability. A homozygous mutation in the INPP5E gene, on chromosome 9q34, is the cause for MORM syndrome. The mutation causes a homozygous transition in the last exon of the INPP5E gene. This transition results in the DNA bases changing from a cytosine residue to a thymine residue. The resulting protein will then have an altered amino acid sequence. In unaffected individuals this specific codon (region of DNA bases) is supposed to code for the amino acid glutamine. In cases of MORM syndrome this codon codes for a termination sequence, which prematurely stops the production of the protein. In unaffected individuals the protein is evenly disbursed throughout the cilia axoneme, which stabilizes the cilia, which are antenna like structures which protrude from the extracellular surface of the cell. They play an important role in extracellular signalling/communication between cells and their environment. | 11
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top Exploitation Through Trafficking Act passed in 2013 aimed at preventing the prosecution of sexually exploited youth being sex trafficked, redirecting abused and exploited youth from the criminal justice system to the child welfare system. This and other laws redirecting victims of child sex trafficking to the child welfare system are known as "Safe Harbor" laws.As of April 2019, 18 states had legislation requiring that mandated reporters report based on suspicion of child abuse of neglect. Advocacy organizations
United States
There are organizations at national, state, and county levels in the United States that provide community leadership in preventing child abuse and neglect. Mary Ellen Wilson, also called Mary Ellen McCormack, was an American whose case of child abuse, the first documented case of child abuse in the United States, led to the creation of the New York Society for the Prevention of Cruelty to Children, which was incorporated in 1875. It was the worlds first child protective agency.Prevent Child Abuse America, founded in 1976, operates in 46 states to provide child abuse and neglect protection.Founded in 1985, the National Childrens Advocacy Center, along with National Childrens Alliance, coordinates efforts and sets standards and policy for child advocacy centers across the US and abroad. The Childrens Trust Fund Alliance, established in 1989, provides funding support to state level child abuse organisations. Many investigations into child abuse in the US are handled on the local level by 924 child advocacy centers, some of which are distributed among 34 other countries. Other organizations focus on specific prevention strategies. | The presence of intracellular bacteria in chronic osteomyelitis is likely an unrecognized contributing factor in its persistence.In infants, the infection can spread to a joint and cause arthritis. In children, large subperiosteal abscesses can form because the periosteum is loosely attached to the surface of the bone.Because of the particulars of their blood supply, the tibia, femur, humerus, vertebrae, maxilla and the mandibular bodies are especially susceptible to osteomyelitis. Abscesses of any bone, however, may be precipitated by trauma to the affected area. Many infections are caused by Staphylococcus aureus, a member of the normal flora found on the skin and mucous membranes. In patients with sickle cell disease, the most common causative agent is Salmonella, with a relative incidence more than twice that of S. aureus. Diagnosis
The diagnosis of osteomyelitis is complex and relies on a combination of clinical suspicion and indirect laboratory markers such as a high white blood cell count and fever, although confirmation of clinical and laboratory suspicion with imaging is usually necessary.Radiographs and CT are the initial method of diagnosis, but are not sensitive and only moderately specific for the diagnosis. They can show the cortical destruction of advanced osteomyelitis, but can miss nascent or indolent diagnoses.Confirmation is most often by MRI. The presence of edema, diagnosed as increased signal on T2 sequences, is sensitive, but not specific, as edema can occur in reaction to adjacent cellulitis. Confirmation of bony marrow and cortical destruction by viewing the T1 sequences significantly increases specificity. The administration of intravenous gadolinium-based contrast enhances specificity further. | 0-1
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