<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 Egg allergy and can you explain it in depth? [/INST] Egg allergy is an immune hypersensitivity to proteins found in chicken eggs, and possibly goose, duck, or turkey eggs. Symptoms can be either rapid or gradual in onset. The latter can take hours to days to appear. The former may include anaphylaxis, a potentially life-threatening condition which requires treatment with epinephrine. Other presentations may include atopic dermatitis or inflammation of the esophagus.In the United States, 90% of allergic responses to foods are caused by cows milk, eggs, wheat, shellfish, peanuts, tree nuts, fish, and soy beans.  The declaration of the presence of trace amounts of allergens in foods is not mandatory in any country, with the exception of Brazil.Prevention is by avoiding eating eggs and foods that may contain eggs, such as cake or cookies. It is unclear if the early introduction of the eggs to the diet of babies aged 4–6 months decreases the risk of egg allergies.Egg allergy appears mainly in children but can persist into adulthood. In the United States, it is the second most common food allergy in children after cows milk. Most children outgrow egg allergy by the age of five, but some people remain allergic for a lifetime. In North America and Western Europe, egg allergy occurs in 0.5% to 2.5% of children under the age of five years. The majority grow out of it by school age, but for roughly one-third, the allergy persists into adulthood. Strong predictors for adult-persistence are anaphylaxis, high egg-specific serum immunoglobulin E (IgE), robust response to the skin prick test and absence of tolerance to egg-containing baked foods.

Signs and symptoms
Food allergies usually have an onset from minutes to one to two hours. Symptoms may include: rash, hives, itching of mouth, lips, tongue, throat, eyes, skin, or other areas, swelling of lips, tongue, eyelids, or the whole face, difficulty swallowing, runny or congested nose, hoarse voice, wheezing, shortness of breath, diarrhea, abdominal pain, lightheadedness, fainting, nausea, or vomiting. Symptoms of allergies vary from person to person and may vary from incident to incident. Serious danger regarding allergies can begin when the respiratory tract or blood circulation is affected. The former can be indicated by wheezing, a blocked airway and cyanosis, the latter by weak pulse, pale skin, and fainting. When these symptoms occur the allergic reaction is called anaphylaxis. Anaphylaxis occurs when IgE antibodies are involved, and areas of the body that are not in direct contact with the food become affected and show severe symptoms. Untreated, this can proceed to vasodilation and a low blood pressure situation called anaphylactic shock.Young children may exhibit dermatitis/eczema on face, scalp and other parts of the body, in older children knees and elbows are more commonly affected. Children with dermatitis are at greater than expected risk of also exhibiting asthma and allergic rhinitis.

Causes
Eating egg
The cause is typically the eating of eggs or foods that contain eggs. Briefly, the immune system over-reacts to proteins found in eggs. This allergic reaction may be triggered by small amounts of egg, even egg incorporated into cooked foods, such as cake. People with an allergy to chicken eggs may also be reactive to goose, duck, or turkey eggs.

Vaccines
Influenza vaccines are created by injecting a live virus into fertilized chicken eggs. The viruses are harvested, killed and purified, but a residual amount of egg white protein remains. For adults ages 18 and older there is an option to receive recombinant flu vaccines (RIV3 or RIV4) which are grown on mammalian cell cultures instead of in eggs, and so are no risk for people with severe egg allergy. Recommendations are that for people with a history of mild egg allergy should receive any IIV or RIV vaccine. People with a more severe allergic reaction may also receive any IIV or RIV, but in an inpatient or outpatient medical setting, administered by a healthcare provider. People with a known severe allergic reaction to influenza vaccine (which could be egg protein or the gelatin or the neomycin components of the vaccine) should not receive a flu vaccine.Each year the American Academy of Pediatrics (AAP) publishes recommendations for prevention and control of influenza in children. In the 2016-2017 guidelines a change was made, that children with a history of egg allergy may receive the IIV3 or IIV4 vaccine without special precautions. It did, however, state that "Standard vaccination practice should include the ability to respond to acute hypersensitivity reactions." Prior to this, AAP recommended precautions based on egg allergy history: if no history, immunize; if a history of mild reaction, i.e., hives, immunize in a medical setting with healthcare professionals and resuscitative equipment available; if a history of severe reactions, refer to an allergist.The measles and mumps parts of the "MMR vaccine" (for measles, mumps, and rubella) are cultured on chick embryo cell culture and contain trace amounts of egg protein. The amount of egg protein is lower than in influenza vaccines and the risk of an allergic reaction is much lower. One guideline stated that all infants and children should get the two MMR vaccinations, mentioning that "Studies on large numbers of egg-allergic children show there is no increased risk of severe allergic reactions to the vaccines." Another guideline recommended that if a child has a known medical history of severe anaphylaxis reaction to eggs, then the vaccination should be done in a hospital center, and the child be kept for observation for 60 minutes before being allowed to leave. The second guideline also stated that if there was a severe reaction to the first vaccination - which could have been to egg protein or the gelatin and neomycin components of the vaccine - the second is contraindicated.

Exercise as a contributing factor
There is a condition called food-dependent, exercise-induced anaphylaxis (FDEIAn). Exercise can trigger hives and more severe symptoms of an allergic reaction. For some people with this condition, exercise alone is not sufficient, nor consumption of a food to which they are mildly allergic sufficient, but when the food in question is consumed within a few hours before high intensity exercise, the result can be anaphylaxis. Egg are specifically mentioned as a causative food. One theory is that exercise is stimulating the release of mediators such as histamine from IgE-activated mast cells. Two of the reviews postulate that exercise is not essential for the development of symptoms, but rather that it is one of several augmentation factors, citing evidence that the culprit food in combination with alcohol or aspirin will result in a respiratory anaphylactic reaction.

Mechanisms
Conditions caused by food allergies are classified into three groups according to the mechanism of the allergic response:
IgE-mediated (classic) – the most common type, manifesting acute changes that occur shortly after eating, and may progress to anaphylaxis
Non-IgE mediated – characterized by an immune response not involving immunoglobulin E; may occur hours to days after eating, complicating diagnosis
IgE and non-IgE-mediated – a hybrid of the above two typesAllergic reactions are hyperactive responses of the immune system to generally innocuous substances, such as proteins in the foods we eat. Why some proteins trigger allergic reactions while others do not is not entirely clear, although in part thought to be due to resistance to digestion. Because of this, intact or largely intact proteins reach the small intestine, which has a large presence of white blood cells involved in immune reactions. The heat of cooking structurally degrades protein molecules, potentially making them less allergenic.The pathophysiology of allergic responses can be divided into two phases. The first is an acute response that occurs within minutes to an hour or two exposure to an allergen. This phase can either subside or progress into a "late-phase reaction" which can substantially prolong the symptoms of a response, and result in more tissue damage. In the early stages of acute allergic reaction, lymphocytes previously sensitized to a specific protein or protein fraction react by quickly producing a particular type of antibody known as secreted IgE (sIgE), which circulates in the blood and binds to IgE-specific receptors on the surface of other kinds of immune cells called mast cells and basophils. Both of these are involved in the acute inflammatory response. Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators called (cytokines, interleukins, leukotrienes, and prostaglandins) into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth-muscle contraction. This results in runny nose, itchiness, shortness of breath, and potentially anaphylaxis. Depending on the individual, the allergen, and the mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system while eczema is localized to the skin.After the chemical mediators of the acute response subside, late-phase responses can often occur due to the migration of other white blood cells such as neutrophils, lymphocytes, eosinophils, and macrophages to the initial reaction sites. This is usually seen 2–24 hours after the original reaction. Cytokines from mast cells may also play a role in the persistence of long-term effects. Late-phase responses seen in asthma are slightly different from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils.Five major allergenic proteins from the egg of the domestic chicken (Gallus domesticus) have been identified; these are designated Gal d 1–5. Four of these are in egg white: ovomucoid (Gal d 1), ovalbumin (Gal d 2), ovotransferrin (Gal d 3) and lysozyme (Gal d 4). Of these, ovomucoid is the dominant allergen, and one that is less likely to be outgrown as children get older. Ingestion of under-cooked egg may trigger more severe clinical reactions than well-cooked egg. In egg yolk, alpha-livetin (Gal d 5) is the major allergen, but various vitellins may also trigger a reaction. People allergic to alpha-livetin may experience respiratory symptoms such as rhinitis and/or asthma when exposed to chickens, because the yolk protein is also found in live birds. In addition to IgE-mediated responses, egg allergy can manifest as atopic dermatitis, especially in infants and young children. Some will display both, so that a child could react to an oral food challenge with allergic symptoms, followed a day or two later with a flare up of atopic dermatitis and/or gastrointestinal symptoms, including allergic eosinophilic esophagitis.

Non-allergic intolerance
Egg whites, which are potentially histamine liberators, also provoke a nonallergic response in some people. In this situation, proteins in egg white directly trigger the release of histamine from mast cells. Because this mechanism is classified as a pharmacological reaction, or "pseudoallergy", the condition is considered a food intolerance instead of a true immunoglobulin E (IgE) based allergic reaction.
The response is usually localized, typically in the gastrointestinal tract. Symptoms may include abdominal pain, diarrhea, or any other symptoms typical to histamine release. If sufficiently strong, it can result in an anaphylactoid reaction, which is clinically indistinguishable from true anaphylaxis. Some people with this condition tolerate small quantities of egg whites. They are more often able to tolerate well-cooked eggs, such as found in cake or dried egg-based pasta, than incompletely cooked eggs, such as fried eggs or meringues, or uncooked eggs.

Diagnosis
Diagnosis of egg allergy is based on the persons history of allergic reactions, skin prick test (SPT), patch test and measurement of egg-specific serum immunoglobulin E (IgE or sIgE). Confirmation is by double-blind, placebo-controlled food challenges. SPT and sIgE have sensitivity greater than 90% but specificity in the 50-60% range, meaning these tests will detect an egg sensitivity, but will also be positive for other allergens. For young children, attempts have been made to identify SPT and sIgE responses strong enough to avoid the need for a confirming oral food challenge.

Prevention
When eggs are introduced to a babys diet is thought to affect risk of developing allergy, but there are contradictory recommendations. A 2016 review acknowledged that introducing peanuts early appears to have a benefit, but stated "The effect of early introduction of egg on egg allergy are controversial." A meta-analysis published the same year supported the theory that early introduction of eggs into an infants diet lowers risk, and a review of allergens in general stated that introducing solid foods at 4–6 months may result in the lowest subsequent allergy risk. However, an older consensus document from the American College of Allergy, Asthma and Immunology recommended that introduction of chicken eggs be delayed to 24 months of age.

Treatment
The mainstay of treatment is total avoidance of egg protein intake. This is complicated because the declaration of the presence of trace amounts of allergens in foods is not mandatory (see regulation of labelling).
Treatment for accidental ingestion of egg products by allergic individuals varies depending on the sensitivity of the person. An antihistamine such as diphenhydramine (Benadryl) may be prescribed. Sometimes prednisone will be prescribed to prevent a possible late phase Type I hypersensitivity reaction. Severe allergic reactions (anaphalaxis) may require treatment with an epinephrine pen, an injection device designed to be used by a non-healthcare professional when emergency treatment is warranted.

Immunotherapy
There is active research on trying oral immunotherapy (OIT) to desensitize people to egg allergens. A Cochrane Review concluded that OIT can desensitize people, but it remains unclear whether long-term tolerance develops after treatment ceases, and 69% of the people enrolled in the trials had adverse effects. They concluded there was a need for standardized protocols and guidelines prior to incorporating OIT into clinical practice. A second review noted that allergic reactions, up to anaphylaxis, can occur during OIT, and recommends this treatment not be routine medical practice. A third review limited its scope to trials of baked egg-containing goods such as bread or cake as a means of resolving egg allergy. Again, there were some successes, but also some severe allergic reactions, and the authors came down on the side of not recommending this as treatment.

Avoiding eggs
Prevention of egg-allergic reactions means avoiding eggs and egg-containing foods. People with an allergy to chicken eggs may also be allergic to other types of eggs, such as goose, duck, or turkey eggs. In cooking, eggs are multifunctional: they may act as an emulsifier to reduce oil/water separation (mayonnaise), a binder (water binding and particle adhesion, as in meatloaf), or an aerator (cakes, especially angel food). Some commercial egg substitutes can substitute for particular functions (potato starch and tapioca for water binding, whey protein or bean water for aeration or particle binding, or soy lecithin or avocado for emulsification). Food companies produce egg-free mayonnaise and other replacement foods. Alfred Bird invented egg-free Birds Custard, the original version of what is known generically as custard powder today.Most people find it necessary to strictly avoid any item containing eggs, including:

Ingredients that sometimes include egg protein include: artificial flavoring, natural flavoring, lecithin and nougat candy.
Probiotic products have been tested, and some found to contain milk and egg proteins which were not always indicated on the labels.

Prognosis
The majority of children outgrow egg allergy. One review reported that 70% of children will outgrow this allergy by 16 years. In subsequently published longitudinal studies, one reported that for 140 infants who had challenge-confirmed egg allergy, 44% had resolved by two years. A second reported that for 203 infants with confirmed IgE-mediated egg allergy, 45% resolved by two years of age, 66% by four years, and 71% by six years. Children will be able to tolerate eggs as an ingredient in baked goods and well-cooked eggs sooner than under-cooked eggs. Resolution was more likely if baseline serum IgE was lower, and if the baseline symptoms did not include anaphylaxis.

Epidemiology
In countries in North America and western Europe, where use of cows milk based infant formula is common, chicken egg allergy is the second most common food allergy in infants and young children after cows milk. However, in Japan, egg allergy is first and cows milk second, followed by wheat and then the other common allergenic foods. A review from South Africa reported egg and peanut as the two most common allergenic foods.Incidence and prevalence are terms commonly used in describing disease epidemiology. Incidence is newly diagnosed cases, which can be expressed as new cases per year per million people. Prevalence is the number of cases alive, expressible as existing cases per million people during a period of time. Egg allergies are usually observed in infants and young children, and often disappear with age (see Prognosis), so prevalence of egg allergy may be expressed as a percentage of children under a set age. One review estimates that in North American and western European populations the prevalence of egg allergy in children under the age of five years is 1.8-2.0%. A second described the range in young children as 0.5-2.5%. Although the majority of children develop tolerance as they age into school age years, for roughly one-third the allergy persists into adulthood. Strong predictors for adult-persistent allergy are anaphylactic symptoms as a child, high egg-specific serum IgE, robust response to the skin prick test and absence of tolerance to egg-containing baked foods. Self-reported allergy prevalence is always higher than food-challenge confirmed allergy.
For all age groups, a review of fifty studies conducted in Europe estimated 2.5% for self-reported egg allergy and 0.2% for confirmed. National survey data in the United States collected in 2005 and 2006 showed that from age six and older, the prevalence of serum IgE confirmed egg allergy was under 0.2%.Adult-onset of egg allergy is rare, but there is confirmation of cases. Some were described as having started in late teenage years; another group were workers in the baking industry who were exposed to powdered egg dust.

Regulation
Whether food allergy prevalence is increasing or not, food allergy awareness has definitely increased, with impacts on the quality of life for children, their parents and their immediate caregivers. In the United States, the Food Allergen Labeling and Consumer Protection Act of 2004  (FALCPA) causes people to be reminded of allergy problems every time they handle a food package, and restaurants have added allergen warnings to menus. The Culinary Institute of America, a premier school for chef training, has courses in allergen-free cooking and a separate teaching kitchen. School systems have protocols about what foods can be brought into the school. Despite all these precautions, people with serious allergies are aware that accidental exposure can easily occur at other peoples houses, at school or in restaurants.

Regulation of labelling
In response to the risk that certain foods pose to those with food allergies, some countries have responded by instituting labeling laws that require food products to clearly inform consumers if their products contain major allergens or byproducts of major allergens among the ingredients intentionally added to foods. Nevertheless, there are no labeling laws to mandatory declare the presence of trace amounts in the final product as a consequence of cross-contamination, except in Brazil.

Ingredients intentionally added
FALCPA became effective 1 January 2006, requiring companies selling foods in the United States to disclose on labels whether a packaged food product contains any of these eight major food allergens, added intentionally: cows milk, peanuts, eggs, shellfish, fish, tree nuts, soy and wheat. This list originated in 1999 from the World Health Organisation Codex Alimentarius Commission. To meet FALCPA labeling requirements, if an ingredient is derived from one of the required-label allergens, then it must either have its "food sourced name" in parentheses, for example "Casein (milk)," or as an alternative, there must be a statement separate but adjacent to the ingredients list: "Contains milk" (and any other of the allergens with mandatory labeling).FALCPA applies to packaged foods regulated by the FDA, which does not include poultry, most meats, certain egg products, and most alcoholic beverages. However, some meat, poultry, and egg processed products may contain allergenic ingredients. These products are regulated by the Food Safety and Inspection Service (FSIS), which requires that any ingredient be declared in the labeling only by its common or usual name. Neither the identification of the source of a specific ingredient in a parenthetical statement nor the use of statements to alert for the presence of specific ingredients, like "Contains: milk", are mandatory according to FSIS.  FALCPA also does not apply to food prepared in restaurants. The EU Food Information for Consumers Regulation 1169/2011 – requires food businesses to provide allergy information on food sold unpackaged, for example, in catering outlets, deli counters, bakeries and sandwich bars.

Trace amounts as a result of cross-contamination
The value of allergen labeling other than for intentional ingredients is controversial. This concerns labeling for ingredients present unintentionally as a consequence of cross-contact or cross-contamination at any point along the food chain (during raw material transportation, storage or handling, due to shared equipment for processing and packaging, etc.). Experts in this field propose that if allergen labeling is to be useful to consumers, and healthcare professionals who advise and treat those consumers, ideally there should be agreement on which foods require labeling, threshold quantities below which labeling may be of no purpose, and validation of allergen detection methods to test and potentially recall foods that were deliberately or inadvertently contaminated.Labeling regulations have been modified to provide for mandatory labeling of ingredients plus voluntary labeling, termed precautionary allergen labeling (PAL), also known as "may contain" statements, for possible, inadvertent, trace amount, cross-contamination during production. PAL labeling can be confusing to consumers, especially as there can be many variations on the wording of the warning </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 Dermatopolymyositis 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 Gapeworm and can you explain it in depth? [/INST] A gapeworm (Syngamus trachea), also known as a red worm and forked worm, is a parasitic nematode worm that infects the tracheas of certain birds. The resulting disease, known as "gape"  occurs when the worms clog and obstruct the airway. The worms are also known as "red worms" or "forked worms" due to their red color and the permanent procreative conjunction of males and females. Gapeworms are common in young, domesticated chickens and turkeys.
When the female gapeworm lays her eggs in the trachea of an infected bird, the eggs are coughed up, swallowed, then defecated. Birds are infected with the parasite when they consume the eggs found in the feces, or by consuming a transport host such as earthworms, snails (Planorbarius corneus, Bithynia tentaculata and others)

Morphology
Males and females are joined together in a state of permanent copulation forming, a Y shape (forked worms). They are also known as the red worms because of their color. Females (up to 20mm long) are much longer than males (up to 6mm long). The life cycle of the gapeworm is peculiar in that transmission from bird to bird may be successfully accomplished either directly (by ingesting embryonated eggs or infective larvae) or indirectly (by ingestion of earthworms containing free or encysted gapeworm larvae they had obtained by feeding on contaminated soil).

Life cycle and pathogenesis
In the preparasitic phase, third stage infective larvae (L3) develop inside the eggs at which time they may hatch. Earthworms serve as transport (paratenic) hosts. Larvae have been shown to remain viable for more than three years encapsulated in earthworm muscles. Other invertebrates may also serve as paratenic hosts, including terrestrial snails and slugs.
The parasitic phase involves substantial migration in the definitive host to reach the predilection site. Young birds are most severely affected with migration of larvae and adults through the lungs causing a severe pneumonia. Lymphoid nodules form at the point of attachment of the worms in the bronchi and trachea. Adult worms also appear to feed on blood. Worms in the bronchi and trachea provoke a hemorrhagic tracheitis and bronchitis, forming large quantities of mucus, plugging the air passages and, in severe cases, causing asphyxiation.
Pheasants appear to be particularly susceptible to infections resulting in mortality rates as high as 25% during outbreaks. The rapidly growing worms soon obstruct the lumen of the trachea, causing suffocation. Turkey poults, baby chicks and pheasant chicks are most susceptible to infection. Turkey poults usually develop gapeworm signs earlier and begin to die sooner after infection than young chickens. Lesions are usually found in the trachea of turkeys and pheasants but seldom if ever in the tracheas of young chickens and guinea fowl.
The male worm, in the form of lesions, remains permanently attached to the tracheal wall throughout the duration of its life. The female worms apparently detach and reattach from time to time in order to obtain a more abundant supply of food.

Epidemiology
Earthworm transport hosts are important factors in the transmission of Syngamus trachea when poultry and game birds are reared on soil. The longevity of L3s in earthworms (up to 3 years) is particularly important in perpetuating the infection from year to year.
Wild birds may serve as reservoirs of infection and have been implicated as the sources of infections in outbreaks on game-bird farms as well as poultry farms. Wild reservoir hosts may include pheasants, ruffed grouse, partridges, wild turkeys, magpies, meadowlarks, American robins, grackles, jays, jackdaws, rooks, starlings and crows.
There is also evidence to suggest that strains of Syngamus trachea from wild bird reservoir hosts may be less effective in domestic birds; if they have an earthworm transport host rather than direct infections via ingestion of L3s, or eggs containing L3s.

Clinical signs
Blockage of the bronchi and trachea with worms and mucus will cause infected birds to gasp for air. They stretch out their necks, open their mouths and gasp for air producing a hissing noise as they do so. This "gaping" posture has given rise to the common term "gapeworm" to describe Syngamus trachea.
These clinical signs first appear approximately 1–2 weeks after infection.  Birds infected with gapeworms show signs of weakness and emaciation, usually spending much of their time with eyes closed and head drawn back against the body. An infected bird may give its head a convulsive shake in an attempt to remove the obstruction from the trachea so that normal breathing may be resumed.
Severely affected birds, particularly young ones, will deteriorate rapidly; they stop drinking and become anorexic. At this stage, death is the usual outcome. Adult birds are usually less severely affected and may only show an occasional cough or even no obvious clinical signs.

Diagnosis
A diagnosis is usually made on the basis of the classical clinical signs of  "gaping".  Subclinical infections with few worms may be confirmed at necropsy by finding copulating worms in the trachea and also by finding the characteristic eggs in the feces of infected birds. Examination of the tracheas of infected birds shows that the mucous membrane is extensively irritated and inflamed. Coughing is apparently the result of this irritation to the mucous lining.

Control and treatment
Prevention
In the artificial rearing of pheasants, gapes are a serious menace. Confinement rearing of young birds has reduced the problem in chickens compared to a few years ago. However, this parasite continues to present an occasional problem with turkeys raised on range. Confinement rearing of broilers/pullets and caging of laying hens, have significantly influenced the quantity and variety of nematode infections in poultry.
For most nematodes, control measures consist of sanitation and breaking the life cycle rather than chemotherapy. Confinement rearing on litter largely prevents infections with nematodes using intermediate hosts such as earthworms or grasshoppers, which are not normally found in poultry houses. Conversely, nematodes with direct life cycles or those that utilize intermediate hosts such as beetles, which are common in poultry houses, may prosper.
Treatment of the soil or litter to kill intermediate hosts may be beneficial. Insecticides suitable for litter treatment include carbaryl, tetrachlorvinphos (stirofos). However, treatment is usually done only between grow-outs. Extreme care should be taken to ensure that feed and water are not contaminated. Treatment of range soil to kill ova is only partially successful.
Changing litter can reduce infections, but treating floors with oil is not very effective </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 Eclampsia and can you explain it in depth? [/INST] Eclampsia is the onset of seizures (convulsions) in a woman with pre-eclampsia. Pre-eclampsia is one of the hypertensive disorders of pregnancy that presents with three main features: new onset of high blood pressure, large amounts of protein in the urine or other organ dysfunction, and edema. The diagnostic criteria for pre-eclampsia is high blood pressure occurring after 20 weeks gestation or during the second half of pregnancy. Most often it occurs during the 3rd trimester of pregnancy and may occur before, during, or after delivery. The seizures are of the tonic–clonic type and typically last about a minute. Following the seizure, there is either a period of confusion or coma. Other complications include aspiration pneumonia, cerebral hemorrhage, kidney failure, pulmonary edema, HELLP syndrome, coagulopathy, placental abruption and cardiac arrest.Low dose aspirin is recommended to prevent pre-eclampsia and eclampsia in those at high risk. Other preventative recommendation include calcium supplementation in areas with low calcium intake and treatment of prior hypertension with anti-hypertensive medications. Exercise during pregnancy may also be useful. The use of intravenous or intramuscular magnesium sulfate improves outcomes in those with severe pre-eclampsia and eclampsia and is generally safe. Treatment options include blood pressure medications such as hydralazine and emergency delivery of the baby either vaginally or by cesarean section.Pre-eclampsia is estimated to globally affect about 5% of deliveries while eclampsia affects about 1.4% of deliveries. In the developed world eclampsia rates are about 1 in 2,000 deliveries due to improved medical care whereas in developing countries it can impact 10-30 times as many women. Hypertensive disorders of pregnancy are one of the most common causes of death in pregnancy. They resulted in 46,900 deaths in 2015. Around one percent of women with eclampsia die. The word eclampsia is from the Greek term for lightning. The first known description of the condition was by Hippocrates in the 5th century BC.

Signs and symptoms
Eclampsia is a disorder of pregnancy characterized by seizures in the setting of pre-eclampsia. Most women have premonitory signs/symptoms in the hours before the initial seizure. Typically the woman develops hypertension before the onset of a convulsion (seizure). Other signs and symptoms to looks out for include:
Long-lasting (persistent) frontal or occipital headaches or thunderclap headaches)
Visual disturbance (blurred vision, photophobia, diplopopia)
Photophobia (i.e. bright light causes discomfort)
Abdominal pain
Either in the epigastric region (the center of the abdomen above the navel, or belly-button)
And/or in the right upper quadrant of the abdomen (below the right side of the rib cage)
Altered mental status (confusion)Any of these symptoms may be present before or after the seizure. It is also possible for the woman to be asymptomatic prior to the onset of the seizure.
Other cerebral signs that may precede the convulsion include nausea, vomiting, headaches, and cortical blindness. If the complication of multi-organ failure ensues, signs and symptoms of those failing organs will appear, such as abdominal pain, jaundice, shortness of breath, and diminished urine output.

Onset
The seizures of eclampsia typically present during pregnancy and prior to delivery (the antepartum period), but may also occur during labor and delivery (the intrapartum period) or after the baby has been delivered (the postpartum period). If postpartum seizures develop, it is most likely to occur within the first 48 hours after delivery. However, late postpartum seizures of eclampsia may occur as late as 4 weeks after delivery.

Characteristics
Eclamptic seizure is typically described as a tonic–clonic seizure which may cause an abrupt loss of consciousness at onset. This is often associated with a shriek or scream followed by stiffness of the muscles of the arms, legs, back and chest. During the tonic phase, the mother may begin to appear cyanotic. This presentation lasts for about a minute, after which the muscles begin in jerk and twitch for an additional one to two minutes. Other signs include tongue biting, frothy and bloody sputum coming out of the mouth.

Complications
There are risks to both the mother and the fetus when eclampsia occurs. The fetus may grow more slowly than normal within the womb (uterus) of a woman with eclampsia, which is termed intrauterine growth restriction and may result in the child appearing small for gestational age or being born with low birth weight. Eclampsia may also cause problems with the placenta. The placenta may bleed (hemorrhage) or begin to separate early from the wall of the uterus. It is normal for the placenta to separate from the uterine wall during delivery, but it is abnormal for it to separate prior to delivery; this condition is called placental abruption and can be dangerous for the fetus. Placental insufficiency may also occur, a state in which the placenta fails to support appropriate fetal development because it cannot deliver the necessary amount of oxygen or nutrients to the fetus. During an eclamptic seizure, the beating of the fetal heart may become slower than normal (bradycardia). If any of these complications occurs, fetal distress may develop. Treatment of the mothers seizures may also manage fetal bradycardia. If the risk to the health of the fetus or the mother is high, the definitive treatment for eclampsia is delivery of the baby. Delivery by cesarean section may be necessary, especially if the instance of fetal bradycardia does not resolve after 10 to 15 minutes of resuscitative interventions. It may be safer to deliver the infant preterm than to wait for the full 40 weeks of fetal development to finish, and as a result prematurity is also a potential complication of eclampsia.In the mother, changes in vision may occur as a result of eclampsia, and these changes may include blurry vision, one-sided blindness (either temporary due to amaurosis fugax or potentially permanent due to retinal detachment), or cortical blindness, which affects the vision from both eyes. There are also potential complications in the lungs. The woman may have fluid slowly collecting in the lungs in a process known as pulmonary edema. During an eclamptic seizure, it is possible for a person to vomit the contents of the stomach and to inhale some of this material in a process known as aspiration. If aspiration occurs, the woman may experience difficulty breathing immediately or could develop an infection in the lungs later, called aspiration pneumonia. It is also possible that during a seizure breathing will stop temporarily or become inefficient, and the amount of oxygen reaching the womans body and brain will be decreased (in a state known as hypoxia). If it becomes difficult for the woman to breathe, she may need to have her breathing temporarily supported by an assistive device in a process called mechanical ventilation. In some severe eclampsia cases, the mother may become weak and sluggish (lethargy) or even comatose. These may be signs that the brain is swelling (cerebral edema) or bleeding (intracerebral hemorrhage).

Risk factors
Eclampsia, like pre-eclampsia, tends to occur more commonly in first pregnancies than subsequent pregnancies. Women who have long term high blood pressure before becoming pregnant have a greater risk of pre-eclampsia. Patients who have gestational hypertension and pre-eclampsia have an increased risk of eclampsia. Furthermore, women with other pre-existing vascular diseases (diabetes or nephropathy) or thrombophilia disease such as the antiphospholipid syndrome are at higher risk to develop pre-eclampsia and eclampsia. Having a placenta that is enlarged by multiple gestation or hydatidiform mole also increases risk of eclampsia. In addition, there is a genetic component: a woman whose mother or sister had the condition is at higher risk than otherwise. Patients who have experienced eclampsia are at increased risk for pre-eclampsia/eclampsia in a later pregnancy. The occurrence of pre-eclampsia was 5% in white, 9% in Hispanic, and 11% in African American patients and this may reflect disproportionate risk of developing pre-eclampsia among ethnic groups. Additionally, black patients were also shown to have a disproportionately higher risk of dying from eclampsia.

Mechanism
The mechanisms of eclampsia and preeclampsia are not definitively understood, but following provides some insight. The presence of a placenta is required, and eclampsia resolves if it is removed. Reduced blood flow to the placenta (placental hypoperfusion) may be a key feature of the process. It is typically accompanied by increased sensitivity of the maternal vasculature to agents which cause constriction of the small arteries, leading to reduced blood flow to multiple organs. Vascular dysfunction-associated maternal conditions such as Lupus, hypertension, and renal disease, or obstetric conditions that increase placental volume without an increase in placental blood flow (such as multifetal gestation) may increase risk for pre-eclampsia. Also, activation of the coagulation cascade can lead to microthrombi formation, which may further impair blood flow. Thirdly, increased vascular permeability results in the shift of extracellular fluid from the blood to the interstitial space which reduces blood flow and causes edema. These events can lead to hypertension, renal dysfunction, pulmonary dysfunction, hepatic dysfunction, and cerebral edema with cerebral dysfunction and convulsions. In clinical context, increased platelet and endothelial activation may be detected before symptoms appear.Hypoperfusion of the placenta is associated with abnormal modelling of the fetal–maternal placental interface that may be immunologically mediated. The pathogenesis of pre-eclampsia is poorly understood and may be attributed to factors related to the woman and placenta since pre-eclampsia is seen in molar pregnancies absent of a fetus or fetal tissue. The placenta normally produces the potent vasodilator adrenomedullin but it is reduced in pre-eclampsia and eclampsia. Other vasodilators, including prostacyclin, thromboxane A2, nitric oxide, and endothelins, are reduced in eclampsia and may lead to vasoconstriction.Eclampsia is associated with hypertensive encephalopathy in which cerebral vascular resistance is reduced, leading to increased blood flow to the brain, cerebral edema and resultant convulsions. An eclamptic convulsion usually does not cause chronic brain damage unless intracranial haemorrhage occurs.

Diagnosis
If a pregnant woman has already been diagnosed with pre-eclampsia during the current pregnancy and then develops a seizure, she may be assigned a clinical diagnosis of eclampsia without further workup. While seizures are most common in the third trimester, they may occur any time from 20 weeks of pregnancy until 6 weeks after birth. Because pre-eclampsia and eclampsia are common conditions in women, eclampsia can be assumed to be the correct diagnosis until proven otherwise in pregnant or postpartum women who experience seizures. However, if a woman has a seizure and it is unknown whether or not they have pre-eclampsia, testing can help make the diagnosis clear.
Pre-eclampsia is diagnosed when repeated blood pressure measurements are greater or equal to 140/90mmHg, in addition to any signs of organ dysfunction, including: proteinuria, thrombocytopenia, renal insufficiency, impaired liver function, pulmonary edema, cerebral symptoms, or abdominal pain.

Vital signs
One of the core features of pre-eclampsia is the new onset of high blood pressure. Blood pressure is a measurement of two numbers: systolic blood pressure and diastolic blood pressure. A systolic blood pressure (the top number) of greater than 140 mmHg and/or a diastolic blood pressure (the bottom number) of greater than 90 mmHg is higher than the normal range. If the blood pressure is high on at least two separate occasions after the first 20 weeks of pregnancy and the woman has signs of organ dysfunction (e.g. proteinuria), then they meet the criteria for a diagnosis of pre-eclampsia. If the systolic blood pressure is greater than 160 or the diastolic pressure is greater than 110, the hypertension is considered to be severe.

Laboratory testing
Another common feature of pre-eclampsia is proteinuria, which is the presence of excess protein in the urine. To determine if proteinuria is present, the urine can be collected and tested for protein; if there is 0.3 grams of protein or more in the urine of a pregnant woman collected over 24 hours, this is one of the diagnostic criteria for pre-eclampsia and raises the suspicion that a seizure is due to eclampsia.In cases of severe eclampsia or pre-eclampsia, the woman can have low levels of platelets in the blood, a condition termed thrombocytopenia. A complete blood count, or CBC, is a test of the blood that can be performed to check platelet levels.
Other investigations include: kidney function test, liver function tests (LFT), coagulation screen, 24-hour urine creatinine, and fetal/placental ultrasound.

Differential diagnosis
Convulsions during pregnancy that are unrelated to pre-eclampsia need to be distinguished from eclampsia. Such disorders include seizure disorders as well as brain tumor, aneurysm of the brain, and medication- or drug-related seizures. Usually, the presence of the signs of severe pre-eclampsia precede and accompany eclampsia, facilitating the diagnosis.

Prevention
Detection and management of pre-eclampsia is critical to reduce the risk of eclampsia. The USPSTF recommends regular checking of blood pressure through pregnancy in order to detect preeclampsia. Appropriate management of a woman with pre-eclampsia generally involves the use of magnesium sulfate to prevent eclamptic seizures. In some cases, low-dose aspirin has been shown to decrease the risk of pre-eclampsia in women, especially when taken in the late first trimester.

Treatment
The four goals of the treatment of eclampsia are to stop and prevent further convulsions, to control the elevated blood pressure, to deliver the baby as promptly as possible, and to monitor closely for the onset of multi-organ failure.

Convulsions
Convulsions are prevented and treated using magnesium sulfate. The study demonstrating the effectiveness of magnesium sulfate for the management of eclampsia was first published in 1955.  Effective anticonvulsant serum levels range from 2.5 to 7.5 mEq/L.With intravenous administration, the onset of anticonvulsant action is fast and lasts about 30 minutes. Following intramuscular administration the onset of action is about one hour and lasts for three to four hours. Magnesium is excreted solely by the kidneys at a rate proportional to the plasma concentration (concentration in the blood) and glomerular filtration (rate at which the blood is filtered through the kidneys). Magnesium sulfate is associated with several minor side effects; serious side effects are uncommon, occurring at elevated magnesium serum concentrations greater than 7.0 mEq/L. Serious toxicity can be counteracted with calcium gluconate.Even with therapeutic serum magnesium concentrations, recurrent convulsions may occur, and additional magnesium may be needed, but with close monitoring for respiratory, cardiac, and neurological depression. If magnesium administration with resultant high serum concentrations fails to control convulsions, the addition of other intravenous anticonvulsants may be used and  intubation and mechanical ventilation may be initiated. It is important to avoid magnesium toxicity, including thoracic muscle paralysis, which could cause respiratory failure and death.
Magnesium sulfate results in better outcomes than diazepam, phenytoin or a combination of chlorpromazine, promethazine, and pethidine.

Blood pressure management
Blood pressure control is used to prevent stroke, which accounts for 15 to 20 percent of deaths in women with eclampsia </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 Anxiety disorder and can you explain it in depth? [/INST] Anxiety disorders are a cluster of mental disorders characterized by significant and uncontrollable feelings of anxiety and fear such that a persons social, occupational, and personal function are significantly impaired. Anxiety may cause physical and cognitive symptoms, such as restlessness, irritability, easy fatiguability, difficulty concentrating, increased heart rate, chest pain, abdominal pain, and a variety of other symptoms that may vary based on the individual.In casual discourse, the words anxiety and fear are often used interchangeably. In clinical usage, they have distinct meanings: anxiety is defined as an unpleasant emotional state for which the cause is either not readily identified or perceived to be uncontrollable or unavoidable, whereas fear is an emotional and physiological response to a recognized external threat. The umbrella term anxiety disorder refers to a number of specific disorders that include fears (phobias) or anxiety symptoms.
There are several types of anxiety disorders, including generalized anxiety disorder, specific phobia, social anxiety disorder, separation anxiety disorder, agoraphobia, panic disorder, and selective mutism. The individual disorder can be diagnosed using the specific and unique symptoms, triggering events, and timing. If a person is diagnosed with an anxiety disorder, a medical professional must have evaluated the person to ensure the anxiety cannot be attributed to another medical illness or mental disorder.  It is possible for an individual to have more than one anxiety disorder during their life or at the same time and anxiety disorders are marked by a typical persistent course. Anxiety disorders are the most common of mental disorders and affect nearly 30% of adults at some point in their lives. However, anxiety disorders are treatable and a number of effective treatments are available. Treatment helps most people lead normal productive lives.

Sub-types
Generalized anxiety disorder
Generalized anxiety disorder (GAD) is a common disorder, characterized by long-lasting anxiety which is not focused on any one object or situation. Those with generalized anxiety disorder experience non-specific persistent fear and worry, and become overly concerned with everyday matters. Generalized anxiety disorder is "characterized by chronic excessive worry accompanied by three or more of the following symptoms: restlessness, fatigue, concentration problems, irritability, muscle tension, and sleep disturbance". Generalized anxiety disorder is the most common anxiety disorder to affect older adults. Anxiety can be a symptom of a medical or substance use disorder problem, and medical professionals must be aware of this. A diagnosis of GAD is made when a person has been excessively worried about an everyday problem for six months or more.  These stresses can include family life, work, social life, or their own health. A person may find that they have problems making daily decisions and remembering commitments as a result of lack of concentration and/or preoccupation with worry. A symptom can be a strained appearance, with increased sweating from the hands, feet, and axillae, and they may be tearful, which can suggest depression. Before a diagnosis of anxiety disorder is made, physicians must rule out drug-induced anxiety and other medical causes.In children, GAD may be associated with headaches, restlessness, abdominal pain, and heart palpitations. Typically it begins around 8 to 9 years of age.

Specific phobias
The single largest category of anxiety disorders is that of specific phobias, which includes all cases in which fear and anxiety are triggered by a specific stimulus or situation. Between 5% and 12% of the population worldwide have specific phobias. According to the National Institute of Mental Health, a phobia is an intense fear of or aversion to specific objects or situations. Individuals with a phobia typically anticipate terrifying consequences from encountering the object of their fear, which can be anything from an animal to a location to a bodily fluid to a particular situation. Common phobias are flying, blood, water, highway driving, and tunnels. When people are exposed to their phobia, they may experience trembling, shortness of breath, or rapid heartbeat.  Thus meaning that people with specific phobias often go out of their way to avoid encountering their phobia. People understand that their fear is not proportional to the actual potential danger but still are overwhelmed by it.

Panic disorder
With panic disorder, a person has brief attacks of intense terror and apprehension, often marked by trembling, shaking, confusion, dizziness, nausea, and/or difficulty breathing. These panic attacks, defined by the APA as fear or discomfort that abruptly arises and peaks in less than ten minutes, can last for several hours. Attacks can be triggered by stress, irrational thoughts, general fear or fear of the unknown, or even exercise. However, sometimes the trigger is unclear and the attacks can arise without warning. To help prevent an attack, one can avoid the trigger. This can mean avoiding places, people, types of behaviors, or certain situations that have been known to cause a panic attack. This being said, not all attacks can be prevented.
In addition to recurrent unexpected panic attacks, a diagnosis of panic disorder requires that said attacks have chronic consequences: either worry over the attacks potential implications, persistent fear of future attacks, or significant changes in behavior related to the attacks. As such, those with panic disorder experience symptoms even outside specific panic episodes. Often, normal changes in heartbeat are noticed, leading them to think something is wrong with their heart or they are about to have another panic attack. In some cases, a heightened awareness (hypervigilance) of body functioning occurs during panic attacks, wherein any perceived physiological change is interpreted as a possible life-threatening illness (i.e., extreme hypochondriasis).

Agoraphobia
Agoraphobia is the specific anxiety about being in a place or situation where escape is difficult or embarrassing or where help may be unavailable. Agoraphobia is strongly linked with panic disorder and is often precipitated by the fear of having a panic attack. A common manifestation involves needing to be in constant view of a door or other escape route. In addition to the fears themselves, the term agoraphobia is often used to refer to avoidance behaviors that individuals often develop. For example, following a panic attack while driving, someone with agoraphobia may develop anxiety over driving and will therefore avoid driving. These avoidance behaviors can have serious consequences and often reinforce the fear they are caused by. In a severe case of agoraphobia, the person may never leave their home.

Social anxiety disorder
Social anxiety disorder (SAD; also known as social phobia) describes an intense fear and avoidance of negative public scrutiny, public embarrassment, humiliation, or social interaction. This fear can be specific to particular social situations (such as public speaking) or, more typically, is experienced in most (or all) social interactions. Roughly 7% of American adults have social anxiety disorder, and more than 75% of people experience their first symptoms in their childhood or early teenage years. Social anxiety often manifests specific physical symptoms, including blushing, sweating, rapid heart rate, and difficulty speaking. As with all phobic disorders, those with social anxiety often will attempt to avoid the source of their anxiety; in the case of social anxiety this is particularly problematic, and in severe cases can lead to complete social isolation.
Children are also affected by social anxiety disorder, although their associated symptoms are different than that of teenagers and adults. They may experience difficulty processing or retrieving information, sleep deprivation, disruptive behaviors in class, and irregular class participation.Social physique anxiety (SPA) is a subtype of social anxiety, involving concern over the evaluation of ones body by others. SPA is common among adolescents, especially females.

Post-traumatic stress disorder
Post-traumatic stress disorder (PTSD) was once an anxiety disorder (now moved to trauma- and stressor-related disorders in DSM-V) that results from a traumatic experience. PTSD affects approximately 3.5% of U.S. adults every year, and an estimated one in eleven people will be diagnosed with PTSD in their lifetime. Post-traumatic stress can result from an extreme situation, such as combat, natural disaster, rape, hostage situations, child abuse, bullying, or even a serious accident. It can also result from long-term (chronic) exposure to a severe stressor— for example, soldiers who endure individual battles but cannot cope with continuous combat. Common symptoms include hypervigilance, flashbacks, avoidant behaviors, anxiety, anger and depression. In addition, individuals may experience sleep disturbances. People who have PTSD often try to detach themselves from their friends and family, and have difficulty maintaining these close relationships. There are a number of treatments that form the basis of the care plan for those with PTSD. Such treatments include cognitive behavioral therapy (CBT), prolonged exposure therapy, stress inoculation therapy, medication, and psychotherapy and support from family and friends.Post-traumatic stress disorder (PTSD) research began with Vietnam veterans, as well as natural and non-natural disaster victims. Studies have found the degree of exposure to a disaster has been found to be the best predictor of PTSD.

Separation anxiety disorder
Separation anxiety disorder (SepAD) is the feeling of excessive and inappropriate levels of anxiety over being separated from a person or place. Separation anxiety is a normal part of development in babies or children, and it is only when this feeling is excessive or inappropriate that it can be considered a disorder. Separation anxiety disorder affects roughly 7% of adults and 4% of children, but the childhood cases tend to be more severe; in some instances, even a brief separation can produce panic. Treating a child earlier may prevent problems. This may include training the parents and family on how to deal with it. Often, the parents will reinforce the anxiety because they do not know how to properly work through it with the child. In addition to parent training and family therapy, medication, such as SSRIs, can be used to treat separation anxiety.

Obsessive–compulsive disorder
Obsessive–compulsive disorder (OCD) is not classified as an anxiety disorder by the DSM-5, but is by the ICD-10. It was previously classified as an anxiety disorder in the DSM-IV. It is a condition where the person has obsessions (distressing, persistent, and intrusive thoughts or images) and compulsions (urges to repeatedly perform specific acts or rituals), that are not caused by drugs or physical disorder, and which cause distress or social dysfunction. The compulsive rituals are personal rules followed to relieve the feeling of discomfort. OCD affects roughly 1–2% of adults (somewhat more women than men), and under 3% of children and adolescents.A person with OCD knows that the symptoms are unreasonable and struggles against both the thoughts and the behavior. Their symptoms could be related to external events they fear (such as their home burning down because they forget to turn off the stove) or worry that they will behave inappropriately.It is not certain why some people have OCD, but behavioral, cognitive, genetic, and neurobiological factors may be involved. Risk factors include family history, being single (although that may result from the disorder), and higher socioeconomic class or not being in paid employment. Of those with OCD about 20% of people will overcome it, and symptoms will at least reduce over time for most people (a further 50%).

Selective mutism
Selective mutism (SM) is a disorder in which a person who is normally capable of speech does not speak in specific situations or to specific people. Selective mutism usually co-exists with shyness or social anxiety. People with selective mutism stay silent even when the consequences of their silence include shame, social ostracism or even punishment. Selective mutism affects about 0.8% of people at some point in their life.Testing for selective mutism is important because doctors must determine if it is an issue associated with the childs hearing, movements associated with the jaw or tongue, and if the child can understand when others are speaking to them.

Diagnosis
The diagnosis of anxiety disorders is made by symptoms, triggers, and a persons personal and family histories.  There are no objective biomarkers or laboratory tests that can diagnose anxiety.  It is important for a medical professional to evaluate a person for other medical and mental causes for prolonged anxiety because treatments will vary considerably.Numerous questionnaires have been developed for clinical use and can be used for an objective scoring system. Symptoms may be vary between each subtype of generalized anxiety disorder.  Generally, symptoms must be present for at least six months, occur more days than not, and significantly impair a persons ability to function in daily life.  Symptoms may include: feeling nervous, anxious, or on edge; worrying excessively; difficulty concentrating; restlessness; irritability.Questionnaires developed for clinical use include the State-Trait Anxiety Inventory (STAI), the Generalized Anxiety Disorder 7 (GAD-7), the Beck Anxiety Inventory (BAI), the Zung Self-Rating Anxiety Scale, and the Taylor Manifest Anxiety Scale. Other questionnaires combine anxiety and depression measurement, such as the Hamilton Anxiety Rating Scale, the Hospital Anxiety and Depression Scale (HADS), the Patient Health Questionnaire (PHQ), and the Patient-Reported Outcomes Measurement Information System (PROMIS). Examples of specific anxiety questionnaires include the Liebowitz Social Anxiety Scale (LSAS), the Social Interaction Anxiety Scale (SIAS), the Social Phobia Inventory (SPIN), the Social Phobia Scale (SPS), and the Social Anxiety Questionnaire (SAQ-A30).

Differential diagnosis
Anxiety disorders differ from developmentally normal fear or anxiety by being excessive or persisting beyond developmentally appropriate periods. They differ from transient fear or anxiety, often stress-induced, by being persistent (e.g., typically lasting 6 months or more), although the criterion for duration is intended as a general guide with allowance for some degree of flexibility and is sometimes of shorter duration in children.The diagnosis of an anxiety disorder requires first ruling out an underlying medical cause. Diseases that may present similar to an anxiety disorder, including certain endocrine diseases (hypo- and hyperthyroidism, hyperprolactinemia), metabolic disorders (diabetes), deficiency states (low levels of vitamin D, B2, B12, folic acid), gastrointestinal diseases (celiac disease, non-celiac gluten sensitivity, inflammatory bowel disease), heart diseases, blood diseases (anemia), and brain degenerative diseases (Parkinsons disease, dementia, multiple sclerosis, Huntingtons disease).Several drugs can also cause or worsen anxiety, whether in intoxication, withdrawal, or from chronic use. These include alcohol, tobacco, cannabis, sedatives (including prescription benzodiazepines), opioids (including prescription painkillers and illicit drugs like heroin), stimulants (such as caffeine, cocaine and amphetamines), hallucinogens, and inhalants.

Prevention
Focus is increasing on prevention of anxiety disorders. There is tentative evidence to support the use of cognitive behavioral therapy and mindfulness therapy. A 2013 review found no effective measures to prevent GAD in adults. A 2017 review found that psychological and educational interventions had a small benefit for the prevention of anxiety. Research indicates that predictors of the emergence of anxiety disorders partly differ from the factors that predict their persistence.

Perception and Discrimination
Stigma
People with an anxiety disorder may be challenged by prejudices and stereotypes that the world believes, most likely as a result of misconception around anxiety and anxiety disorders. Misconceptions found in a data analysis from the National Survey of Mental Health Literacy and Stigma include (1)  many people believe anxiety is not a real medical illness; and (2) many people believe that people with anxiety could turn it off if they wanted to. For people experiencing the physical and mental symptoms of an anxiety disorder, stigma and negative social perception can make an individual less likely to seek treatment.There are two prevalent types of stigmas that surround anxiety disorders: Public and Self-Stigma. Public stigma in this context is the reaction that the general population has to people with an anxiety disorder. Self-Stigma is described as the prejudice which people with mental illness turn against themselves.There is no explicit evidence that announces the exact cause of stigma towards anxiety, however there are three highlighted perspectives. The macro, intermediate, and micro levels. The macro level marks society as whole with the influence from mass media. The intermediate level includes health care professionals and their perspective. The micro level details the individuals contributions to the process through self-stigmatization.Stigma can be described in three conceptual ways: cognitive, emotional, and behavioural. This allows for differentiation between stereotypes, prejudice, and discrimination.

Treatment
Treatment options include lifestyle changes, therapy, and medications. There is no clear evidence as to whether therapy or medication is most effective; the specific medication decision can be made by a doctor and patient with consideration to the patients specific circumstances and symptoms. If while on treatment with a chosen medication, the persons anxiety does not improve, another medication may be offered. Specific treatments will vary by subtype of anxiety disorder, a persons other medical conditions, and medications.

Lifestyle and diet
Lifestyle changes include exercise, for which there is moderate evidence for some improvement, regularizing sleep patterns, reducing caffeine intake, and stopping smoking. Stopping smoking has benefits in anxiety as large as or larger than those of medications. Omega-3 polyunsaturated fatty acids, such as fish oil, may reduce anxiety, particularly in those with more significant symptoms.

Psychotherapy
Cognitive behavioral therapy (CBT) is effective for anxiety disorders and is a first-line treatment. CBT appears to be equally effective when carried out via the internet compared to sessions completed face to face.Mindfulness-based programs also appear to be effective for managing anxiety disorders. It is unclear if meditation has an effect on anxiety and transcendental meditation appears to be no different than other types of meditation.A 2015 Cochrane review of Morita therapy for anxiety disorder in adults found not enough evidence to draw a conclusion.Adventure-based counseling can be an effective way to anxiety. Using rock-climbing as an example, climbing can often bring on fear or frustration, and tackling these negative feelings in a nurturing environment can help people develop coping mechanisms necessary to deal with these negative feelings.

Medications
First-line choices for medications include SSRIs or SNRIs to treat generalized anxiety disorder. For adults there is no good evidence supporting which specific medication in the SSRI or SNRI class is best for treating anxiety, so cost often drives drug choice. Fluvoxamine is effective in treating a range of anxiety disorders in children and adolescents. Fluoxetine, sertraline and paroxetine can also help with some forms of anxiety in children and adolescents. If the chosen medicine is effective, it is recommended that it is continued for at least a year. Stopping medication results in a greater risk of relapse.Buspirone and pregabalin are second-line treatments for people who do not respond to SSRIs or SNRIs; there is also evidence that benzodiazepines, including diazepam and clonazepam, are effective. Pregabalin and gabapentin are effective in treating some anxiety disorders but there is concern regarding their off-label use due to the lack of strong scientific evidence for their efficacy in multiple conditions and their proven side effects.Medications need to be used with care among older adults, who are more likely to have side effects because of coexisting physical disorders. Adherence problems are more likely among older people, who may have difficulty understanding, seeing, or remembering instructions.In general, medications are not seen as helpful in specific phobia, but a benzodiazepine is sometimes used to help resolve acute episodes. In 2007, data were sparse for efficacy of any drug.

Cannabis
As of 2019, there is little evidence for cannabis in treating anxiety disorders.

Children
Both therapy and a number of medications have been found to be useful for treating childhood anxiety disorders. Therapy is generally preferred to medication.Cognitive behavioral therapy (CBT) is a good first therapy approach. Studies have gathered substantial evidence for treatments that are not CBT-based as being effective forms of treatment, expanding treatment options for those who do not respond to CBT. Although studies have demonstrated the effectiveness of CBT for anxiety disorders in children and adolescents, evidence that it is more effective than treatment as usual, medication, or wait list controls is inconclusive. Like adults, children may undergo psychotherapy, cognitive-behavioral therapy, or counseling. Family therapy is a form of treatment in which the child meets with a therapist together with the primary guardians and siblings. Each family member may attend individual therapy, but family therapy is typically a form of group therapy. Art and play therapy are also used. Art therapy is most commonly used when the child will not or cannot verbally communicate, due to trauma or a disability in which they are nonverbal. Participating in art activities allows the child to express what they otherwise may not be able to communicate to others. In play therapy, the child is allowed to play however they please as a therapist observes them. The therapist may intercede from time to time with a question, comment, or suggestion. This is often most effective when the family of the child plays a role in the treatment.If a medication option is warranted, antidepressants such as SSRIs and SNRIs can be effective. Fluvoxamine is effective in treating a range of anxiety disorders in children and adolescents </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 Seizure and can you explain it in depth? [/INST] An epileptic seizure, informally known as a seizure, is a period of symptoms due to abnormally excessive or synchronous neuronal activity in the brain. Outward effects vary from uncontrolled shaking movements involving much of the body with loss of consciousness (tonic-clonic seizure), to shaking movements involving only part of the body with variable levels of consciousness (focal seizure), to a subtle momentary loss of awareness (absence seizure). Most of the time these episodes last less than two minutes and it takes some time to return to normal. Loss of bladder control may occur.Seizures may be provoked and unprovoked. Provoked seizures are due to a temporary event such as low blood sugar, alcohol withdrawal, abusing alcohol together with prescription medication, low blood sodium, fever, brain infection, or concussion. Unprovoked seizures occur without a known or fixable cause such that ongoing seizures are likely. Unprovoked seizures may be exacerbated by stress or sleep deprivation.  Epilepsy describes brain disease in which there has been at least one unprovoked seizure and where there is a high risk of additional seizures in the future. Conditions that look like epileptic seizures but are not include: fainting, nonepileptic psychogenic seizure  and tremor.A seizure that lasts for more than a brief period is a medical emergency. Any seizure lasting longer than five minutes should be treated as status epilepticus. A first seizure generally does not require long-term treatment with anti-seizure medications unless a specific problem is found on electroencephalogram (EEG) or brain imaging. Typically it is safe to complete the work-up following a single seizure as an outpatient. In many, with what appears to be a first seizure, other minor seizures have previously occurred.Up to 10% of people have at least one epileptic seizure. Provoked seizures occur in about 3.5 per 10,000 people a year while unprovoked seizures occur in about 4.2 per 10,000 people a year. After one seizure, the chance of experiencing a second is about 50%. Epilepsy affects about 1% of the population at any given time with about 4% of the population affected at some point in time.  Many places require people to stop driving until they have not had a seizure for a specific period.

Signs and symptoms
The signs and symptoms of seizures vary depending on the type. The most common and stereotypical type of seizure is convulsive (60%), typically called a tonic-clonic seizure. Two-thirds of these begin as focal seizures prior to developing into tonic-clonic seizures. The remaining 40% of seizures are non-convulsive, an example of which is absence seizure. When EEG monitoring shows evidence of a seizure, but no symptoms are present, it is referred to as a subclinical seizure.

Focal seizures
Focal seizures often begin with certain experiences, known as an aura. These may include sensory (including visual, auditory, etc.), cognitive, autonomic, olfactory or motor phenomena.In a complex partial seizure a person may appear confused or dazed and cannot respond to questions or direction.Jerking activity may start in a specific muscle group and spread to surrounding muscle groups—known as a Jacksonian march. Unusual activities that are not consciously created may occur. These are known as automatisms and include simple activities like smacking of the lips or more complex activities such as attempts to pick something up.

Generalized seizures
There are six main types of generalized seizures: tonic-clonic, tonic, clonic, myoclonic, absence, and atonic seizures. They all involve a loss of consciousness and typically happen without warning.
Tonic-clonic seizures present with a contraction of the limbs followed by their extension, along with arching of the back for 10–30 seconds. A cry may be heard due to contraction of the chest muscles. The limbs then begin to shake in unison. After the shaking has stopped it may take 10–30 minutes for the person to return to normal.
Tonic seizures produce constant contractions of the muscles. The person may turn blue if breathing is impaired.
Clonic seizures involve shaking of the limbs in unison.
Myoclonic seizures involve spasms of muscles in either a few areas or generalized through the body.
Absence seizures can be subtle, with only a slight turn of the head or eye blinking. The person often does not fall over and may return to normal right after the seizure ends, though there may also be a period of post-ictal disorientation.
Atonic seizures involve the loss of muscle activity for greater than one second. This typically occurs bilaterally (on both sides of the body).

Duration
A seizure can last from a few seconds to more than five minutes, at which point it is known as status epilepticus. Most tonic-clonic seizures last less than two or three minutes. Absence seizures are usually around 10 seconds in duration.

Postictal
After the active portion of a seizure, there is typically a period of confusion called the postictal period before a normal level of consciousness returns. This usually lasts 3 to 15 minutes but may last for hours. Other common symptoms include: feeling tired, headache, difficulty speaking, and abnormal behavior. Psychosis after a seizure is relatively common, occurring in between 6 and 10% of people. Often people do not remember what occurred during this time.

Causes
Seizures have a number of causes. Of those who have a seizure, about 25% have epilepsy. A number of conditions are associated with seizures but are not epilepsy including: most febrile seizures and those that occur around an acute infection, stroke, or toxicity. These seizures are known as "acute symptomatic" or "provoked" seizures and are part of the seizure-related disorders. In many the cause is unknown.
Different causes of seizures are common in certain age groups.

Seizures in babies are most commonly caused by hypoxic ischemic encephalopathy, central nervous system (CNS) infections, trauma, congenital CNS abnormalities, and metabolic disorders.
The most frequent cause of seizures in children is febrile seizures, which happen in 2–5% of children between the ages of six months and five years.
During childhood, well-defined epilepsy syndromes are generally seen.
In adolescence and young adulthood, non-compliance with the medication regimen and sleep deprivation are potential triggers.
Pregnancy and labor and childbirth, and the post-partum, or post-natal period (after birth) can be at-risk times, especially if there are certain complications like pre-eclampsia.
During adulthood, the likely causes are alcohol related, strokes, trauma, CNS infections, and brain tumors.
In older adults, cerebrovascular disease is a very common cause. Other causes are CNS tumors, head trauma, and other degenerative diseases that are common in the older age group, such as dementia.

Metabolic
Dehydration can trigger epileptic seizures if it is severe enough. A number of disorders including: low blood sugar, low blood sodium, hyperosmolar nonketotic hyperglycemia, high blood sodium, low blood calcium and high blood urea levels may cause seizures. As may hepatic encephalopathy and the genetic disorder porphyria.

Structural
Cavernoma or cavernous malformation is a treatable medical condition that can cause seizures, headaches, and brain hemorrhages.
Arteriovenous malformation (AVM) is a treatable medical condition that can cause seizures, headaches, and brain hemorrhages.
Space-occupying lesions in the brain (abscesses, tumours). In people with brain tumours, the frequency of epilepsy depends on the location of the tumor in the cortical region.

Medications
Both medication and drug overdoses can result in seizures, as may certain medication and drug withdrawal. Common drugs involved include: antidepressants, antipsychotics, cocaine, insulin, and the local anaesthetic lidocaine. Difficulties with withdrawal seizures commonly occurs after prolonged alcohol or sedative use, a condition known as delirium tremens. In people who are at risk of developing epileptic seizures, common herbal medicines such as ephedra, ginkgo biloba and wormwood can provoke seizures.

Infections
Infection with the pork tapeworm, which can cause neurocysticercosis, is the cause of up to half of epilepsy cases in areas of the world where the parasite is common.
Parasitic infections such as cerebral malaria. In Nigeria this is one of the most common causes of seizures among children under five years of age.
Infection, such as encephalitis or meningitis

Stress
Stress can induce seizures in people with epilepsy, and is a risk factor for developing epilepsy. Severity, duration, and time at which stress occurs during development all contribute to frequency and susceptibility to developing epilepsy. It is one of the most frequently self-reported triggers in patients with epilepsy.Stress exposure results in hormone release that mediates its effects in the brain. These hormones act on both excitatory and inhibitory neural synapses, resulting in hyper-excitability of neurons in the brain. The hippocampus is known to be a region that is highly sensitive to stress and prone to seizures. This is where mediators of stress interact with their target receptors to produce effects.

Other
Seizures may occur as a result of high blood pressure, known as hypertensive encephalopathy, or in pregnancy as eclampsia when accompanied by either seizures or a decreased level of consciousness. Very high body temperatures may also be a cause. Typically this requires a temperature greater than 42 °C (107.6 °F).
Head injury may cause non-epileptic post-traumatic seizures or post-traumatic epilepsy
About 3.5 to 5.5% of people with celiac disease also have seizures.
Seizures in a person with a shunt may indicate failure
Hemorrhagic stroke can occasionally present with seizures, embolic strokes generally do not (though epilepsy is a common later complication); cerebral venous sinus thrombosis, a rare type of stroke, is more likely to be accompanied by seizures than other types of stroke
Multiple sclerosis may cause seizures
Electroconvulsive therapy (ECT) deliberately sets out to induce a seizure for the treatment of major depression.
Reflex seizure induced by a specific stimulus or trigger (extrinsic or intrinsic stimuli)

Mechanism
Normally, brain electrical activity is non-synchronous. In epileptic seizures, due to problems within the brain, a group of neurons begin firing in an abnormal, excessive, and synchronized manner. This results in a wave of depolarization known as a paroxysmal depolarizing shift.Normally after an excitatory neuron fires it becomes more resistant to firing for a period of time. This is due in part from the effect of inhibitory neurons, electrical changes within the excitatory neuron, and the negative effects of adenosine. In epilepsy the resistance of excitatory neurons to fire during this period is decreased. This may occur due to changes in ion channels or inhibitory neurons not functioning properly. Forty-one ion-channel genes and over 1,600 ion-channel mutations have been implicated in the development of epileptic seizure. These ion channel mutations tend to confer a depolarized resting state to neurons resulting in pathological hyper-excitability. This long-lasting depolarization in individual neurons is due to an influx of Ca2+ from outside of the cell and leads to extended opening of Na+ channels and repetitive action potentials. The following hyperpolarization is facilitated by γ-aminobutyric acid (GABA) receptors or potassium (K+) channels, depending on the type of cell. Equally important in epileptic neuronal hyper-excitability, is the reduction in the activity of inhibitory GABAergic neurons, an effect known as disinhibition. Disinhibition may result from inhibitory neuron loss, dysregulation of axonal sprouting from the inhibitory neurons in regions of neuronal damage, or abnormal GABAergic signaling within the inhibitory neuron. Neuronal hyper-excitability results in a specific area from which seizures may develop, known as a "seizure focus". Following an injury to the brain, another mechanism of epilepsy may be the up regulation of excitatory circuits or down regulation of inhibitory circuits. These secondary epilepsies occur through processes known as epileptogenesis. Failure of the blood–brain barrier may also be a causal mechanism. While blood-brain barrier disruption alone does appear to cause epileptogenesis, it has been correlated to increased seizure activity. Furthermore, it has been implicated in chronic epileptic conditions through experiments inducing barrier permeability with chemical compounds. Disruption may lead to fluid leaking out of the blood vessels into the area between cells and driving epileptic seizures. Preliminary findings of blood proteins in the brain after a seizure support this theory.Focal seizures begin in one hemisphere of the brain while generalized seizures begin in both hemispheres. Some types of seizures may change brain structure, while others appear to have little effect. Gliosis, neuronal loss, and atrophy of specific areas of the brain are linked to epilepsy but it is unclear if epilepsy causes these changes or if these changes result in epilepsy.Seizure activity may be propagated through the brains endogenous electrical fields. Proposed mechanisms that may cause the spread and recruitment of neurons include an increase in K+ from outside the cell, and increase of Ca2+ in the presynaptic terminals. These mechanisms blunt hyperpolarization and depolarizes nearby neurons, as well as increasing neurotransmitter release.

Diagnosis
Seizures may be divided into provoked and unprovoked. Provoked seizures may also be known as "acute symptomatic seizures" or "reactive seizures". Unprovoked seizures may also be known as "reflex seizures". Depending on the presumed cause blood tests and lumbar puncture may be useful. Hypoglycemia may cause seizures and should be ruled out. An electroencephalogram and brain imaging with CT scan or MRI scan is recommended in the work-up of seizures not associated with a fever.

Classification
Seizure types are organized by whether the source of the seizure is localized (focal seizures) or distributed (generalized seizures) within the brain. Generalized seizures are divided according to the effect on the body and include tonic-clonic (grand mal), absence (petit mal), myoclonic, clonic, tonic, and atonic seizures. Some seizures such as epileptic spasms are of an unknown type.Focal seizures (previously called partial seizures) are divided into simple partial or complex partial seizure. Current practice no longer recommends this, and instead prefers to describe what occurs during a seizure.The classification of seizures can also be made according to dynamical criteria, observable in electrophysiological measurements. It is a classification according to their type of onset and offset.

Physical examination
Most people are in a postictal state (drowsy or confused) following a seizure. They may show signs of other injuries. A bite mark on the side of the tongue helps confirm a seizure when present, but only a third of people who have had a seizure have such a bite. When present in people thought to have had a seizure, this physical sign tentatively increases the likelihood that a seizure was the cause.

Tests
An electroencephalography is only recommended in those who likely had an epileptic seizure and may help determine the type of seizure or syndrome present. In children it is typically only needed after a second seizure. It cannot be used to rule out the diagnosis and may be falsely positive in those without the disease. In certain situations it may be useful to prefer the EEG while sleeping or sleep deprived.Diagnostic imaging by CT scan and MRI is recommended after a first non-febrile seizure to detect structural problems inside the brain. MRI is generally a better imaging test except when intracranial bleeding is suspected. Imaging may be done at a later point in time in those who return to their normal selves while in the emergency room. If a person has a previous diagnosis of epilepsy with previous imaging repeat imaging is not usually needed with subsequent seizures.In adults, testing electrolytes, blood glucose and calcium levels is important to rule these out as causes, as is an electrocardiogram. A lumbar puncture may be useful to diagnose a central nervous system infection but is not routinely needed. Routine antiseizure medical levels in the blood are not required in adults or children. In children additional tests may be required.A high blood prolactin level within the first 20 minutes following a seizure may be useful to confirm an epileptic seizure as opposed to psychogenic non-epileptic seizure. Serum prolactin level is less useful for detecting partial seizures. If it is normal an epileptic seizure is still possible and a serum prolactin does not separate epileptic seizures from syncope. It is not recommended as a routine part of diagnosis epilepsy.

Differential diagnosis
Differentiating an epileptic seizure from other conditions such as syncope can be difficult. Other possible conditions that can mimic a seizure include: decerebrate posturing, psychogenic seizures, tetanus, dystonia, migraine headaches, and strychnine poisoning. In addition, 5% of people with a positive tilt table test may have seizure-like activity that seems due to cerebral hypoxia. Convulsions may occur due to psychological reasons and this is known as a psychogenic non-epileptic seizure. Non-epileptic seizures may also occur due to a number of other reasons.

Prevention
A number of measures have been attempted to prevent seizures in those at risk. Following traumatic brain injury anticonvulsants decrease the risk of early seizures but not late seizures.In those with a history of febrile seizures, some medications (both antipyretics and anticonvulsants) have been found effective for reducing reoccurrence, however due to the frequency of adverse effects and the benign nature of febrile seizures the decision to use medication should be weighted carefully against potential negative effects.There is no clear evidence that antiepileptic drugs are effective or not effective at preventing seizures following a craniotomy, following subdural hematoma, after a stroke, or after subarachnoid haemorrhage, for both people who have had a previous seizure, and those who have not.

Management
Potentially sharp or dangerous objects should be moved from the area around a person experiencing a seizure so that the individual is not hurt. After the seizure, if the person is not fully conscious and alert, they should be placed in the recovery position. A seizure longer than five minutes, or two or more seizures occurring within the time of five minutes is a medical emergency known as status epilepticus. Contrary to a common misconception, bystanders should not attempt to force objects into the mouth of the person having a seizure, as doing so may cause injury to the teeth and gums.Treatments of a person that is actively seizing follows a progression from initial response, through first line, second line, and third line treatments. The initial response involves ensuring the person is protected from potential harms (such as nearby objects) and managing their airway, breathing, and circulation. Airway management should include placing the person on their side, known as the recovery position, to prevent them from choking. If they are unable to breathe because something is blocking their airway, they may require treatments to open their airway.

Medication
The first line medication for an actively seizing person is a benzodiazepine, with most guidelines recommending lorazepam. Diazepam and midazolam are alternatives. This may be repeated if there is no effect after 10 minutes. If there is no effect after two doses, barbiturates or propofol may be used.Second-line therapy for adults is phenytoin or fosphenytoin and phenobarbital for children. Third-line medications include phenytoin for children and phenobarbital for adults.Ongoing anti-epileptic medications are not typically recommended after a first seizure except in those with structural lesions in the brain. They are generally recommended after a second one has occurred. Approximately 70% of people can obtain full control with continuous use of medication. Typically one type of anticonvulsant is preferred. Following a first seizure, while immediate treatment with an anti-seizure drug lowers the probability of seizure recurrence up to five years it does not change the risk of death and there are potential side effects.In seizures related to toxins, up to two doses of benzodiazepines should be used. If this is not effective pyridoxine is recommended. Phenytoin should generally not be used.There is a lack of evidence for preventive anti-epileptic medications in the management of seizures related to intracranial venous thrombosis.

Other
Helmets may be used to provide protection to the head during a seizure. Some claim that seizure response dogs, a form of service dog, can predict seizures. Evidence for this, however, is poor. At present there is not enough evidence to support the use of cannabis for the management of seizures, although this is an ongoing area of research. There is low quality evidence that a ketogenic diet may help in those who have epilepsy and is reasonable in those who do not improve following typical treatments.

Prognosis
Following a first seizure, the risk of more seizures in the next two years is 40–50%. The greatest predictors of more seizures are problems either on the electroencephalogram or on imaging of the brain. In adults, after 6 months of being seizure-free after a first seizure, the risk of a subsequent seizure in the next year is less than 20% regardless of treatment. Up to 7% of seizures that present to the emergency department (ER) are in status epilepticus. In those with a status epilepticus, mortality is between 10% and 40%. Those who have a seizure that is provoked (occurring close in time to an acute brain event or toxic exposure) have a low risk of re-occurrence, but have a higher risk of death compared to those with epilepsy.

Epidemiology
Approximately 8–10% of people will experience an epileptic seizure during their lifetime. In adults, the risk of seizure recurrence within the five years following a new-onset seizure is 35%; the risk rises to 75% in persons who have had a second seizure. In children, the risk of seizure recurrence within the five years following a single unprovoked seizure is about 50%; the risk rises to about 80% after two unprovoked seizures. In the United States in 2011, seizures resulted in an estimated 1.6 million emergency department visits; approximately 400,000 of these visits were for new-onset seizures. The exact incidence of epileptic seizures in low-income and middle-income countries is unknown, however it probably exceeds that in high-income countries. This may be due to increased risks of traffic accidents, birth injuries, and malaria and other parasitic infections.

History
Epileptic seizures were first described in an Akkadian text from 2000 B.C </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 Localized hypertrichosis 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 Bacteriuria and can you explain it in depth? [/INST] Bacteriuria is the presence of bacteria in urine. Bacteriuria accompanied by symptoms is a urinary tract infection while that without is known as asymptomatic bacteriuria. Diagnosis is by urinalysis or urine culture. Escherichia coli is the most common bacterium found. People without symptoms should generally not be tested for the condition. Differential diagnosis include contamination.If symptoms are present treatment is generally with antibiotics. Bacteriuria without symptoms generally does not require treatment. Exceptions may include pregnant women, those who have had a recent kidney transplant, young children with significant vesicoureteral reflux, and those undergoing surgery of the urinary tract.Bacteriuria without symptoms is present in about 3% of otherwise healthy middle aged women. In nursing homes rates are as high as 50% among women and 40% in men. In those with a long term indwelling urinary catheter rates are 100%. Up to 10% of women have a urinary tract infection in a given year and half of all women have at least one infection at some point in their lives. There is an increased risk of asymptomatic or symptomatic bacteriuria in pregnancy due to physiological changes that occur in a pregnant women which promotes unwanted pathogen growth in the urinary tract.

Signs and symptoms
Asymptomatic
Asymptomatic bacteriuria is bacteriuria without accompanying symptoms of a urinary tract infection and is commonly caused by the bacterium Escherichia coli. Other potential pathogens are Klebsiella spp., and group B streptococci. It is more common in women, in the elderly, in residents of long-term care facilities, and in people with diabetes, bladder catheters, and spinal cord injuries. People with a long-term Foley catheter always show bacteriuria. Chronic asymptomatic bacteriuria occurs in as many as 50% of the population in long-term care.There is an association between asymptomatic bacteriuria in pregnant women with low birth weight, preterm delivery, cystitis, infection of the newborn and fetus death. However, most of these studies were graded as poor quality. Bacteriuria in pregnancy also increases the risk of preeclampsia.

Symptomatic
Symptomatic bacteriuria is bacteriuria with the accompanying symptoms of a urinary tract infection (such as frequent urination, painful urination, fever, back pain, abdominal pain and blood in the urine) and includes pyelonephritis or cystitis. The most common cause of urinary tract infections is Escherichia coli.

Diagnosis
Testing for bacteriuria is usually performed in people with symptoms of a urinary tract infection. Certain populations that cannot feel or express symptoms of infection are also tested when showing nonspecific symptoms. For example, confusion or other changes in behaviour can be a sign of an infection in the elderly. Screening for asymptomatic bacteriuria in pregnancy is a common routine in many countries, but controversial.

The gold standard for detecting bacteriuria is a bacterial culture which identifies the concentration of bacterial cells in the urine. The culture is usually combined with subsequent testing using biochemical methods or MALDI-TOF, which allows to identify the causal bacterial species, and antibiotic susceptibility testing. Urine culture is quantitative and very reliable, but can take at least one day to obtain a result and it is expensive.Miniaturization of bacterial culture within dipstick format, Digital Dipstick, allows bacterial detection, identification and quantification for bacteriuria within 10–12 hours at the point-of-care. Clinicians will often treat symptomatic bacteriuria based on the results of the urine dipstick test while waiting for the culture results.
Bacteriuria can usually be detected using a urine dipstick test. The nitrite test detects nitrate-reducing bacteria if growing in high numbers in urine. A negative dipstick test does not exclude bacteriuria, as not all bacteria which can colonise the urinary tract are nitrate-reducing. The leukocyte esterase test indirectly detects the presence of leukocytes (white blood cells) in urine which can be associated with a urinary tract infection. In the elderly, the leukocyte esterase test is often positive even in the absence of an infection. The urine dipstick test is readily available and provides fast, but often unreliable results.
Microscopy can also be used to detect bacteriuria. It is rarely used in clinical routine since it requires more time and equipment and does not allow reliable identification or quantification of the causal bacterial species.Bacteriuria is assumed if a single bacterial species is isolated in a concentration greater than 100,000 colony forming units per millilitre of urine in clean-catch midstream urine specimens. In urine samples obtained from women, there is a risk for bacterial contamination from the vaginal flora </s>