<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Riedels thyroiditis and can you explain it in depth? [/INST] Riedels thyroiditis, is a chronic form of thyroiditis. It is now believed that Riedels thyroiditis is one manifestation of a systemic disease that can affect many organ systems called IgG4-related disease. It is often a multi-organ disease affecting pancreas, liver, kidney, salivary and orbital tissues and retroperitoneum. The hallmarks of the disease are fibrosis and infiltration by IgG4 secreting plasma cells.

Signs and symptoms
Pathophysiology
Riedels thyroiditis is characterized by a replacement of the normal thyroid parenchyma by a dense fibrosis that invades adjacent structures of the neck and extends beyond the thyroid capsule </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Telangiectasia macularis eruptiva perstans and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Morquio syndrome and can you explain it in depth? [/INST] Morquio syndrome, also known as Mucopolysaccharidosis Type IV (MPS IV), is a rare metabolic disorder in which the body cannot process certain types of sugar molecules called glycosaminoglycans (AKA GAGs, or mucopolysaccharides). In Morquio syndrome, the specific GAG which builds up in the body is called keratan sulfate. This birth defect, which is autosomal recessive, is a type of lysosomal storage disorder. The buildup of GAGs in different parts of the body causes symptoms in many different organ systems.: 544  In the US, the incidence rate for Morquio syndrome is estimated at between 1 in 200,000 and 1 in 300,000 live births.

Signs and symptoms
Patients with Morquio syndrome appear healthy at birth. Types A and B have similar presentations, but Type B generally has milder symptoms. The age of onset is usually between 1 and 3 years of age. Morquio syndrome causes progressive changes to the skeleton of the ribs and chest, which may lead to neurological complications such as nerve compression. Patients may also have hearing loss and clouded corneas. Intelligence is usually normal unless a patient has untreated hydrocephalus.Physical growth slows and often stops around age 8. Skeletal abnormalities include a bell-shaped chest, a flattening or curvature of the spine, shortened long bones, and dysplasia of the hips, knees, ankles, and wrists. The bones that stabilize the connection between the head and neck can be malformed (odontoid hypoplasia); in these cases, a surgical procedure called spinal cervical bone fusion can be lifesaving. Restricted breathing, joint stiffness, and heart disease are also common. Children with the more severe form of MPS IV may not live beyond their twenties or thirties.

Cause
Morquio syndrome is inherited from an autosomal recessive inherited gene. Every person has two copies of the genes needed to break down keratan sulfate, but only one healthy copy is needed. Both parents pass down one defective copy to their child, resulting in a child with no functional copies of the gene. As such, the body is incapable breaking down keratan sulfate for disposal. The incompletely broken down GAGs remain stored in cells in the body, causing progressive damage. Babies may show little sign of the disease, but as more and more cells become damaged, symptoms start to appear.

Diagnosis
Classification
This syndrome has two forms, A and B, referred to as Morquio A and Morquio B syndrome or MPS IVA and MPS IVB. The two forms are distinguished by the gene product involved; Type A involves a malfunction in the GALNS gene, while Type B involves a malfunction of the GLB1 gene.

Treatment
The treatment for Morquio syndrome consists of prenatal identification and of enzyme replacement therapy. On 12 February 2014, the US Food and Drug Administration approved the drug elosulfase alfa (Vimizim) for treating Type A </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Disseminated superficial actinic porokeratosis and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Bickerstaff brainstem encephalitis and can you explain it in depth? [/INST] Bickerstaff brainstem encephalitis is a rare inflammatory disorder of the central nervous system, first described by Edwin Bickerstaff in 1951. It may also affect the peripheral nervous system, and has features in common with both Miller Fisher syndrome and Guillain–Barré syndrome.

Signs and symptoms
In order to diagnose Bickerstaff brainstem encephalitis, ataxia and ophthalmoplegia must be present. These are also diagnostic features of Miller Fisher syndrome, and so Bickerstaffs is only diagnosed if other features are present which exclude Miller Fisher syndrome. These may include drowsiness, coma or hyperreflexia. When the condition is defined in this way, a number of other features are commonly but not always found: among these are weakness of the limbs, the face, and/or the bulbar muscles; abnormalities of the pupils; and absent reflexes.Like some other autoimmune diseases, the condition usually follows a minor infection, such as a respiratory tract infection or gastroenteritis.

Pathophysiology
The clinical features and course of the condition, the associated auto-antibodies against relevant antigens, and the response to treatment, all suggest that Bickerstaff brainstem encephalitis is an autoimmune disease. However, each of these criteria fails to fit a substantial proportion of patients, and there is no single test or feature which is diagnostic of Bickerstaff brainstem encephalitis </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Thyroid dysgenesis and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Vulvar vestibulitis and can you explain it in depth? [/INST] Vulvar vestibulitis syndrome (VVS), vestibulodynia, or simply vulvar vestibulitis, is vulvodynia localized to the vulvar vestibule. It tends to be associated with a highly localized "burning" or "cutting" type of pain. Until recently, "vulvar vestibulitis" was the term used for localized vulvar pain: the suffix "-itis" would normally imply inflammation, but in fact there is little evidence to support an inflammatory process in the condition. "Vestibulodynia" is the term now recognized by the International Society for the Study of Vulvovaginal Disease.Provoked vestibulodynia, pain provoked by contact localized to the vulvar vestibule, is the most common subtype of vulvodynia among premenopausal women </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Lupus erythematosus panniculitis and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Whipples disease and can you explain it in depth? [/INST] Whipples disease is a rare systemic infectious disease caused by the bacterium Tropheryma whipplei. First described by George Hoyt Whipple in 1907 and commonly considered as a gastrointestinal disorder, Whipples disease primarily causes malabsorption, but may affect any part of the human body, including the heart, brain, joints, skin, lungs and the eyes. Weight loss, diarrhea, joint pain, and arthritis are common presenting symptoms, but the presentation can be highly variable in certain individuals, and about 15% of patients do not have the standard signs and symptoms.Whipples disease is significantly more common in men, with 87% of patients diagnosed being male. When recognized and treated, Whipples disease can usually be cured with long-term antibiotic therapy, but if the disease is left undiagnosed or untreated, it can ultimately be fatal.

Signs and symptoms
The most common symptoms are diarrhea, abdominal pain, weight loss, and joint pains. The joint pains may be due to migratory nondeforming arthritis, which may occur many years before any digestive-tract symptoms develop; they tend to involve the large joints, but can occur in any pattern and tend not to damage the joint surface to the point that the joint becomes deformed. Fever and chills occur in a small proportion of people.In its more advanced form, malabsorption (insufficient absorption of nutrients from the diet) leads to wasting and the enlargement of lymph nodes in the abdomen. Neurological symptoms (discussed below) are more common in those with the severe form of the abdominal disease. Chronic malabsorptive diarrhea leads to the poor absorption of fat, causing steatorrhea (fatty, offensive-smelling stool), flatulence, and abdominal distension. Protein-losing enteropathy may also occur, causing depletion of albumin, a blood protein, which may lead to peripheral edema caused by the lowered oncotic pressures.Hyperpigmentation of the skin occurs in almost half; some also have skin nodules. Various eye problems, such as uveitis, may occur; this is typically associated with deteriorating vision and pain in the affected eye. Endocarditis (infection of the heart valve) has been reported in a small number of cases, sometimes in people with no other symptoms of Whipples disease; this is typically noticed as breathlessness and leg swelling due to fluid accumulation as the heart is unable to pump fluid through the body.Of those affected by Whipples disease, 10–40% have problems related to the involvement of the brain; the symptoms relate to the part of the brain that is affected. The most common problems are dementia, memory loss, confusion, and decreased level of consciousness. Eye-movement disturbances and myorhythmia (rapidly repetitive movements of the muscles) of the face, together referred to as oculomasticatory myorhythmia, are highly characteristic for Whipples disease. Weakness and poor coordination of part of the body, headaches, seizures, and a number of more uncommon neurological features are present in some cases.

Mechanism
T. whipplei is one of the Actinomycetes, and is a distant relative of the Mycobacterium avium complex, explaining in part why Whipples disease is similar to the diseases caused by MAC bacteria. The disease is common in farmers and those exposed to soil and animals, suggesting that the infection is acquired from these sources.Individuals who are most susceptible to the disease are those with decreased ability to perform intracellular degradation of ingested pathogens or particles, particularly within macrophages. Several studies indicate that defective T-lymphocyte (particularly TH1 population) function may be an important predisposing factor for the disease. In particular, circulating cells which are CD11b (also known as integrin alpha) expressive are reduced in susceptible individuals. CD11b has a vital role in activation of macrophages to destroy intracellularly ingested T. whipplei bacteria.

Diagnosis
Common clinical signs and symptoms of Whipples disease include diarrhea, steatorrhea, abdominal pain, weight loss, migratory arthropathy, fever, and neurological symptoms. Weight loss and diarrhea are the most common symptoms that lead to identification of the process, but may be preceded by chronic, unexplained, relapsing episodes of nondestructive seronegative arthritis, often of large joints.Endoscopy of the duodenum and jejunum can reveal pale yellow shaggy mucosa with erythematous eroded patches in patients with classic intestinal Whipples disease, and small bowel X-rays may show some thickened folds. Other pathological findings may include enlarged mesenteric lymph nodes, hypercellularity of lamina propria with "foamy macrophages", and a concurrent decreased number of lymphocytes and plasma cells, per high power field view of the biopsy.Diagnosis is made by biopsy, usually by duodenal endoscopy, which reveals PAS-positive macrophages in the lamina propria containing nonacid-fast, Gram-positive bacilli. Immunohistochemical staining for antibodies against T. whipplei has been used to detect the organism in a variety of tissues, and a polymerase chain reaction-based assay is also available,  which can be confirmatory if performed on blood, vitreous fluid, synovial fluid, heart valves, or cerebrospinal fluid. PCR of saliva, gastric or intestinal fluid, and stool specimens is highly sensitive, but not specific enough, indicating that healthy individuals can also harbor the causative bacterium without the manifestation of Whipples disease, but that a negative PCR is most likely indicative of a healthy individual.

Treatment
Treatment is with penicillin, ampicillin, tetracycline, or co-trimoxazole for one to two years. Any treatment lasting less than a year has a relapse rate around 40%. Expert opinion as of 2007 is that Whipples disease should be treated with doxycycline with hydroxychloroquine for 12 to 18 months. Sulfonamides (sulfadiazine or sulfamethoxazole) may be added for treatment of neurological symptoms.

Epidemiology
The disease is regarded as extremely rare, with an incidence (new number of cases per year) of one case per million people. The patients are predominantly male (86% in a survey of American patients), although in some countries, the rate of women receiving a diagnosis of Whipples disease has increased in recent years. It occurs predominantly in those of Caucasian ethnicity, suggesting a genetic predisposition in that population. T. whipplei appears to be an environmental organism that is commonly present in the gastrointestinal tract, but remains asymptomatic. Several lines of evidence suggest that some defect—inherited or acquired—in immunity is required for it to become pathogenic </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tufted folliculitis and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Panniculitis and can you explain it in depth? [/INST] Panniculitis is a group of diseases whose hallmark is inflammation of subcutaneous adipose tissue (the fatty layer under the skin – panniculus adiposus). Symptoms include tender skin nodules, and systemic signs such as weight loss and fatigue.
Restated, an inflammatory disorder primarily localized in the subcutaneous fat is termed a "panniculitis", a group of disorders that may be challenging both for the clinician and the dermatopathologist.: 487  The general term for inflammation of any adipose tissue is steatitis.

Signs and symptoms
Panniculitis can also be classified based on the presence or absence of systemic symptoms. Panniculitis without systemic disease can be a result of trauma or cold. Panniculitis with systemic disease can be caused by:

connective tissue disorders such as lupus erythematosus or scleroderma;
lymphoproliferative disease such as lymphoma or histiocytosis;
pancreatitis or pancreatic cancer;
sarcoidosis with cutaneous involvement (seen in up to 20 percent);
Alpha 1-antitrypsin deficiency
Crohns diseaseThis is not a complete list of possible causes.

Associated conditions
Lipoatrophy or lipodystrophy (the loss of subcutaneous adipose tissue) can occur in any of these conditions.

Diagnosis
Classification
It can occur in any fatty tissue (cutaneous or visceral) and is often diagnosed on the basis of a deep skin biopsy, and can be further classified by histological characteristics based on the location of the inflammatory cells (within fatty lobules or in the septa which separate them) and on the presence or absence of vasculitis.There are thus four main histological subtypes:
lobular panniculitis without vasculitis (acute panniculitis, previously termed Weber–Christian disease, systemic nodular panniculitis)
lobular panniculitis with vasculitis
septal panniculitis without vasculitis
septal panniculitis with vasculitis

Lobular
With vasculitis
Erythema induratum, or "Bazin disease", is a panniculitis on the back of the calves </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Multiple chemical sensitivity and can you explain it in depth? [/INST] Multiple chemical sensitivity (MCS), also known as idiopathic environmental intolerances (IEI), is an unrecognized and controversial diagnosis characterized by chronic symptoms attributed to exposure to low levels of commonly used chemicals. Symptoms are typically vague and non-specific. They may include fatigue, headaches, nausea, and dizziness.
Although these symptoms can be debilitating, MCS is not recognized as an organic, chemical-caused illness by the World Health Organization, American Medical Association, nor any of several other professional medical organizations. Blinded clinical trials show that people with MCS react as often and as strongly to placebos as they do to chemical stimuli; the existence and severity of symptoms is seemingly related to the perception that a chemical stimulus is present.Commonly attributed substances include scented products (e.g. perfumes), pesticides, plastics, synthetic fabrics, smoke, petroleum products, and paint fumes.

Symptoms
Symptoms are typically vague and non-specific, such as fatigue or headaches.  These symptoms, although they can be disabling, are called non-specific because they are not associated with any single specific medical condition.
A 2010 review of MCS literature said that the following symptoms, in this order, were the most reported in the condition: headache, fatigue, confusion, depression, shortness of breath, arthralgia, myalgia, nausea, dizziness, memory problems, gastrointestinal symptoms, respiratory symptoms.Symptoms mainly arise from the autonomic nervous system (such as nausea or dizziness) or have psychiatric or psychological aspects (such as difficulty concentrating).

Possible causes
Various different causes for MCS have been hypothesized.There is a general agreement among most MCS researchers that the cause is not specifically related to sensitivity to chemicals, but this does not preclude the possibility that symptoms are caused by other known or unknown factors. Various health care professionals and government agencies are working on giving those who report the symptoms proper care while searching for a cause.In 2017, a Canadian government Task Force on Environmental Health said that there had been very little rigorous peer-reviewed research into MCS and almost a complete lack of funding for such research in North America. "Most recently," it said, "some peer-reviewed clinical research has emerged from centres in Italy, Denmark and Japan suggesting that there are fundamental neurobiologic, metabolic, and genetic susceptibility factors that underlie ES/MCS."The US Occupational Safety and Health Administration (OSHA) says that MCS is highly controversial and that there is insufficient scientific evidence to explain the relationship between any of the suggested causes of MCS – it lists "allergy, dysfunction of the immune system, neurobiological sensitization, and various psychological theories" as the suggested causes – and its symptoms.

Immunological
Researchers have studied immunity biomarkers in people with MCS to determine whether MCS could be an autoimmune disorder or allergic response, but the results have been inconclusive. Some people with MCS appear to have excess production of inflammatory cytokines, but this phenomenon is not specific to MCS and overall there is no evidence that low-level chemical exposure causes an immune response.

Genetic
It has been hypothesized that there is a heritable genetic trait which pre-disposes people to be hypersensitive to low-level chemical exposure and so develop MCS. To investigate, researchers compared the genetic makeup of people with MCS, to people without. The results were generally inconclusive and contradictory, thus failing to support the hypothesis.Gaétan Carrier and colleagues write that the genetic hypothesis appears implausible when the evidence around it is judged by the Bradford Hill criteria.

Psychological
Several mechanisms for a psychological etiology of the condition have been proposed, including theories based on misdiagnoses of an underlying mental illness, stress, or classical conditioning. Many people with MCS also meet the criteria for major depressive disorder or anxiety disorder. Other proposed explanations include somatic symptom disorder, panic disorder, migraine, chronic fatigue syndrome, or fibromyalgia and brain fog. Through behavioral conditioning, it has been proposed that people with MCS may develop real, but unintentionally psychologically produced, symptoms, such as anticipatory nausea, when they encounter certain odors or other perceived triggers. It has also been proposed in one study that individuals may have a tendency to "catastrophically misinterpret benign physical symptoms"  or simply have a disturbingly acute sense of smell. The personality trait absorption, in which individuals are predisposed to becoming deeply immersed in sensory experiences, may be stronger in individuals reporting symptoms of MCS.  In the 1990s, behaviors exhibited by MCS sufferers were hypothesized by some to reflect broader sociological fears about industrial pollution and broader societal trends of technophobia and chemophobia.These theories have attracted criticism.In Canada, in 2017, following a three-year government inquiry into environmental illness, it was recommended that a public statement be made by the health department.A 2018 systematic review concluded that the evidence suggests that abnormalities in sensory processing pathways combined with peculiar personality traits best explains this condition.

Diagnosis
In practice, diagnosis relies entirely upon the self-reported claim that symptoms are triggered by exposure to various substances.Many other tests have been promoted by various people over the years, including testing of the immune system, porphyrin metabolism, provocation-neutralization testing, autoantibodies, the Epstein–Barr virus, testing for evidence of exposure to pesticides or heavy metals, and challenges involving exposure to chemicals, foods, or inhalants.  None of these tests correlate with MCS symptoms, and none are useful for diagnosing MCS.The stress and anxiety experienced by people reporting MCS symptoms are significant.  Neuropsychological assessments do not find differences between people reporting MCS symptoms and other people in areas such as verbal learning, memory functioning, or psychomotor performance.  Neuropsychological tests are sensitive but not specific, and they identify differences that may be caused by unrelated medical, neurological, or neuropsychological conditions.Another major goal for diagnostic work is to identify and treat any other medical conditions the person may have.  People reporting MCS-like symptoms may have other health issues, ranging from common conditions, such as depression or asthma, to less common circumstances, such a documented chemical exposure during a work accident.  These other conditions may or may not have any relationship to MCS symptoms, but they should be diagnosed and treated appropriately, whenever the patient history, physical examination, or routine medical tests indicates their presence.  The differential diagnosis list includes solvent exposure, occupational asthma, and allergies.

Definitions
Different researchers and proponents use different definitions, which complicates research and can affect diagnosis.  For example, the 1987 definition that requires symptoms to begin suddenly after an identifiable, documented exposure to a chemical, but the 1996 definition by the WHO/ICPS says that the cause can be anything, including other medical conditions or psychological factors.In 1996, an expert panel at WHO/ICPS was set up to examine MCS. The panel accepted the existence of "a disease of unclear pathogenesis", rejected the claim that MCS was caused by chemical exposure, and proposed these three diagnostic requirements for what they re-named idiopathic environmental intolerances (IEI):

the disease was acquired (not present from birth) and must produce multiple relapsing symptoms;
the symptoms must be closely related to "multiple environmental influences, which are well tolerated by the majority of the population"; and
it could not be explained by any other medical condition.In Japan, MCS is called chemical hypersensitivity or chemical intolerance (化学物質過敏症; kagaku bushitsu kabinsho), and the 1999 Japanese definition requires one or more of four major symptoms – headaches; malaise and fatigue; muscle pain; joint pain – combined with laboratory findings and/or some minor symptoms, such as mental effects or skin conditions.  The defined lab findings are abnormalities in parasympathetic nerves, cerebral cortical dysfunction diagnosed by SPECT testing, visuospatial abnormalities, abnormalities of eye movement, or a positive provocation test.

International Statistical Classification of Diseases
The International Statistical Classification of Diseases and Related Health Problems (ICD), maintained by the World Health Organization, is a medical coding system used for medical billing and statistical purposes – not for deciding whether any person is sick, or whether any collection of symptoms constitutes a single disease.  The ICD does not list MCS as a discrete disease.  However, this does not mean that people with MCS-related symptoms cannot be treated or billed for medical services.  For example, the public health service in Germany permits healthcare providers to bill for MCS-related medical services under the ICD-10 code T78.4, which is for idiosyncratic reactions, classified under the heading T78, Unerwünschte Nebenwirkungen, anderenorts nicht klassifiziert ("adverse reactions, not otherwise specified").  Being able to get paid for medical services and collect statistics about unspecified, idiosyncratic reactions does not mean that MCS is recognized as a specific disease or that any particular cause has been defined by the German government.  Healthcare providers can also bill for MCS-related services under the ICD-10 codes of F45.0 for somatization disorder.  MCS is named in evidence-based ("S3") guidelines for the management of patients with nonspecific, functional, and somatoform physical symptoms.

Management
There is no single proven treatment for MCS. The goal of treatment is to improve quality of life, with fewer distressing symptoms and the ability to maintain employment and social relationships, rather than to produce a permanent cure.A multidisciplinary treatment approach is recommended.  It should take into account the uncommon personality traits often seen in affected individuals and physiological abnormalities in sensory pathways and the limbic system. There is also no scientific consensus on supportive therapies for MCS, "but the literature agrees on the need for patients with MCS to avoid the specific substances that trigger reactions for them and also on the avoidance of xenobiotics in general, to prevent further sensitization.": 17 Common self-care strategies include avoiding exposure to known triggers and emotional self-care.  Healthcare providers can provide useful education on the bodys natural ability to eliminate and excrete toxins on its own and support positive self-care efforts.  Avoiding triggers, such as by removing smelly cleaning products from the home, can reduce symptoms and increase the persons sense of being able to reclaim a reasonably normal life.  However, for other people with MCS, their efforts to avoid suspected triggers will backfire, and instead produce harmful emotional side effects that interfere with the overall goal of reducing distress and disability. Treatments that have not been scientifically validated, such as detoxification, have been used by MCS patients. Unproven treatments can be expensive, may cause side effects, and may be counterproductive.

Epidemiology
Prevalence rates for MCS vary according to the diagnostic criteria used. The condition is reported across industrialized countries and it affects women more than men.: 37 In 2018, the same researchers reported that the prevalence rate of diagnosed MCS had increased by more than 300% and self-reported chemical sensitivity by more than 200% in the previous decade. They found that 12.8% of those surveyed reported medically diagnosed MCS and 25.9% reported having chemical sensitivities.A 2014 study by the Canadian Ministry of Health estimated, based on its survey, that 0.9% of Canadian males and 3.3% of Canadian females had a diagnosis of MCS by a health professional.: 37 While a 2018 study at the University of Melbourne found that 6.5% of Australian adults reported having a medical diagnosis of MCS and that 18.9 per cent reported having adverse reactions to multiple chemicals. The study also found that for 55.4% of those with MCS, the symptoms triggered by chemical exposures could be disabling.

Gulf War syndrome
Symptoms attributed to Gulf War syndrome are similar to those reported for MCS, including headache, fatigue, muscle stiffness, joint pain, inability to concentrate, sleep problems, and gastrointestinal issues.A population-based, cross-sectional epidemiological study involving American veterans of the Gulf War, non-Gulf War veterans, and non-deployed reservists enlisted both during Gulf War era and outside the Gulf War era concluded the prevalence of MCS-type symptoms in Gulf War veterans was somewhat higher than in non-Gulf War veterans. After adjusting for potentially confounding factors (age, sex, and military training), there was a robust association between individuals with MCS-type symptoms and psychiatric treatment (either therapy or medication) before deployment and, therefore, before any possible deployment-connected chemical exposures.The odds of reporting MCS or chronic multiple-symptom illness was 3.5 times greater for Gulf War veterans than non-Gulf veterans </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Frotteurism and can you explain it in depth? [/INST] Frotteurism is a paraphilic interest in rubbing, usually ones pelvic area or erect penis, against a non-consenting person for sexual pleasure. It may involve touching any part of the body, including the genital area. A person who practices frotteuristic acts is known as a frotteur.
Toucherism is sexual arousal based on grabbing or rubbing ones hands against an unexpecting (and non-consenting) person. It usually involves touching breasts, buttocks or genital areas, often while quickly walking across the victims path. Some psychologists consider toucherism a manifestation of frotteurism, while others distinguish the two. In clinical medicine, treatment of frotteuristic disorder involves cognitive behavioral therapy coupled with the administration of an SSRI.

Etymology and history
Frotteuristic acts were probably first interpreted as signs of a psychological disorder by French psychiatrist Valentin Magnan, who described three acts of "frottage" in an 1890 study. "Frottage" derives from the French verb frotter, meaning "to rub". Frotteur is a French noun literally meaning "one who rubs". It was popularized by German sexologist Richard von Krafft-Ebing in his book Psychopathia Sexualis, borrowing from Magnans French terminology </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Bicuspid aortic valve and can you explain it in depth? [/INST] Bicuspid aortic valve (aka BAV) is a form of heart disease in which two of the leaflets of the aortic valve fuse during development in the womb resulting in a two-leaflet (bicuspid) valve instead of the normal three-leaflet (tricuspid) valve. BAV is the most common cause of heart disease present at birth and affects approximately 1.3% of adults. Normally, the mitral valve is the only bicuspid valve and this is situated between the hearts left atrium and left ventricle. Heart valves play a crucial role in ensuring the unidirectional flow of blood from the atrium to the ventricles, or from the ventricle to the aorta or pulmonary trunk. BAV is normally inherited.

Signs and symptoms
In many cases, a bicuspid aortic valve will cause no problems. People with BAV may become tired more easily than those with normal valvular function and have difficulty maintaining stamina for cardio-intensive activities due to poor heart performance caused by stress on the aortic wall.

Complications
Calcification
BAV may become calcified later in life, which may lead to varying degrees of severity of aortic stenosis that will manifest as murmurs. If the leaflets do not close correctly, aortic regurgitation can occur. If these become severe enough, they may require heart surgery. The heart is put under more stress in order to either pump more blood through a stenotic valve or attempt to circulate regurgitation blood through a leaking valve. Ultimately there is a risk of rupture in the aortic valve due to bicuspid aortopathy which is a result of progressive aortic dilation from the stress of having only two values where three are normal.

Aortic lesions
One of the most notable associations with BAV is the tendency for these patients to present with ascending aortic aneurysmal lesions.
The extracellular matrix of the aorta in patients with BAV shows marked deviations from that of the normal tricuspid aortic valve.
It is currently believed that an increase in the ratio of MMP2 (Matrix Metalloproteinases 2) to TIMP1 (tissue inhibitors of metalloproteinase) may be responsible for the abnormal degradation of the valve matrix and therefore lead to aortic dissection and aneurysm. However, other studies have also shown MMP9 involvement with no differences in TIMP expression. The size of the proximal aorta should be evaluated carefully during the workup. The initial diameter of the aorta should be noted and annual evaluation with CT scan, or MRI to avoid ionizing radiation, should be recommended to the patient; the examination should be conducted more frequently if a change in aortic diameter is seen. From this monitoring, the type of surgery that should be offered to the patient can be determined based on the change in size of the aorta.

Aortic narrowing
A bicuspid aortic valve may cause the hearts aortic valve to narrow (aortic stenosis). This narrowing prevents the valve from opening fully, which reduces or blocks blood flow from the heart to the body. In some cases, the aortic valve does not close tightly, causing blood to leak backward into the left ventricle.Coarctation of the aorta (a congenital narrowing in the region of the ductus arteriosus) has also been associated with BAV.

Pathophysiology
Fusion of aortic valve leaflets occurs most commonly (≈80%) between the right coronary and left coronary leaflets (RL), which are the anterior leaflets of the aortic valve. Fusion also occurs between the right coronary and noncoronary leaflets (RN, ≈17%), and least commonly between the noncoronary and left coronary leaflets (≈2%). In comparison to other fusion patterns, RN leaflet fusion has a stronger association with future complications such as aortic valve regurgitation and stenosis. However, all fusion patterns associate with a specific area or areas of dilated enlargement in either the root of the ascending aorta, the ascending aorta, or the transverse aortic arch.

Hemodynamics
Identifying hemodynamic patterns in the aorta after left ventricle systole aids in predicting consequential complications of bicuspid aortic valve. The patient-specific risk of developing complications such as aortic aneurysms is dependent on the particular aortic leaflet fusion pattern, with each pattern varying in 4D MRI measurements of wall shear stress (WSS), blood flow velocity, asymmetrical flow displacement and flow angle of the aorta.BAV outflow is helical and occurs at high velocities (>1 m/s) throughout the ascending aorta. This is potentially more damaging to the aorta in comparison to the streamline flow and short-lived burst of high velocity at the beginning of the aorta, as seen within a healthy tricuspid valve. This eccentric outflow from the BAV results in blood hitting and reflecting off the aortic wall in a non-streamline fashion.  The specific zones where blood hits is dependent on the varying BAV leaflet fusion patterns and consequently correlates with increases in WSS. WSS measurements in RL fusion indicate an increase in pressure applied predominantly to the right-anterior side of the vessel wall, while RN fusion increases WSS on the right-posterior wall. The resulting rise in WSS is supported by the asymmetrical displacement of blood flow produced by an increased angle of outflow from the BAV. Displacement is measured as the distance in millimeters from the center of the aorta to the center of the high velocity outflow. Blood does not flow centrally through the aorta in BAV, but along the right-anterior and right-posterior vessel wall for RL and RN leaflet fusion respectively.

Aortic disease
Identification of hemodynamics for RL, RN, and left coronary and noncoronary leaflet fusion patterns enables detection of specific aortic regions susceptible to dysfunction and the eventual development of disease. Specifically, RL and RN fusion patterns are more likely to develop into these aortic disease states. The blood flow information associated with RL fusion causes dilation of the mid-ascending aorta, while RN fusion is associated with dilation in the root, distal ascending aorta and transverse arch. BAV helical and high velocity outflow patterns are consistent with aortic dilation hemodynamics seen in those with tricuspid aortic valves. However, it is the increase and variance in WSS and flow displacement in BAV that demonstrate the importance of aortic leaflet morphology. Flow displacement measurements taken from 4D MRI may be best for detecting irregularities in hemodynamics. Displacement measurements were highly sensitive and distinguishable between different valve morphologies. Hemodynamic measurements from 4D MRI in patients with BAV are advantageous in determining the timing and location of repair surgery to the aorta in aortopathy states.Most patients with bicuspid aortic valve whose valve becomes dysfunctional will need careful follow-up and potentially valve replacement at some point in life. Regular EchoCG and MRI may be performed.If the valve is normally functioning or minimally dysfunctional, average lifespan is similar to that of those without the anomaly.

Diagnosis
A bicuspid aortic valve can be associated with a heart murmur located at the right second intercostal space. Often there will be differences in blood pressures between upper and lower extremities </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Left ventricular thrombus and can you explain it in depth? [/INST] Left ventricular thrombus is a blood clot (thrombus) in the left ventricle of the heart. LVT is a common complication of acute myocardial infarction (AMI). Typically the clot is a mural thrombus, meaning it is on the wall of the ventricle. The primary risk of LVT is the occurrence of cardiac embolism, in which the thrombus detaches from the ventricular wall and travels through the circulation and blocks blood vessels. Blockage can be especially damaging in the heart or brain (stroke).

Pathophysiology
LVT occurs most often during the first 2 weeks following AMI. AMI patients most at risk display the 3 characteristics of Virchows triad:

Stagnation of blood
The risk of LVT formation increases as infarction size increases. A larger infarction means a larger area of tissue injury, which may be akinetic or dyskinetic, resulting in stagnation of ventricular blood.

Endothelial injury
Monocytes and macrophages play important roles in healing after myocardial infarction. With the absence of monocytes and macrophages, chances of LVT formation are very high. Failure to clear cellular debris from the infarct compromises the endothelial lining of the left ventricle and exposes the damaged tissue to the blood. The response is to build a thrombus composed of fibrin, red blood cells and platelets.

Hypercoagulable state
For several days after AMI, the levels of tissue factor and D-dimer, which are involved in coagulation, are high, which increases the risk of LVT formation. LVT may be good for the heart when tissues are severely damaged because it acts to thicken the wall, thus protecting it against rupture.

Diagnosis
Echocardiography is the main diagnostic tool for LVT </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Obstructed labour and can you explain it in depth? [/INST] Obstructed labour, also known as labour dystocia, is when the baby does not exit the pelvis during childbirth due to being physically blocked, despite the uterus contracting normally. Complications for the baby include not getting enough oxygen which may result in death. It increases the risk of the mother getting an infection, having uterine rupture, or having post-partum bleeding. Long-term complications for the mother include obstetrical fistula. Obstructed labour is said to result in prolonged labour, when the active phase of labour is longer than 12 hours.The main causes of obstructed labour include: a large or abnormally positioned baby, a small pelvis, and problems with the birth canal. Abnormal positioning includes shoulder dystocia where the anterior shoulder does not pass easily below the pubic bone. Risk factors for a small pelvis include malnutrition and a lack of exposure to sunlight causing vitamin D deficiency. It is also more common in adolescence as the pelvis may not have finished growing by the time they give birth. Problems with the birth canal include a narrow vagina and perineum which may be due to female genital mutilation or tumors. A partograph is often used to track labour progression and diagnose problems. This combined with physical examination may identify obstructed labour.The treatment of obstructed labour may require cesarean section or vacuum extraction with possible surgical opening of the symphysis pubis. Other measures include: keeping the women hydrated and antibiotics if the membranes have been ruptured for more than 18 hours. In Africa and Asia obstructed labor affects between two and five percent of deliveries. In 2015 about 6.5 million cases of obstructed labour or uterine rupture occurred. This resulted in 23,000 maternal deaths down from 29,000 deaths in 1990 (about 8% of all deaths related to pregnancy). It is also one of the leading causes of stillbirth. Most deaths due to this condition occur in the developing world.

Cause
The main causes of obstructed labour include: a large or abnormally positioned baby, a small pelvis, and problems with the birth canal.  Both the size and the position of the fetus can lead to obstructed labor. Abnormal positioning includes shoulder dystocia where the anterior shoulder does not pass easily below the pubic bone. A small pelvis of the mother can be a result of many factors. Risk factors for a small pelvis include malnutrition and a lack of exposure to sunlight causing vitamin D deficiency. A deficiency in calcium can also result in a small pelvis as the structures of the pelvic bones will be weak due to the lack of calcium. A relationship between maternal height and pelvis size is present and can be used to predict the possibility of obstructed labor. This relationship is a result of the mothers nutritional health throughout her life leading up to childbirth. Younger mothers are also at more risk for obstructed labor due to growth of the pelvis not being completed. Problems with the birth canal include a narrow vagina and perineum which may be due to female genital mutilation or tumors. All of these factors lead to a failure in the progress of labor.

Evolution
Obstructed labor is more common in humans than any other species and continues to be a main cause of birth complications today. Modern humans have morphologically evolved to survive as bipeds, however, bipedalism has resulted in skeletal changes that have consequently narrowed the pelvis and the birth canal. The combination of increased brain size and changes in pelvic structure are the major contributors of obstructed labor in modern humans. It is also common for obstructed labor in humans to be caused by the fetus’ broad shoulders. However, morphological shifts in pelvic structure still account for the inability of a fetus to effectively pass through the birth canal without major complications Other primates have a wider and straighter birth canal that allows a fetus to pass through more effectively. Mismatch between birth canal size and infant cranial width and length due to bipedal locomotion requirements have often been referred to as the obstetric dilemma, since compared to other great apes, modern humans have the greatest disproportion between infant cranial size and birth canal size. Shrinking of upper extremities and curvature of the spine have also affected the way modern humans give birth. Quadruped apes have longer upper limbs that allow them to reach down and pull their fetus out of the birth canal unassisted. Other primates also have a wider and straighter birth canal that allows a fetus to pass through more effectively. Modern human’s shorter upper extremities and evolution of bipedal locomotion may have placed a premium on assistance during labor. For this reason, researchers argue that assisted labor may have evolved with bipedalism. Obstructed labor has been documented as a complication of childbirth since the field of obstetrics originated. For over 1,000 years obstetricians have had to forcibly remove obstructed labor fetuses to prevent the death of the mother.Prior to the existence of the cesarean section, fetuses that were obstructed had a low survival rate. Even in the 21st century, if obstructed labor is left untreated, it could result in mother and infant death. Although surgical removal of the fetus is the preferred method of managing obstructed labor, manual removal using medical tools is also common.Obstructed labor is unique to humans compared to other primates. The evolution of humans to become obligate bipedal and increase in brain size create the problems associated with obstructed labor. In order for bipedal locomotion to be possible, many changes had to occur to the skeletal structure of humans, especially in the pelvis. Both the shape and orientation of the pelvis changed. Other primates have straighter and wider pelvises compared to humans. A narrow pelvis is better for bipedal locomotion but makes childbirth more difficult. The pelvis is sexually dimorphic, with females having a wider pelvis to be better suited for childbirth. However, the female pelvis still must accommodate for bipedal locomotion which is what creates the challenges for obstructed labor. The brain size of humans has also increased as the species has evolved, resulting in a larger head of the fetus that must exit the womb. This requires human infants to be born less developed when compared to other species. The bones of the skull are not yet fused when a human infant is born in order to prevent the head from becoming too large to exit the womb. However, the head of the fetus is still large and poses the possibility for obstructed labor.

Diagnosis
Obstructed labour is usually diagnosed based on physical examination. Ultrasound can be used to predict malpresentation of the fetus. In examination of the cervix once labor has begun, all examinations are compared to regular cervical assessments. The comparison between the average cervical assessment and the current state of the mother allows for a diagnosis of obstructed labor. An increasingly long time in labor also indicates a mechanical issue that is preventing the fetus from exiting the womb.

Prevention
Access to proper health services can reduce the prevalence of obstructed labor. Less developed areas have inadequate health services to attend to obstructed labor, resulting in a higher prevalence among less developed area. Improving nutrition of female, both before and during pregnancy, is important for reducing the risk of obstructive labor. Creating education programs about reproduction and increasing access to reproductive services such as contraception and family planning in developing areas can also reduce the prevalence of obstructed labor.

Treatment
Before considering surgical options, changing the posture of the mother during labor can help to progress labor. The treatment of obstructed labour may require cesarean section or vacuum extraction with possible surgical opening of the symphysis pubis. Caesarean section is an invasive method but is often the only method that will save the lives of both the mother and the infant. Symphysiotomy is the surgical opening of the symphysis pubis. This procedure can be completed more rapidly than Caesarean sections and does not require anesthesia, making it a more accessible option in places with less advanced medical technology. This procedure also leaves no scars on the uterus which makes further pregnancies and births safer for the mother. Another important factor in treating obstructed labor is monitoring the energy and hydration of the mother. Contractions of the uterus require energy, so the longer the mother is in labor the more energy she expends. When the mother is depleted of energy, the contractions become weaker and labor will become increasingly longer. Antibiotics are also an important treatment as infection is a possible result of obstructed labor.

Prognosis
If cesarean section is obtained in a timely manner, prognosis is good </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Erythema marginatum and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Organic personality disorder and can you explain it in depth? [/INST] Organic personality disorder (OPD) or secondary personality change, is a condition described in the ICD-10 and ICD-11 respectively. It is characterized by a significant personality change featuring abnormal behavior due to an underlying traumatic brain injury or another pathophysiological medical condition affecting the brain. Abnormal behavior can include but is not limited to apathy, paranoia and disinhibition.In the ICD-10, it is described as a mental disorder and not included in the classification group of personality disorders. In the ICD-11, it is described as a syndrome. The condition has not been described in any edition of the Diagnostic and Statistical Manual of Mental Disorders.

Signs and symptoms
OPD is associated with a large variety of symptoms, such as deficits in cognitive function, dysfunctional/abnormal behaviour, psychosis, neurosis, higher irritability and altered emotional expression. Those with OPD can experience emotional lability, meaning that their emotional expressions are unstable and fluctuating. In addition, patients may show a reduction in ability of perseverance with goals and they disinhibition, often characterised by inappropriate sexual and antisocial behavior. Those affected can experience cognitive disturbances, suspiciousness and paranoia. Altered language processing in the brain can also occur. Furthermore, patients may show changes in their sexual preference and hyposexuality symptoms.

Causes
OPD is associated with "personality change due to general medical condition". The OPD is included in a group of personality and behavioural disorders - in the ICD-10 this is "Personality and behavioural disorders due to brain disease, damage and dysfunction", and in the ICD-11 this is "Secondary Mental or Behavioural Syndromes Associated with Disorders or Diseases Classified Elsewhere". This mental health disorder can be caused by disease, brain damages or dysfunctions in specific brain areas in frontal lobe. The most common reason for this profound change in personality is the traumatic brain injury. Children whose brain areas have been injured or damaged, may present with attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder or OPD.OPD is most often caused by lesions in three brain areas of frontal lobe: traumatic brain injuries in orbitofrontal cortex, anterior cingulate cortex and dorsolateral prefrontal cortex. OPD may also be caused by lesions in other circumscribed brain areas.Another common feature of personality of patients with OPD is their dysfunctional and maladaptive behaviour that causes serious problems in these patients, because they face problems with pursuit and achievement of their goals. Patients with OPD express a feeling of unreasonable satisfaction and euphoria. Patients can show aggressive behaviour and these dysfunctions in behaviour can have effects on interpersonal relationships. One explanation of signs of anger and aggression is due to an inability to handle their impulses, this type of aggression being called "impulsive aggression".

Diagnosis
ICD-11
In the ICD-11, the condition is called secondary personality change rather than organic personality disorder. To meet diagnosis there must be a clinically significant personality disturbance that represents a change from the individual’s previous characteristic personality pattern. This personality disturbance must be explainable directly as a result from a pathophysiological health condition affecting the brain. The duration, onset, and remission of the health condition, along with responses to treatment of the underlying health condition, must be consistent with presentations of the personality disturbance.
There are seven sub-classifications of secondary personality change based on disturbances of affect, which includes "constricted", "blunted", "flat", "labile" and "inappropriate", along with other specified and unspecified categories.

ICD-10
In the ICD-10 there were no specifically listed diagnostic criteria. It is characterized by "a significant alteration of the habitual patterns of behaviour displayed by the subject premorbidly, involving the expression of emotions, needs and impulses." Cognition, thought functions and sexuality are mentioned as potentially altered or affected. Two "organic" and three "syndrome" underlying causes are mentioned respectively: "pseudopsychopathic personality", "pseudoretarded personality", "frontal lobe damage", "limbic epilepsy personality" and post-lobotomy.

Differential diagnosis
Being an organic disorder, differential diagnosis between mental disorders and OPD is necessary. According to the ICD-11, specific considerations for differential diagnosis include delerium, dementia, personality disorders, impulse control disorder, and addictive behavior syndrome. For differential diagnosis in the ICD-10, along with personality disorders, there are two mentioned conditions in the in the ICD-10 under the same diagnostic category "F07" for consideration: postencephalitic parkinsonism (called "postencephalitic syndrome" in the ICD-10) and post-concussion syndrome.
Patients with OPD may present similar symptoms to Huntingtons disease. The symptoms of apathy and irritability are common between these two conditions. OPD is somewhat similar to temporal lobe epilepsy, as patients who have chronic epilepsy may also express aggressive behaviours. Another similar symptom between Temporal lobe epilepsy and OPD is epileptic seizures. The symptom of epileptic seizure has influence on patients personality that means it causes behavioural alterations. Temporal lobe epilepsy is associated with the hyperexcitability of the medial temporal lobe of patients.

Treatment
Patients with OPD show a wide variety of sudden behavioural changes and dysfunctions. There is little information about the treatment of OPD </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Desquamative interstitial pneumonia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Biceps and can you explain it in depth? [/INST] The biceps or biceps brachii (Latin: musculus biceps brachii, "two-headed muscle of the arm") is a large muscle that lies on the front of the upper arm between the shoulder and the elbow. Both heads of the muscle arise on the scapula and join to form a single muscle belly which is attached to the upper forearm. While the biceps crosses both the shoulder and elbow joints, its main function is at the elbow where it flexes the forearm and supinates the forearm.  Both these movements are used when opening a bottle with a corkscrew: first biceps screws in the cork (supination), then it pulls the cork out (flexion).

Structure
The biceps is one of three muscles in the anterior compartment of the upper arm, along with the brachialis muscle and the coracobrachialis muscle, with which the biceps shares a nerve supply. The biceps muscle has two heads, the short head and the long head, distinguished according to their origin at the coracoid process and supraglenoid tubercle of the scapula, respectively. From its origin on the glenoid, the long head remains tendinous as it passes through the shoulder joint and through the intertubercular groove of the humerus. Extending from its origin on the coracoid, the tendon of the short head runs adjacent to the tendon of the coracobrachialis as the conjoint tendon. Unlike the other muscles in the anterior compartment of the arm, the biceps muscle crosses two joints, the shoulder joint and the elbow joint.
Both heads of the biceps join in the middle upper arm to form a single muscle mass usually near the insertion of the deltoid to form a common muscle belly, although several anatomic studies have demonstrated that the muscle bellies remain distinct structures without confluent fibers. As the muscle extends distally, the two heads rotate 90 degrees externally before inserting onto the radial tuberosity. The short head inserts distally on the tuberosity while the long head inserts proximally closer to the apex of the tuberosity. The bicipital aponeurosis, also called the lacertus fibrosus, is a thick fascial band that organizes close to the musculotendinous junction of the biceps and radiates over and inserts onto the ulnar part of the antebrachial fascia.The tendon that attaches to the radial tuberosity is partially or completely surrounded by a bursa, the bicipitoradial bursa, which ensures frictionless motion between the biceps tendon and the proximal radius during pronation and supination of the forearm.Two muscles lie underneath the biceps brachii. These are the coracobrachialis muscle, which like the biceps attaches to the coracoid process of the scapula, and the brachialis muscle which connects to the ulna and along the mid-shaft of the humerus. Besides those, the brachioradialis muscle is adjacent to the biceps and also inserts on the radius bone, though more distally.

Variation
Traditionally described as a two-headed muscle, biceps brachii is one of the most variable muscles of the human body and has a third head arising from the humerus in 10% of cases (normal variation)—most commonly originating near the insertion of the coracobrachialis and joining the short head—but four, five, and even seven supernumerary heads have been reported in rare cases.One study found a higher than expected number of female cadavers with a third head of biceps brachii, equal incidence between sides of the body, and uniform innervation by musculocutaneous nerve.The distal biceps tendons are completely separated in 40% and bifurcated in 25% of cases.

Nerve supply
The biceps shares its nerve supply with the other two muscles of the anterior compartment. The muscles are supplied by the  musculocutaneous nerve. Fibers of the fifth, sixth and seventh cervical nerves make up the components of the musculocutaneous nerve which supply the biceps.

Blood supply
The blood supply of the biceps is the brachial artery. The distal tendon of the biceps can be useful for palpating the brachial pulse, as the artery runs medial to the tendon in the cubital fossa.

Function
The biceps works across three joints.  The most important of these functions is to supinate the forearm and flex the elbow. Besides, the long head of biceps prevents the upward displacement of the head of the humerus. In more detail, the actions are, by joint:
Proximal radioulnar joint of the elbow – The biceps brachii functions as a powerful supinator of the forearm, i.e. it turns the palm upwards. This action, which is aided by the supinator muscle, requires the humeroulnar joint of the elbow to be at least partially flexed. If the  humeroulnar joint, is fully extended, supination is then primarily carried out by the supinator muscle. The biceps is a particularly powerful supinator of the forearm due to the distal attachment of the muscle at the radial tuberosity, on the opposite side of the bone from the supinator muscle. When flexed, the biceps effectively pulls the radius back into its neutral supinated position in concert with the supinator muscle.: 346–347
Humeroulnar joint of the elbow – The biceps brachii also functions as an important flexor of the forearm, particularly when the forearm is supinated. Functionally, this action is performed when lifting an object, such as a bag of groceries or when performing a biceps curl. When the forearm is in pronation (the palm faces the ground), the brachialis, brachioradialis, and supinator function to flex the forearm, with minimal contribution from the biceps brachii. It is also important to note that regardless of forearm position, (supinated, pronated, or neutral) the force exerted by the biceps brachii remains the same; however, the brachioradialis has a much greater change in exertion depending on position than the biceps during concentric contractions. That is, the biceps can only exert so much force, and as forearm position changes, other muscles must compensate.
Glenohumeral joint (shoulder joint) – Several weaker functions occur at the glenohumeral joint. The biceps brachii weakly assists in forward flexion of the shoulder joint (bringing the arm forward and upwards). It may also contribute to abduction (bringing the arm out to the side) when the arm is externally (or laterally) rotated. The short head of the biceps brachii also assists with horizontal adduction (bringing the arm across the body) when the arm is internally (or medially) rotated. Finally, the short head of the biceps brachii, due to its attachment to the scapula (or shoulder blade), assists with stabilization of the shoulder joint when a heavy weight is carried in the arm. The tendon of the long head of the biceps also assists in holding the head of the humerus in the glenoid cavity.: 295
Motor units in the lateral portion of the long head of the biceps are preferentially activated during elbow flexion, while motor units in the medial portion are preferentially activated during forearm supination.The biceps are usually attributed as representative of strength within a variety of worldwide cultures.

Clinical significance
The proximal tendons of the biceps brachii are commonly involved in pathological processes and are a frequent cause of anterior shoulder pain. Disorders of the distal biceps brachii tendon include insertional tendonitis and partial or complete tears of the tendon. Partial tears are usually characterized by pain and enlargement and abnormal contour of the tendon. Complete tears occur as avulsion of the tendinous portion of the biceps away from its insertion on the tuberosity of the radius, and is often accompanied by a palpable, audible "pop" and immediate pain and soft tissue swelling.A soft-tissue mass is sometimes encountered in the anterior aspect of the arm, the so-called Reverse Popeye deformity, which paradoxically leads to a decreased strength during flexion of the elbow and supination of the forearm.

Tendon rupture
Tears of the biceps brachii may occur during athletic activities, however avulsion injuries of the distal biceps tendon are frequently occupational in nature and sustained during forceful, eccentric contraction of the biceps muscle while lifting.Treatment of a biceps tear depends on the severity of the injury.  In most cases, the muscle will heal over time with no corrective surgery. Applying cold pressure and using anti-inflammatory medications will ease pain and reduce swelling. More severe injuries require surgery and post-op physical therapy to regain strength and functionality in the muscle. Corrective surgeries of this nature are typically reserved for elite athletes who rely on a complete recovery.

Training
The biceps can be strengthened using weight and resistance training. Examples of well known biceps exercises are the chin-up and biceps curl.

Etymology and grammar
The biceps brachii muscle is the one that gave all muscles their name: it comes from the Latin musculus, "little mouse", because the appearance of the flexed biceps resembles the back of a mouse.  The same phenomenon occurred in Greek, in which μῦς, mȳs, means both "mouse" and "muscle".The term biceps brachii is a Latin phrase meaning "two-headed [muscle] of the arm", in reference to the fact that the muscle consists of two bundles of muscle, each with its own origin, sharing a common insertion point near the elbow joint. The proper plural form of the Latin adjective biceps is bicipites, a form not in general English use </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Pes anserinus (leg) and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Limbal stem cell and can you explain it in depth? [/INST] Limbal stem cells, also known as corneal epithelial stem cells, are stem cells located in the basal epithelial layer of the corneal limbus. They form the border between the cornea and the sclera. Characteristics of limbal stem cells include a slow turnover rate, high proliferative potential, clonogenicity, expression of stem cell markers, as well as the ability to regenerate the entire corneal epithelium. Limbal stem cell proliferation has the role of maintaining the cornea; for example, by replacing cells that are lost via tears. Additionally, these cells also prevent the conjunctival epithelial cells from migrating onto the surface of the cornea.

Medical conditions and treatments
Damage to the limbus can lead to limbal stem cell deficiency (LSCD); this may be primary - related to an insufficient stromal microenvironment to support stem cell functions, such as aniridia, and other congenital conditions, or secondary – caused by external factors that destroy the limbal stem cells, such as chemical or thermal burns, radiation, surgery, infection, use of contact lenses, or certain drugs.
Signs and symptoms include: conjunctivalisation, corneal vascularisation, edema, ocular discomfort or pain, visual impairment, and blindness, which are likely associated with failure in the process of regenerating the corneal epithelium.
Immediate management aims to limit traumatic or chemical damage to the limbus, control inflammation, and help achieve a healthy corneal epithelium. Initial treatment after trauma/injury includes preservative-free artificial tears, topical steroids, ‘bandage’ contact lenses, and autologous eye drops (eye drops manufactured from the patients own blood serum and plasma). Once the corneal surface has stabilized, surgery is the main approach to treatment.
Types of surgeries:

In the case of a partial LSCD:, a sequential sector conjunctival epitheliectomy (SSCE) can be performed to remove any tissue (pannus) that has grown over the cornea. This procedure is sometimes used as a temporary measure until further surgical interventions are possible.
Transplantation of amniotic membrane from a placenta may also help. Although amniotic membrane does not have stem cells of its own, it supports regeneration of limbal stem cells. However, further surgical intervention may be needed if these approaches are unsuccessful, or when disease is more severe.
Conjunctival limbal autograft (CLAU) involves transplantation of limbal tissue from a patients healthy eye. As the procedure is achieved by transplanting autologous limbal stem cells from the patients healthy eye, there is no risk of immune rejection, and hence no need for systemic immunosuppression. However, this procedure represents a risk for the donor eye, as the patient already has one eye damaged.
In the case of bilateral LSCD, where both eyes are affected, it may be possible to transplant limbal tissue from a living donor (usually a relative). This is known as a conjunctival limbal allograft (CLAL). CLAL can be performed with both partial or total LSCD, the donor tissue is usually from a sibling or parent. As with CLAU, only a part of the donor limbus can be transplanted, as a live donor is being used. Being an allogenic transplant, immunosuppression is required, due to the risk of rejection.
Kerato-limbal allograft (KLAL) involves transplantation from someone who has died and donated their organs. KLAL can be used for cases of bilateral LSCD when a living related donor is not available, or for patients with unilateral LSCD, who dont want to jeopardise their healthy eye. However, most of these types of transplant fail within five years.                                                     KLAL has a number of limitations: the graft is usually up to 24 hours old before retrieval and a further period of time is often required to screen the cadavers blood before the tissue can be used; often the limbus is found to be damaged as the tissue is not immunocompatible, there is a high risk of rejection between the recipient and the donor cadaver and studies report only a temporary success in term of transplant effectiveness, with most failing after 5 years.
A recent procedure, less invasive than CLAU, which so far has been tested only in unilateral cases, is simple limbal epithelial transplantation (SLET). In this procedure, healthy limbal tissue from the patients good eye is cut into a number of pieces and transferred directly to human amniotic membrane covering the cornea in the damaged eye. Studies published so far have only investigated the procedure in unilaterally affected patients, and the long-term effectiveness of the technique is yet to be proven.
Another recent innovation is cultivated limbal epithelial transplant (CLET), either autologous (where donor and recipient are the same patient) or allogenic (where donor and recipient are different patients). This approach can be used when either one or both eyes are affected, providing there is sufficient limbal tissue available (1–2 mm2). A small sample of limbal cells is taken from a healthy part of the eye, and grown in a sterile laboratory to produce a sheet of cells sufficient for transplantation. Once transplanted, they multiply and regrow the corneal epithelium. The manufacturing process is designed to ensure implantation of the right number, size and quality of cells. CLET avoids some of the issues faced by other limbal transplantation procedures and does not pose a threat to the integrity of the donor eye. It also offers the possibility of re-grafting in case of failure of the first graft or need for a further graft.

Types
There are three types of clonogenic keratinocytes involved in the generation of the corneal epithelium: holoclones, meroclones and paraclones.                                                                    1- Holoclones: as true stem cells, have the greatest growth potential, and give rise to               2-meroclones, which have a much lower proliferative capacity, but frequently divide.             3- Paraclones have even lower proliferative capacity. Both meroclones and paraclones are known as transient amplifying cells and their purpose is to form a stratified squamous epithelium. All three types of keratinocytes are present in the basal layer of the limbus, with holoclones in the least abundance (10%–15%). The basal layer of the cornea is populated by meroclones and paraclones at the periphery, and only paraclones in the central cornea, reflecting the above process of cell division and differentiation. Holoclones are identified by high expression of the marker p63 and are also known as p63 bright cells.

Society and culture
In February 2015, the European Commission approved autologous CLET using the stem cell therapy Holoclar for people with severe LSCD due to corneal burns. This is the first time that a stem cell therapy (other than the use of umbilical cord stem cells) has been approved by any regulatory agency in the world </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Frontal fibrosing alopecia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tibial nerve and can you explain it in depth? [/INST] The tibial nerve is a branch of the sciatic nerve.  The tibial nerve passes through the popliteal fossa to pass below the arch of soleus.

Structure
Popliteal fossa
The tibial nerve is the larger terminal branch of the sciatic nerve with root values of L4, L5, S1, S2, and S3. It lies superficial (or posterior) to the popliteal vessels, extending from the superior angle to the inferior angle of the popliteal fossa, crossing the popliteal vessels from lateral to medial side. It gives off branches as shown below:
Muscular branches - Muscular branches arise from the distal part of the popliteal fossa. It supplies the medial and lateral heads of gastrocnemius, soleus, plantaris and popliteus muscles. Nerve to popliteus crosses the popliteus muscle, runs downwards and laterally, winds around the lower border of the popliteus to supply the deep (or anterior) surface of the popliteus. This nerve also supplies the tibialis posterior muscle, superior tibiofibular joint, tibia bone, interosseous membrane of leg, and the inferior tibiofibular joint.
Cutaneous branches - Tibial nerve also gives off a cutaneous nerve called the medial sural nerve from the middle of the popliteal fossa and exits at the inferior angle. It supplies the skin of the lower half of the back of the leg and lateral border of the foot until the tip of the little toe.
Articular branches - There are three articular branches arises from the upper part of the fossa: superior medial genicular nerve (located on the surface of medial condyle of femur, middle genicular nerve (pierces the posterior capsule of the knee joint to supply the structures located in the intercondylar notch of the femur, and inferior genicular nerve (runs along the upper border of the popliteus to reach the medial condyle of tibia).

Back of the leg
At the inferior angle of the popliteal fossa, tibial nerve passes deep to the tendinous arch of soleus to enter the back of the leg. In the leg, it runs downwards and medially to reach the posteromedial side of the ankle, midway between the medial malleolus and medial tubercle of the calcaneum. It terminates deep to the flexor retinaculum at the origin of the abductor hallucis by dividing into medial and lateral plantar nerves to supply the foot. The tibial nerve gives off several branches to supply the back of the leg:
Muscular branches - Supplies tibialis posterior, flexor digitorum longus, flexor hallucis longus, and deep part of soleus.
Cutaneus branches - The medial calcaneal nerve pierces the flexor retinaculum to supply the skin of the back and lower surface of the heel.
Articular branches - Supplies the ankle joint

Foot
In the foot, the nerve terminates by dividing into medial and lateral plantar branches.

Medial plantar nerve - It is the larger terminal branch of the tibial nerve. It passes between the abductor hallucis and flexor digitorum brevis to divide further into branches. Its distribution resembles to that of the distribution of median nerve in the hand. Its muscular branches supply the abductor hallucis, the flexor digitorum brevis, the flexor hallucis brevis and the first lumbrical. Cutaneous distribution of the medial plantar nerve supplies the medial sole and medial three and one half toes through four digital branches. Each digital branch give off a dorsal branch to supply the nail beds on the dorsum </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Dentin dysplasia and can you explain it in depth? [/INST] Dentin dysplasia (DD) is a rare genetic developmental disorder affecting dentine production of the teeth, commonly exhibiting an autosomal dominant inheritance that causes malformation of the root. It affects both primary and permanent dentitions in approximately 1 in every 100,000 patients. It is characterized by presence of normal enamel but atypical dentin with abnormal pulpal morphology. Witkop in 1972 classified DD into two types which are Type I (DD-1) is the radicular type, and type II (DD-2) is the coronal type. DD-1 has been further divided into 4 different subtypes (DD-1a,1b,1c,1d) based on the radiographic features.

Signs and symptoms
Clinically the teeth look normal in colour and morphologic appearance; however, they are commonly very mobile and exfoliated prematurely.Both primary and permanent dentitions can be affected by either type I or type II dentin dysplasia. However, deciduous teeth affected by type II dentin dysplasia have a characteristic blue-amber discolouration, whilst the other dentition appears normal.

Causes
The mutation in collagen type 1 (COL1 A1, COL1 A2) causes DI-1. It is similar to the systemic condition dental features known as osteogenesis imperfect. DI-2, DI-3 and DD-2 share the same genetic mutation of dentin sialophosphoprotein, that is located on chromosome 4. They are autosomal-dominant diseases with complete penetrance and variable expressivity. Due to the same genetic mutation, these diseases would often result in overlapping clinical and radiographic features. Therefore, prevailing theories suggests that DI-2, DI-3 and DD-2 are categorized as a single disease entity with variable severity of expression. However, the causes of DD-1 have yet to be theorized.

Diagnosis
Diagnosis is mostly based on general examination and radiographs, and it should be taken when abnormality of the teeth is suspected as most of the affected teeth have normal clinical appearance.Differential diagnosis is very important to have a definitive diagnosis as some radiographic or histologic features of dentine dysplasia may bear a resemblance to different disorders:
Dentinogenesis imperfecta
Odontodysplasia
Calcinosis
Osteogenesis imperfecta
Ehlers–Danlos syndromes
Goldblatt syndrome
Schimke immuno-osseous dysplasia
Brachio-skeleto-genital syndrome.

Type I: Radicular type
Type I has been known as radicular dentine dysplasia because the teeth have undeveloped root(s) with abnormal pulp tissue. Morphology and colour of the crown mostly appear normal, but occasionally teeth appear slightly amber coloured or bluish-brown shine in primary teeth with no or only immature root development. The teeth are mostly maligned and have higher risk of fracture.

Radiographic feature
In other words, affected primary teeth usually have abnormal shaped or shorter than normal roots. “Crescent/half-moon shaped” pulp chamber remnant in permanent teeth can be seen on x-rays. The roots may appear to be darker or radiolucent/pointy and short with apical constriction. Dentine is laid down abnormally and causes excessive growth within the pulp chamber. This will reduce the pulp space and eventually cause incomplete and total pulp chamber obliteration in permanent teeth. Sometimes periapical pathology or cysts can be seen around the root apex. Most cases of DD associated with peri-apical radiolucency/ pathology have been diagnosed as radicular cysts, but some of them have been as diagnosed peri-apical grauloma instead.

Type II: Coronal type
Type II would mostly cause discolouration to the primary teeth. Affected teeth usually appear as brownish-blue, brown or yellow. Translucent “opalescence” is often one of the characteristics to describe teeth with DD-2. In some cases teeth might show slightly amber coloured but in most of the cases permanent teeth are unaffected and appear normal regardless of colour, shape and size. Dental X-rays are the key to diagnose dentine dysplasia, especially on permanent teeth. Abnormalities of the pulp chamber is the main characteristic to make a definitive diagnosis.In the primary teeth, coronal dentin dysplasia may appear similar to Dentinogenesis Imperfecta type II (DG-II) but if abnormalities features appear to be more pronounced in the permanent teeth, then consider changing the diagnosis to DGI-II instead of DD-2.

Radiographic features
In coronal type, teeth show normal roots containing enlarged pulp with abnormal extensions towards the roots, which is often described as “thistle tube” shaped on dental radiographs. As well as this, numerous pulp stones can be often found in the pulp chambers due to abnormal calcifications. In primary teeth, the pulp chamber is usually completely obliterated but in permanent teeth, the pulp may become partially obliterated after eruption.

Histological features
There are a few studies and proposals that were designed to explain the pathogenesis of DD but the main reason of the cause still remains unclear in the dental literature. Logan et al., suggested that dental papilla is the cause of abnormal root growth or development. They also proposed that calcification of multiple degenerative foci within the papillae reduce the growth and eventually leads to pulpal obliteration. Wesley et al., suggested that odontoblasts with abnormal function and/ or differentiation are mainly due to atypical interaction between odontoblasts and ameloblasts. Histopathologically, deeper layer of the teeth shows abnormal dentine tubular pattern with unstructured, unorganised, atubular areas with normal enamel appearance. Globular or small mass of rounded or irregular shape of atypical dentine is often seen in the pulp.

Treatment
With various options available to dentists, the treatment of this condition can still be difficult. Endodontic treatment is not advised for teeth with complete obliteration of root canals and pulp chambers. An alternative treatment for teeth with periapical abscesses and pulpal necrosis is dental extraction. Retrograde fillings and periapical surgery is a treatment option for teeth with longer roots, as well as orthodontic treatment. However, orthodontic treatment can lead to even more resorption of the roots, which could lead to further tooth mobility and premature exfoliation. Another proposed treatment, for successful oral rehabilitation, is to extract all teeth, curette any cysts and provide the patient with a complete denture. A combination of bone grafting and a sinus lift technique can also be successful to accomplish implant placement.

Management
The best method of maintaining the health of teeth is to practice exemplary oral hygiene. More tooth loss is likely to occur if intervention takes place </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Potts puffy tumor and can you explain it in depth? [/INST] Potts puffy tumor, first described by Sir Percivall Pott in 1760, is a rare clinical entity characterized by subperiosteal abscess associated with osteomyelitis. It is characterized by an osteomyelitis of the frontal bone, either direct or through haematogenic spread. This results in a swelling on the forehead, hence the name. The infection can also spread inwards, leading to an intracranial abscess. Potts puffy tumor can be associated with cortical vein thrombosis, epidural abscess, subdural empyema, and brain abscess.
The cause of vein thrombosis is explained by venous drainage of the frontal sinus, which occurs through diploic veins, which communicate with the dural venous plexus; septic thrombi can potentially evolve from foci within the frontal sinus and propagate through this venous system. This type of chronic osteomyelitis of the frontal bone is confused with acute sub-periosteal abscess of the frontal bone, which presents as a discrete collection over the frontal sinus.
Although it can affect all ages, it is mostly found among teenagers and adolescents. It is usually seen as a complication of frontal sinusitis or trauma.  Medical imaging can be of use in the diagnosis and evaluation of the underlying cause and extent of the condition.  Ultrasound is able to identify frontal bone osteomyelitis, while computed tomography (CT) can evaluate bony erosion, and along with magnetic resonance imaging (MRI), can better appreciate the underlying cause and extent of possible intra-cranial extension/involvement.

Cause
Frontal sinusitis, acute or chronic.
Frontal trauma, usually blunt.
Some cases have been seen in a context of intranasal substance abuse (cocaine, methamphetamine).
Post-surgical: after frontal sinus reconstruction

Diagnosis
Diagnosis is suspected clinically and is confirmed using cross sectional imaging of the sinuses and brain. The patient typically presents with a headache overlying the frontal sinuses and an associated forehead swelling </s>