<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Postural orthostatic tachycardia syndrome and explain in detail? [/INST] Postural orthostatic tachycardia syndrome (POTS) is a condition characterized by an abnormally large increase in heart rate upon standing. Symptoms may include lightheadedness, brain fog, blurred vision, weakness, fatigue, headaches, heart palpitations, exercise intolerance, nausea, diminished concentration, tremulousness (shaking), syncope (fainting), coldness or pain in the extremities, chest pain and shortness of breath. Other conditions associated with POTS include Ehlers–Danlos syndrome, mast cell activation syndrome, irritable bowel syndrome, insomnia, chronic headaches, chronic fatigue syndrome, and fibromyalgia. POTS symptoms may be treated with lifestyle changes such as increasing fluid and salt intake, wearing compression stockings, gentler and slow postural changes, avoiding prolonged bedrest, medication and physical therapy.
The causes of POTS are varied. POTS may develop after a viral infection, surgery, trauma or pregnancy. It has been shown to emerge in previously healthy patients after COVID-19. Risk factors include a family history of the condition. A POTS diagnosis in adults is characterized by an increased heart rate of 30 beats per minute within ten minutes of standing up, while accompanied by symptoms. This increased heart rate should occur in the absence of orthostatic hypotension (>20 mm Hg drop in systolic blood pressure) to be considered POTS. A spinal fluid leak (called spontaneous intracranial hypotension) may have the same signs and symptoms as POTS and should be excluded. Prolonged bedrest may lead to multiple symptoms, including blood volume loss and postural tachycardia. Other conditions which can cause similar symptoms, such as dehydration, orthostatic hypotension, heart problems, adrenal insufficiency, epilepsy, and Parkinsons disease, must not be present.Treatment may include avoiding factors that bring on symptoms, increasing dietary salt and water, small and frequent meals, avoidance of immobilization, wearing compression stockings, and taking medications. Medications used may include beta blockers, pyridostigmine, midodrine or fludrocortisone. More than 50% of patients whose condition was triggered by a viral infection get better within five years. About 80% of patients have symptomatic improvement with treatment, while 25 percent of patients are so disabled they are unable to work. Retrospective studies has shown that five years after diagnosis, 19% of patients had a full resolution of symptoms.It is estimated that 500,000 people in the United States have POTS. The average age for POTS onset is 20 years old, and it occurs about five times more frequently in females than in males.

Signs and symptoms
In adults, the primary manifestation is an increase in heart rate of more than 30 beats per minute within ten minutes of standing up. The resulting heart rate is typically more than 120 beats per minute. For people between ages 12 and 19, the minimum increase for a POTS diagnosis is 40 beats per minute. POTS is often accompanied by common features of orthostatic intolerance—in which symptoms that develop while upright are relieved by reclining. These orthostatic symptoms include palpitations, light-headedness, chest discomfort, shortness of breath, nausea, weakness or "heaviness" in the lower legs, blurred vision, and cognitive difficulties. Symptoms may be exacerbated with prolonged sitting, prolonged standing, alcohol, heat, exercise, or eating a large meal.Up to one-third of POTS patients experience fainting for many reasons, including but not limited to standing, physical exertion, or heat exposure. POTS patients may also experience orthostatic headaches. Some POTS patients may develop blood pooling in the extremities, characterized by a reddish-purple color of the legs and/or hands upon standing. 48% of people with POTS report chronic fatigue and 32% report sleep disturbances. Other POTS patients only exhibit the cardinal symptom of orthostatic tachycardia. Additional signs and symptoms are varied, and may include excessive sweating, lack of sweating, heat intolerance, digestive issues such as nausea, indigestion, constipation, and diarrhea, post-exertional malaise, coat-hanger pain, brain fog, and syncope or presyncope.

Brain fog
One of the most disabling and prevalent symptoms in POTS is "brain fog", a term used by patients to describe the cognitive difficulties they experience. In one survey of 138 POTS patients, brain fog was defined as "forgetful" (91%), "difficulty thinking" (89%), and "difficulty focusing" (88%). Other common description was "Difficulty processing what others say" (80%), Confusion (71%), Lost (64%), and "Thoughts moving too quickly" (40%). The same survey described the most common triggers of brain fog to be fatigue (91%), lack of sleep (90%), prolonged standing (87%) and dehydration (86%).Neuropsychological testing has shown that a POTS patient has reduced attention (Ruff 2&7 speed and WAIS-III digits forward), short-term memory (WAIS-III digits back), cognitive processing speed (Symbol digits modalities test) and executive function (Stroop word color and trails B).A potential cause for brain fog is a decrease in cerebral blood flow (CBF), especially in upright position.There may be a loss of neurovascular coupling and reduced functional hyperemia in response to cognitive challenge under orthostatic stress – perhaps related to a loss of autoregulatory buffering of beat-by-beat fluctuations in arterial blood flow.

Causes
The symptoms of POTS can be caused by several distinct pathophysiological mechanisms. These mechanisms are poorly understood, and can overlap, with many patients showing features of multiple POTS types. Many people with POTS exhibit low blood volume (hypovolemia), which can decrease the rate of blood flow to the heart. To compensate for low blood volume, the heart increases its cardiac output by beating faster, leading to the symptoms of presyncope and reflex tachycardia.In the 30% to 60% of cases classified as hyperadrenergic POTS, norepinephrine levels are elevated on standing, often due to hypovolemia or partial autonomic neuropathy. A smaller minority of people with POTS have (typically very high) standing norepinephrine levels that are elevated even in the absence of hypovolemia and autonomic neuropathy; this is classified as central hyperadrenergic POTS. The high norepinephrine levels contribute to symptoms of tachycardia. Another subtype, neuropathic POTS, is associated with denervation of sympathetic nerves in the lower limbs. In this subtype, it is thought that impaired constriction of the blood vessels causes blood to pool in the veins of the lower limbs. Heart rate increases to compensate for this blood pooling.In up to 50% of cases, there was an onset of symptoms following a viral illness. It may also be linked to vaccination, physical trauma, concussion, pregnancy, or surgery. It is believed that these events could act as a trigger for an autoimmune response that result in POTS.POTS is more common in females than males. It has also been shown to be linked in patients with acute stressors such as pregnancy, recent surgery, or recent trauma. POTS also has been linked to patients with a history of autoimmune diseases, irritable bowel syndrome, anemia, hyperthyroidism, fibromyalgia, diabetes, amyloidosis, sarcoidosis, systemic lupus erythematosus, and cancer. Genetics likely plays a role, with one study finding that one in eight POTS patients reported a history of orthostatic intolerance in their family.

Autoimmunity
There is an increasing number of studies indicating that POTS is an autoimmune disease. A high number of patients has elevated levels of autoantibodies against the adrenergic alpha 1 receptor and against the muscarinic acetylcholine M4 receptor.Elevations of autoantibodies targeting adrenergic α1 receptor has been associated with symptoms severity in patients with POTS.More recently, autoantibodies against other targets have been identified in small cohorts of POTS patients. Signs of innate immune system activation with elaboration of pro-inflammatory cytokines has also been reported in a cohort of POTS patients.

Secondary POTS
If POTS is caused by another condition, it may be classified as secondary POTS. Chronic diabetes mellitus is one common cause. POTS can also be secondary to gastrointestinal disorders that are associated with low fluid intake due to nausea or fluid loss through diarrhea, leading to hypovolemia. Systemic lupus erythematosus and other autoimmune diseases have also been linked to POTS.There is a subset of patients who present with both POTS and mast cell activation syndrome (MCAS), and it is not yet clear whether MCAS is a secondary cause of POTS or simply comorbid, however, treating MCAS for these patients can significantly improve POTS symptoms.POTS can also co-occur in all types of Ehlers–Danlos syndrome (EDS), a hereditary connective tissue disorder marked by loose hypermobile joints prone to subluxations and dislocations, skin that exhibits moderate or greater laxity, easy bruising, and many other symptoms. A trifecta of POTS, EDS, and Mast Cell Activation Syndrome (MCAS) is becoming increasingly more common, with a genetic marker common among all three conditions. POTS is also often accompanied by vasovagal syncope, with a 25% overlap being reported. There are some overlaps between POTS and chronic fatigue syndrome, with evidence of POTS in 10–20% of CFS cases. Fatigue and reduced exercise tolerance are prominent symptoms of both conditions, and dysautonomia may underlie both conditions.POTS can sometimes be a paraneoplastic syndrome associated with cancer.There are case reports of people developing POTS and other forms of dysautonomia post-COVID. There is no good large-scale empirical evidence yet to prove a connection, so for now the evidence is preliminary.

Diagnosis
POTS is most commonly diagnosed by a cardiologist (41%), cardiac electrophysiologist (15%), or Neurologist (19%). The average number of physicians seen before receiving diagnosis is seven, and the average delay before diagnosis is 4.7 years.

Diagnostic criteria
A POTS diagnosis requires the following characteristics:
For patients age 20 or older, increase in heart rate ≥30 bpm within ten minutes of upright posture (tilt table test or standing) from a supine position
For patients age 12–19, heart rate increase must be >40 bpm
Associated with related symptoms that are worse with upright posture and that improve with recumbence
Chronic symptoms that have lasted for longer than six months
In the absence of other disorders, medications, or functional states that are known to predispose to orthostatic tachycardia

Orthostatic intolerance
An increase in heart rate upon moving to an upright posture is known as orthostatic (upright) tachycardia (fast heart rate). It occurs without any coinciding drop in blood pressure, as that would indicate orthostatic hypotension. Certain medications to treat POTS may cause orthostatic hypotension. It is accompanied by other features of orthostatic intolerance—symptoms that develop in an upright position and are relieved by reclining. These orthostatic symptoms include palpitations, light-headedness, chest discomfort, shortness of breath, nausea, weakness or "heaviness" in the lower legs, blurred vision, and cognitive difficulties.

Differential diagnoses
A variety of autonomic tests are employed to exclude autonomic disorders that could underlie symptoms, while endocrine testing is used to exclude hyperthyroidism and rarer endocrine conditions. Electrocardiography is normally performed on all patients to exclude other possible causes of tachycardia. In cases where a particular associated condition or complicating factor are suspected, other non-autonomic tests may be used: echocardiography to exclude mitral valve prolapse, and thermal threshold tests for small-fiber neuropathy.Testing the cardiovascular response to prolonged head-up tilting, exercise, eating, and heat stress may help determine the best strategy for managing symptoms. POTS has also been divided into several types (see § Causes), which may benefit from distinct treatments. People with neuropathic POTS show a loss of sweating in the feet during sweat tests, as well as impaired norepinephrine release in the leg, but not arm. This is believed to reflect peripheral sympathetic denervation in the lower limbs. People with hyperadrenergic POTS show a marked increase of blood pressure and norepinephrine levels when standing, and are more likely to have from prominent palpitations, anxiety, and tachycardia.People with POTS can be misdiagnosed with inappropriate sinus tachycardia (IST) as they present similarly. One distinguishing feature is those with POTS rarely exhibit >100 bpm while in a supine position, while patients with IST often have a resting heart rate >100 bpm. Additionally patients with POTS display a more pronounced change in heart rate in response to postural change.

Treatment
POTS treatment involves using multiple methods in combination to counteract cardiovascular dysfunction, address symptoms, and simultaneously address any associated disorders. For most patients, water intake should be increased, especially after waking, in order to expand blood volume (reducing hypovolemia). Eight to ten cups of water daily are recommended. Increasing salt intake, by adding salt to food, taking salt tablets, or drinking sports drinks and other electrolyte solutions is an effective way to raise blood pressure by helping the body retain water. Different physicians recommend different amounts of sodium to their patients. Combining these techniques with gradual physical training enhances their effect. In some cases, when increasing oral fluids and salt intake is not enough, intravenous saline or the drug desmopressin is used to help increase fluid retention.Large meals worsen symptoms for some people. These people may benefit from eating small meals frequently throughout the day instead. Alcohol and food high in carbohydrates can also exacerbate symptoms of orthostatic hypotension. Excessive consumption of caffeine beverages should be avoided, because they can promote urine production (leading to fluid loss) and consequently hypovolemia. Exposure to extreme heat may also aggravate symptoms.
Prolonged physical inactivity can worsen the symptoms of POTS. Techniques that increase a persons capacity for exercise, such as endurance training or graded exercise therapy, can relieve symptoms for some patients. Aerobic exercise performed for 20 minutes a day, three times a week, is sometimes recommended for patients who can tolerate it. Exercise may have the immediate effect of worsening tachycardia, especially after a meal or on a hot day. In these cases, it may be easier to exercise in a semi-reclined position, such as riding a recumbent bicycle, rowing, or swimming.When changing to an upright posture, finishing a meal, or concluding exercise, a sustained hand grip can briefly raise the blood pressure, possibly reducing symptoms. Compression garments can also be of benefit by constricting blood pressures with external body pressure.

Medication
If nonpharmacological methods are ineffective, medication may be necessary. Medications used may include beta blockers, pyridostigmine, midodrine, or fludrocortisone. As of 2013, no medication has been approved by the U.S. Food and Drug Administration to treat POTS, but a variety are used off-label. Their efficacy has not yet been examined in long-term randomized controlled trials.Fludrocortisone may be used to enhance sodium retention and blood volume, which may be beneficial not only by augmenting sympathetically mediated vasoconstriction, but also because a large subset of POTS patients appear to have low absolute blood volume.While people with POTS typically have normal or even elevated arterial blood pressure, the neuropathic form of POTS is presumed to constitute a selective sympathetic venous denervation. In these patients the selective Alpha-1 adrenergic receptor agonist midodrine may increase venous return, enhance stroke volume, and improve symptoms. Midodrine should only be taken during the daylight hours as it may promote supine hypertension.Sinus node blocker Ivabradine can successfully restrain heart rate in POTS without affecting blood pressure, demonstrated in approximately 60% of people with POTS treated in an open-label trial of ivabradine experienced symptom improvement.Pyridostigmine has been reported to restrain heart rate and improve chronic symptoms in approximately half of people.The selective alpha-1 agonist phenylephrine has been used successfully to enhance venous return and stroke volume in some people with POTS. However, this medication may be hampered by poor oral bioavailability.

Prognosis
POTS has a favorable prognosis when managed appropriately. Symptoms improve within five years of diagnosis for many patients, and 60% return to their original level of functioning. Approximately 90% of people with POTS respond to a combination of pharmacological and physical treatments. Those who develop POTS in their early to mid teens during a period of rapid growth will most likely see complete symptom resolution in two to five years. Outcomes are more guarded for adults newly diagnosed with POTS. Some people do not recover, and a few even worsen with time. The hyperadrenergic type of POTS typically requires continuous therapy. If POTS is caused by another condition, outcomes depend on the prognosis of the underlying disorder.

Epidemiology
The prevalence of POTS is unknown. One study estimated a minimal rate of 170 POTS cases per 100,000 individuals, but the true prevalence is likely higher due to underdiagnosis. Another study estimated that there are at least 500,000 cases in the United States. POTS is more common in women than men, with a female-to-male ratio of 4:1. Most people with POTS are aged between 20 and 40, with an average onset of 21. Diagnoses of POTS beyond age 40 are rare, perhaps because symptoms improve with age.

Co-morbidities
Conditions that are commonly reported with POTS include:
Migraine headaches (11–40%)
Ehlers–Danlos syndrome (20–25%)
Fibromyalgia (11–20%)
Irritable bowel syndrome (7–30%)
Chronic fatigue syndrome (7–21%)
Mast cell activation disorder (6–9%)

History
In 1871, physician Jacob Mendes Da Costa described a condition that resembled the modern concept of POTS. He named it irritable heart syndrome </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Papular xanthoma and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Spanish flu (disambiguation) and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Eosinophilia–myalgia syndrome and explain in detail? [/INST] Eosinophilia–myalgia syndrome is a rare, sometimes fatal neurological condition linked to the ingestion of the dietary supplement L-tryptophan. The risk of developing EMS increases with larger doses of tryptophan and increasing age. Some research suggests that certain genetic polymorphisms may be related to the development of EMS. The presence of eosinophilia is a core feature of EMS, along with unusually severe myalgia (muscle pain).

Signs and symptoms
The initial, acute phase of EMS, which last for three to six months, presents as trouble with breathing and muscle problems, including soreness and spasm, but which may also be intense. Muscle weakness is not a feature of this phase, but some people experience muscle stiffness. Additional features can include cough, fever, fatigue, joint pain, edema, and numbness or tingling, usually in the limbs, hands and feet.The chronic phase follows the acute phase. Eosinophilic fasciitis may develop, primarily in the limbs. CNS signs may appear, including numbness, increased sensation, muscle weakness, and sometimes cardiac or digestive dysfunction. Fatigue is present to some degree, while the muscle pain (which may be extremely intense) and dyspnea continue in this phase.

Causes
Subsequent epidemiological studies suggested that EMS was linked to specific batches of L-tryptophan supplied by a single large Japanese manufacturer, Showa Denko. It eventually became clear that recent batches of Showa Denkos L-tryptophan were contaminated by trace impurities, which were subsequently thought to be responsible for the 1989 EMS outbreak. The L-tryptophan was produced by a bacterium grown in open vats in a Showa Denko fertilizer factory. While a total of 63 trace contaminants were eventually identified, only six of them could be associated with EMS. The compound EBT (1,1-ethylidene-bis-L-tryptophan, also known as "Peak E") was the only contaminant identifiable by initial analysis, but further analysis revealed PAA (3-(phenylamino)-L-alanine, also known as "UV-5"), and peak 200 (2[3-indolyl-methyl]-L-tryptophan). Two of the remaining uncharacterized peaks associated with EMS were later determined to be 3a-hydroxy-1,2,3,3a,8,8a-hexahydropyrrolo-[2,3-b]-indole-2-carboxylic acid (peak C) and 2-(2-hydroxy indoline)-tryptophan (peak FF). These were characterized using accurate mass LC–MS, LC–MS/MS and multistage mass spectrometry (MSn). The last of the six contaminants (peak AAA/"UV-28", being "the contaminant most significantly associated with EMS"  has been characterized as two related chain-isomers; peak AAA1 ((S)-2-amino-3-(2-((S,E)-7-methylnon-1-en-1-yl)-1H-indol-3-yl)propanoic acid, a condensation product between L-tryptophan and 7-methylnonanoic acid) and peak AAA2 ((S)-2-amino-3-(2-((E)-dec-1-en-1-yl)-1H-indol-3-yl)propanoic acid, a condensate between L-tryptophan and decanoic acid). No consistent relationship has ever been firmly established between any specific trace impurity or impurities identified in these batches and the effects of EMS. While EBT in particular has been frequently implicated as the culprit, there is no statistically significant association between EBT levels and EMS. Of the 63 trace contaminants, only the two AAA compounds displayed a statistically significant association with cases of EMS (with a p-value of 0.0014).As most research has focused on attempts to associate individual contaminants with EMS, there is a comparative lack of detailed research on other possible causal or contributing factors. Tryptophan itself has been implicated as a potentially major contributory factor in EMS. While critics of this theory have argued that this hypothesis fails to explain the near-absent reports of EMS prior to and following the EMS outbreak, this fails to take into account the sudden rapid increase in tryptophans usage immediately prior to the 1989 outbreak, and ignores the strong influence of the EMS outbreaks legacy and the extended FDA ban on later usage of tryptophan. Crucially, this also ignores the existence of a number of cases of EMS that developed both prior to and after the primary epidemic, including at least one case where the tryptophan was tested and found to lack the contaminants found in the contaminated lots of Showa Denkos tryptophan, as well as cases with other supplements inducing EMS, and even a case of EMS induced by excessive dietary L-tryptophan intake via overconsumption of cashew nuts. A major Canadian analysis located a number of patients that met the CDC criteria for EMS but had never been exposed to tryptophan, which "brings causal interpretations of earlier studies into question". Other studies have highlighted numerous major flaws in many of the epidemiological studies on the association of tryptophan with EMS, which cast serious doubt on the validity of their results. As the FDA concluded, "other brands of L-tryptophan, or L-tryptophan itself, regardless of the levels or presence of impurities, could not be eliminated as causal or contributing to the development of EMS". Even animal studies have suggested that tryptophan itself "when ingested by susceptible individuals either alone or in combination with some other component in the product, results in the pathological features in EMS".At the time of the outbreak, Showa Denko had recently made alterations to its manufacturing procedures that were thought to be linked to the possible origin of the contaminants detected in the affected lots of tryptophan. A key change was the reduction of the amount of activated charcoal used to purify each batch from >20 kg to 10 kg. A portion of the contaminated batches had also bypassed another filtration step that used reverse-osmosis to remove certain impurities. Additionally, the bacterial culture used to synthesize tryptophan was a strain of Bacillus amyloliquefaciens that had been genetically engineered to increase tryptophan production </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Orbital cellulitis and explain in detail? [/INST] Orbital cellulitis  is inflammation of eye tissues behind the orbital septum. It is most commonly caused by an acute spread of infection into the eye socket from either the adjacent sinuses or through the blood. It may also occur after trauma.  When it affects the rear of the eye, it is known as retro-orbital cellulitis.
It should not be confused with periorbital cellulitis, which refers to cellulitis anterior to the septum.
Without proper treatment, orbital cellulitis may lead to serious consequences, including permanent loss of vision or even death.

Signs and symptoms
Orbital cellulitis commonly presents with painful eye movement, sudden vision loss, chemosis, bulging of the infected eye, and limited eye movement. Along with these symptoms, patients typically have redness and swelling of the eyelid, pain, discharge, inability to open the eye, occasional fever and lethargy.

Complications
Complications include hearing loss, blood infection, meningitis, cavernous sinus thrombosis, cerebral abscess, and blindness. It is possible that children experience more severe complications due to their immature immune system and because they have thinner orbital bones, which makes the infection easier to spread.

Causes
Orbital cellulitis occurs commonly from bacterial infection spread via the paranasal sinuses, usually from a previous sinus infection. Other ways in which orbital cellulitis may occur are from blood stream infections or from eyelid skin infections. Upper respiratory infection, sinus infection, trauma to the eye, ocular or periocular infection, and systemic infection all increase ones risk of orbital cellulitis.
Staphylococcus aureus, Haemophilus influenzae B, Moraxella catarrhalis, Streptococcus pneumoniae, and beta-hemolytic streptococci are bacteria that can be responsible for orbital cellulitis.
Staphylococcus aureus is a gram-positive bacterium, which is the most common cause of staphylococcal infections. Staphylococcus aureus infection can spread from the skin to the orbit. This organism is able to produce toxins which promotes its virulence, leading to the inflammatory response seen in orbital cellulitis. Staphylococcus infections are identified by a cluster arrangement on gram stain. Staphylococcus aureus forms large yellow colonies when cultured (which is distinct from other Staph infections such as Staphylococcus epidermidis, which forms white colonies).
Streptococcus pneumoniae is also a gram-positive bacterium responsible for orbital cellulitis due to its ability to infect the sinuses.  Streptococcal bacteria can invade surrounding tissues, causing the inflammatory response seen in orbital cellulitis (similar to Staphyloccoccus aureus). Streptococcal infections are identified on culture by their formation of pairs or chains. Streptococcus pneumoniae produce green (alpha) hemolysis, or partial reduction of red blood cell hemoglobin.

Risk Factors
Risk factors for the development of orbital cellulitis include, but are not limited to:
Recent upper respiratory illness
Sinus infection
Younger age
Retained foreign bodies within the orbit
Trauma
Immunosuppression
Systemic infection
Dental infection

Diagnosis
Early diagnosis of orbital cellulitis is urgent, and it involves a complete and thorough physical examination. Common presenting signs include: a protruding eye (proptosis), eyelid edema (swelling), eye pain, vision loss, inability to move the eye completely (ophthalmoplegia), and fever. It is important to correlate physical findings with patient history and reported symptoms.CT scan and MRI of the orbits are two imaging modalities that are commonly used to aid in the diagnosis and monitoring of orbital cellulitis, as they can provide detailed images that can show the extent of inflammation along with possible abscess location, size, and involvement of surrounding structures. Ultrasound has also been used as an imaging modality in the past, but it cannot provide the same level of detail as CT or MRI.Blood cultures, electrolytes, and a complete blood count (CBC) with differential showing elevated white blood cell count is a useful laboratory test that may aid in diagnosis.

Differential Diagnosis
A variety of pathologies and diseases can present similarly to orbital cellulitis, including:
Inflammatory causes (thyroid eye disease, idiopathic orbital inflammatory syndrome, sarcoidosis, granulomatosis with polyangiitis)
Infectious causes (subperiosteal abscess)
Neoplastic, benign and malignant (dermoid cyst, capillary hemangioma, rhabdomyosarcoma, optic nerve glioma, lymphangioma, neurofibroma, leukemia)
Trauma (orbital fracture, retrobulbar hemorrhage, orbital foreign body, carotid cavernous fistula)
Malformation (congenital, vascular)

Treatment
Immediate treatment is very important, and it typically involves intravenous (IV) antibiotics in the hospital and frequent observation (every 4–6 hours). Several lab tests should be ordered, including a complete blood count, differential, and blood culture.

Antibiotic therapy – Since orbital cellulitis is commonly caused by Staphylococcus and Streptococcus species, both penicillins and cephalosporins are typically the best choices for IV antibiotics. However, due to the increasing rise of MRSA (methicillin-resistant Staphylococcus aureus) orbital cellulitis can also be treated with Vancomycin, Clindamycin, or Doxycycline. If improvement is noted after 48 hours of IV antibiotics, healthcare professionals can then consider switching a patient to oral antibiotics (which must be used for 2–3 weeks).
Surgical intervention – An abscess can threaten the vision or neurological status of a patient with orbital cellulitis, therefore sometimes surgical intervention is necessary. Surgery typically requires drainage of the sinuses and if a subperiosteal abscess is present in the medial orbit, drainage can be performed endoscopically.  Post-operatively, patients must follow up regularly with their surgeon and remain under close observation.
Corticosteroids - Complications of orbital cellulitis may arise as a result of swelling from the infection. Because the orbit is a small space, increasing the pressure inside can harm the eye. Steroids are drugs that are used to reduce swelling caused by various illnesses, but they can also weaken the immune systems ability to fight the infection. There is inadequate evidence to draw judgments about the use of steroids in the treatment of orbital cellulitis. More research is needed to inform decision making.

Prognosis
Although orbital cellulitis is considered an ophthalmic emergency, the prognosis is good if prompt medical treatment is received.

Death and blindness rates without treatment
Bacterial infections of the orbit have long been associated with a risk of devastating outcomes and intracranial spread.
The natural course of the disease, as documented by Gamble (1933), in the pre-antibiotic era,
resulted in death in 17% of patients and permanent blindness in 20%.

Epidemiology
Orbital cellulitis is an uncommon medical condition, with the reported rates being much higher among the pediatric population compared to the adult population. One study reported that children are approximately 16 times more likely to suffer from orbital cellulitis compared to adults. It is twice as common among male children compared to female children. Some studies reported that orbital cellulitis follows a seasonal pattern, with the highest rates occurring during the fall and winter, which coincides with the higher rates of sinus infection during the colder months.

References
Noel LP, Clarke WN, MacDonald N (1990) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Myelophthisic anemia and explain in detail? [/INST] Myelophthisic anemia (or myelophthisis) is a severe type of anemia found in some people with diseases that affect the bone marrow.  Myelophthisis refers to the displacement of hemopoietic bone-marrow tissue by fibrosis, tumors, or granulomas </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Adult attention deficit hyperactivity disorder and explain in detail? [/INST] Adult attention deficit hyperactivity disorder is the neurological condition of attention deficit hyperactivity disorder (ADHD) in adults. About one-third to two-thirds of children with symptoms from early childhood continue to demonstrate ADHD symptoms throughout life.: 44 Three types of ADHD are identified in the DSM-5 as:

Predominantly Inattentive Type (ADHD-PI or ADHD-I)
Predominantly Hyperactive or Hyperactive-Impulsive Type (ADHD-PH or ADHD-HI)
Combined Type (ADHD-C)In later life, the hyperactive/impulsive subtype manifests less frequently.: 44  The hyperactivity symptoms tend to turn more into "inner restlessness", starting in adolescence and carrying on in adulthood.Adult ADHD is typically marked by inattention and hyperfocus, hyperactivity (often internalised as restlessness), emotional dysregulation, and excessive mind wandering. Specifically, adults with ADHD present with persistent difficulties in following directions, remembering information, concentrating, organizing tasks, completing work within specified time frames and appearing timely in appointments. These difficulties affect several different areas of an ADHD adults life, causing emotional, social, vocational, marital, legal, financial and/or academic problems.Diagnosis follows one or several psychiatric assessment which may include examination of personal history, observational evidence from family members or friends, academic reports, often going back to school years, as well as evaluation to diagnose additional possible conditions which often coexist with ADHD, called comorbidities or comorbid disorders.
The condition often runs in families, and while its exact causes are not fully known, genetic or environmental factors are understood to play a part. ADHD often - but not always - is a childhood-onset condition. Children under treatment will migrate to adult health services if necessary as they transit into adulthood, however diagnosis of adults involves full examination of their history.
Treatment of ADHD is usually based on a combination of behavioral interventions and medication. Stimulant medication is the first line treatment for ADHD in adults, particularly amphetamines. Non-stimulant medications, such as atomoxetine, or Viloxazine, are also recommended for some ADHD adults. Psychotherapy such as cognitive behavioural therapy is helpful, particularly in combination with medication. Similarly, exercise, sufficient sleep and nutritious food are also known to have a positive effect. Within school and work, reasonable accommodations may be put in place, such as by structuring work tasks, and setting up clear rules and limits for tasks.

Classification
The DSM-5, or Diagnostic and Statistical Manual of Mental Disorders, 2013 edition, defines three types of ADHD:

a Predominantly Inattentive presentation
a Predominantly Hyperactive-Impulsive presentation
a Combined Type, that displays symptoms from both presentationTo meet the diagnostic criteria of ADHD, an individual must display:

at least six inattentive-type symptoms for the inattentive type
at least six hyperactive-type symptoms for the hyperactive-impulsive type
all of the above to have the combined typeThe symptoms (see below) were required to have been present since before the individual was seven years old, and must have interfered with at least two spheres of his or her functioning (at home and at school or work, for example) over the last six months. The DSM-IV criteria for ADHD were, however, tailored towards the type of symptoms that children would show, and might therefore have underestimated the prevalence of ADHD in adults. In 2013, the newer DSM-5 reviewed some of these criteria, with more lenient requirements for the diagnosis, especially in adults, and the age limit for symptoms first arising raised to twelve years.

Signs and symptoms
ADHD is a chronic condition, beginning in early childhood that can persist throughout a persons lifetime. It is estimated that 33–66% of children with ADHD will continue to have significant ADHD-related symptoms persisting into adulthood, resulting in a significant impact on education, employment, and interpersonal relationships.Individuals with ADHD exhibit deficiencies in self-regulation and self-motivation which in turn foster problematic characteristics such as distractibility, procrastination, and disorganization. They are often perceived by others as chaotic, with a tendency to need high stimulation to be less distracted and function effectively. The learning potential and overall intelligence of an adult with ADHD, however, is no different from the potential and intelligence of adults who do not have the disorder.Whereas teachers and caregivers responsible for children are often attuned to the symptoms of ADHD, employers and others who interact with adults are less likely to regard such behaviors as a symptom. In part, this is because symptoms do change with maturity; adults who have ADHD are less likely to exhibit obvious hyperactive behaviors. Instead, they may report constant mental activity and inner restlessness as their hyperactivity internalizes.Symptoms of ADHD (see table below) can vary widely between individuals and throughout the lifetime of an individual. As the neurobiology of ADHD is becoming increasingly understood, it is becoming evident that difficulties exhibited by individuals with ADHD are due to problems with the parts of the brain responsible for executive functions (see below: Pathophysiology). These result in problems with sustaining attention, planning, organization, prioritization, time management, impulse control, and decision making.The difficulties generated by these deficiencies can range from moderate to extreme, resulting in the inability to effectively structure their lives, plan daily tasks, or think of and act accordingly even when aware of potential consequences. These can lead to poor performance in school and work and can be followed by underachievement in these areas. In young adults, poor driving records with traffic violations may surface.As problems accumulate, a negativistic self-view becomes established and a vicious circle of failure is set up. Up to 80% of adults may have some form of psychiatric comorbidity, such as depression or anxiety. Many with ADHD also have associated learning disabilities, such as dyslexia, which contributes to their difficulties.Studies on adults with ADHD have shown that, more often than not, they experience self-stigma and depression in childhood, commonly resulting from feeling neglected and different from their peers. These problems may play a role in the high levels of depression, substance abuse, and relationship problems that affect adults with ADHD later in life.

Pathophysiology
Over the last 30 years, research into ADHD has greatly increased. There is no single, unified theory that explains the cause of ADHD. Genetic factors are presumed important, and it has been suggested that environmental factors may affect how symptoms manifest.It is becoming increasingly accepted that individuals with ADHD have difficulty with "executive functioning". In higher organisms, such as humans, these functions are thought to reside in the frontal lobes. They enable recall of tasks that need accomplishing, organization to accomplish these tasks, assessment of consequences of actions, prioritization of thoughts and actions, keeping track of time, awareness of interactions with surroundings, the ability to focus despite competing stimuli, and adaptation to changing situations.Several lines of research based on structural and/or functional imaging techniques, stimulant drugs, psychological interventions have identified alterations in the dopaminergic and adrenergic pathways of individuals with ADHD. In particular, areas of the prefrontal cortex appear to be the most affected. Dopamine and norepinephrine are neurotransmitters which play an important role in brain function. The uptake transporters for dopamine and norepinephrine are overly active and clear these neurotransmitters from the synapse a lot faster than in other individuals. This is thought to increase processing latency and salience, and diminish working memory.

Adult ADHD in Men
Studies have shown that adult men with ADHD-type symptoms have issues with interpersonal and romantic relationships. Adult men with ADHD have reported, in a study done by Canu in 2007, to have more romantic partners than their counterparts. They are commonly rated as less desirable to women than people without ADHD-type symptoms. Stimulant medication does not appear to affect the rating given by women. Ratings of self worth also appear to be lower in adult men who are diagnosed with ADHD (Canu, 2007). Canus study looked at adult men with ADHD and found that they did not have higher levels of rejection sensitivity. This may be due to the possibility that individuals with ADHD may not recognize their own impairment of judgement and will overestimate their ability to interact with others to the point that they may not be aware of how poorly a social interaction may go. This may result in lower reports of rejection sensitivity.Other results of adult ADHD are higher reported incidences of traffic citations, missed workdays, and accidents. According to Fritz in a 2016 study, adult men with ADHD may be able to focus better on mental tasks after completing some type of physical exertion. This may help individuals that suffer with adult ADHD. Mood improvements were shown to be statistically significant for a short while but quickly the mood would return to pre-exertion levels.

Diagnosis
While there is no single medical, physical, or genetic test for ADHD, an evaluation can be provided by a qualified mental health care professional or physician who gathers information from multiple sources. These can include ADHD symptom checklists, standardized behavior rating scales, a detailed history of past and current functions including the persons history of childhood behavior and school experiences, and information obtained from family members, friends, or significant others. The evaluations also seek to rule out other conditions or differential diagnoses such as depression, anxiety, or substance use disorders. Other diseases such as hyperthyroidism may exhibit symptoms similar to those of ADHD, and it is imperative to rule these out as well. Autism is sometimes mistaken for ADHD, due to impairments in executive functioning found in some people with autism. However, autism also typically involves difficulties in social interaction, restricted and repetitive patterns of behavior and interests, and problems with sensory processing, including hypersensitivity. Along with this, the quality of diagnosing an adult with ADHD can often be skewed being that the majority of adults with ADHD also have other complications, ranging from anxiety and depression to substance abuse.Formal tests and assessment instruments such as IQ tests, standardized achievement tests, or neuropsychological tests typically are not helpful for identifying people with ADHD. Furthermore, no currently available physiological or medical measure is definitive diagnostically. However, psycho-educational, such as the Continuous Performance Test (CPT), and medical tests are helpful in ruling in or out other conditions (e.g. learning disabilities, allergies) that may be associated with ADHD-like behaviors.The use of neuroimaging is also steadily increasing to help in an ADHD diagnosis. Some of these include:

single-photon emission computed tomography (SPECT)
positron emission tomography (PET)
functional magnetic resonance imaging (fMRI)United States medical and mental health professionals follow the Diagnostic and Statistical Manual of Mental Disorders (DSM) of the American Psychiatric Association; the International Classification of Diseases (ICD) published by the World Health Organisation (WHO) is often used by health professionals elsewhere.
Until recently ADHD in adults was considered as a continuation of child-onset ADHD. It is now established, however, that also an adult-onset version exists. In a large longitudinal study from 2015 it was found that 28 of the 31 persons who had an ADHD-diagnosis at the age of 38 never had received an ADHD-diagnosis when tested at the ages of 11, 13 and 15.

Treatment
As a first step, adults with ADHD should receive psychoeducation about ADHD, so they understand the diagnosis. This is vital to ensure that adults with ADHD can make informed decisions about their treatment, and has other benefits such as improved relationships with others. Treatment often begins with medication selected to address the symptoms of ADHD, along with any comorbid conditions that may be present. Medication alone, while sometimes effective in correcting the physiological symptoms of ADHD, will not address the paucity of skills which many adults will have acquired because of their ADHD (e.g., one might regain ability to focus with medication, but skills such as organizing, prioritizing and effectively communicating have taken others time to cultivate). Suggested treatment for adult ADHD is to include a combined approach of psychosocial interventions (behavioural or cognitive), medication, vocational interventions, and regular follow-up support.

Medications
Medications to help treat ADHD include psychostimulants and non-stimulants. Guidelines and availability of the different options available for medication may vary depending on what country the person lives in.

Stimulants
Stimulants have moderate-to-high effects, which have higher average effects than non-stimulant medications. For adults, amphetamines in particular are the most efficacious medications and they (along with methylphenidate) have the least adverse effects. While there is some debate about whether to treat ADHD adults with substance use disorder (SUD) with stimulants, the 2019 Updated European Consensus Statement on diagnosis and treatment of adult ADHD notes that "in SUD patients, treatment of ADHD [with stimulants] can be useful to reduce ADHD symptoms without worsening the SUD, and should not be avoided".Amphetamine and its derivatives, prototype stimulants, are available in immediate and long-acting formulations. Amphetamines act by multiple mechanisms including reuptake inhibition, displacement of transmitters from vesicles, reversal of uptake transporters and reversible MAO inhibition. Thus amphetamines actively increases the release of these neurotransmitters into the synaptic cleft. In the short term, methylphenidate, a benzylpiperidine and phenethylamine derivative stimulant medication, is well tolerated. As of a 2008 review, long-term studies had not been conducted in adults, although no serious side effects had been reported to regulatory authorities.In the UK, clinical guidelines recommend that psychostimulants are used as a first-line treatment. For people who cannot be treated with stimulants due to a substance use disorder or other contraindications, atomoxetine is the suggested first line treatment in the UK. In Canada, clinical guidelines suggest that first line treatment be methylphenidate or lisdexamfetamine. Non-stimulant medications are generally second-line treatments in Canada.

Non-stimulant medications
The non-stimulant atomoxetine (Strattera), may be an effective treatment for adult ADHD. Although atomoxetine has a half life similar to stimulants it exhibits delayed onset of therapeutic effects similar to antidepressants. Unlike stimulants which are generally controlled substances, atomoxetine lacks addictive potential. It is particularly effective for those with the predominantly inattentive concentration type of attention deficit due to being primarily a norepinephrine reuptake inhibitor. It is often prescribed in adults who cannot tolerate the side effects of amphetamines or methylphenidate. It is also approved for ADHD by the US Food and Drug Administration. A rare but potentially severe side effect includes liver damage and increased suicidal ideation.Viloxazine is a selective norepinephrine reuptake inhibitor that was FDA-approved to treat ADHD in children, adolescents, and adults.Bupropion and desipramine are two antidepressants that have demonstrated some evidence of effectiveness in the management of ADHD particularly when there is comorbid major depression, although antidepressants have lower treatment effect sizes.

Psychotherapy
Psychotherapy, including behavioral therapy, can help an adult with ADHD monitor their own behaviour and provide skills for improving organization and efficiency in daily tasks. Research has shown that, alongside medication, psychological interventions in adults can be effective in reducing symptomatic deficiencies. Cognitive behavioral therapy in particular can provide benefits, especially alongside medication, in the treatment of adult ADHD.

Epidemiology
In North America and Europe, it is estimated that three to five percent of adults have ADHD. Of those adults with ADHD, an estimated 10% of those have received a formal diagnosis. It has been estimated that 5% of the global population has ADHD (including cases not yet diagnosed). In the context of the World Health Organization World Mental Health Survey Initiative, researchers screened more than 11,000 people aged 18 to 44 years in ten countries in the Americas, Europe and the Middle East. On this basis they estimated the adult ADHD proportion of the population to average 3.5 percent with a range of 1.2 to 7.3 percent, with a significantly lower prevalence in low-income countries (1.9%) compared to high-income countries (4.2%). The researchers concluded that adult ADHD often co-occurs with other disorders, and that it is associated with considerable role disability. Although they found that few adults are treated for ADHD itself, in many instances treatment is given for the co-occurring disorders.

History
Early work on disorders of attention was conducted by Alexander Crichton in 1798 writing about "mental restlessness". The underlying condition came to be recognized from the early 1900s by Sir George Still. Efficacy of medications on symptoms was discovered during the 1930s and research continued throughout the twentieth century. ADHD in adults began to be studied from the early 1970s and research has increased as worldwide interest in the condition has grown.In the 1970s researchers began to realize that the condition now known as ADHD did not always disappear in adolescence, as was once thought </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Wandering spleen and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Epidemic typhus and explain in detail? [/INST] Epidemic typhus, also known as louse-borne typhus, is a form of typhus so named because the disease often causes epidemics following wars and natural disasters where civil life is disrupted. Epidemic typhus is spread to people through contact with infected body lice, in contrast to endemic typhus which is usually transmitted by fleas.Though typhus has been responsible for millions of deaths throughout history, it is still considered a rare disease that occurs mainly in populations that suffer unhygienic extreme overcrowding. Typhus is most rare in industrialized countries. It occurs primarily in the colder, mountainous regions of central and east Africa, as well as Central and South America. The causative organism is Rickettsia prowazekii, transmitted by the human body louse (Pediculus humanus corporis). Untreated typhus cases have a fatality rate of approximately 40%.Epidemic typhus should not be confused with Murine typhus, which is more endemic to the United States, particularly Southern California and Texas. This form of typhus has similar symptoms, but is caused by Rickettsia typhi. It is carried primarily in rat feces and fleas, as well as other rodents. It is not as deadly as louse-born typhus. It occurs only during the summer and fall, when rodents are active among humans.

Signs and symptoms
Symptoms of this disease typically begin within 2 weeks of contact with the causative organism. Signs/Symptoms may include:
Fever
Chills
Headache
Confusion
Cough
Rapid Breathing
Body/Muscle Aches
Rash
Nausea
VomitingAfter 5–6 days, a macular skin eruption develops: first on the upper trunk and spreading to the rest of the body (rarely to the face, palms, or soles of the feet, however).Brill–Zinsser disease, first described by Nathan Brill in 1913 at Mount Sinai Hospital in New York City, is a mild form of epidemic typhus that recurs in someone after a long period of latency (similar to the relationship between chickenpox and shingles). This recurrence often arises in times of relative immunosuppression, which is often in the context of a person suffering malnutrition or other illnesses. In combination with poor sanitation and hygiene in times of social chaos and upheaval, which enable a greater density of lice, this reactivation is why typhus generates epidemics in such conditions.

Complications
Complications are as follows
Myocarditis
Endocarditis
Mycotic aneurysm
Pneumonia
Pancreatitis
Kidney or bladder infections
Acute renal failure
Meningitis
Encephalitis
Myelitis
Septic shock

Transmission
Feeding on a human who carries the bacterium infects the louse. R. prowazekii grows in the louses gut and is excreted in its feces. The louse transmits the disease by biting an uninfected human, who scratches the louse bite (which itches) and rubs the feces into the wound. The incubation period is one to two weeks. R. prowazekii can remain viable and virulent in the dried louse feces for many days. Typhus will eventually kill the louse, though the disease will remain viable for many weeks in the dead louse.Epidemic typhus has historically occurred during times of war and deprivation. For example, typhus killed millions of prisoners in German Nazi concentration camps during World War II. The unhygenic conditions in camps such as Auschwitz, Theresienstadt, and Bergen-Belsen allowed diseases such as typhus to flourish. Situations in the twenty-first century with potential for a typhus epidemic would include refugee camps during a major famine or natural disaster. In the periods between outbreaks, when human to human transmission occurs less often, the flying squirrel serves as a zoonotic reservoir for the Rickettsia prowazekii bacterium.
In 1916, Henrique da Rocha Lima proved that the bacterium Rickettsia prowazekii was the agent responsible for typhus; he named it after H. T. Ricketts and Stanislaus von Prowazek, two zoologists who had died from typhus while investigating epidemics. Once these crucial facts were recognized, Rudolf Weigl in 1930 was able to fashion a practical and effective vaccine production method. He ground up the insides of infected lice that had been drinking blood. It was, however, very dangerous to produce, and carried a high likelihood of infection to those who were working on it.
A safer mass-production-ready method using egg yolks was developed by Herald R. Cox in 1938. This vaccine was widely available and used extensively by 1943.

Diagnosis
IFA, ELISA or PCR positive after 10 days.

Treatment
The infection is treated with antibiotics. Intravenous fluids and oxygen may be needed to stabilize the patient. There is a significant disparity between the untreated mortality and treated mortality rates: 10-60% untreated versus close to 0% treated with antibiotics within 8 days of initial infection. Tetracycline, chloramphenicol, and doxycycline are commonly used. Infection can also be prevented by vaccination.Some of the simplest methods of prevention and treatment focus on preventing infestation of body lice. Completely changing the clothing, washing the infested clothing in hot water, and in some cases also treating recently used bedsheets all help to prevent typhus by removing potentially infected lice. Clothes left unworn and unwashed for 7 days also result in the death of both lice and their eggs, as they have no access to a human host. Another form of lice prevention requires dusting infested clothing with a powder consisting of 10% DDT, 1% malathion, or 1% permethrin, which kill lice and their eggs.Other preventive measures for individuals are to avoid unhygienic, extremely overcrowded areas where the causative organisms can jump from person to person. In addition, they are warned to keep a distance from larger rodents that carry lice, such as rats, squirrels, or opossums.

History
History of outbreaks
Before 19th century
During the second year of the Peloponnesian War (430 BC), the city-state of Athens in ancient Greece had an epidemic, known as the Plague of Athens, which killed, among others, Pericles and his two elder sons. The plague returned twice more, in 429 BC and in the winter of 427/6 BC. Epidemic typhus is proposed as a strong candidate for the cause of this disease outbreak, supported by both medical and scholarly opinions.

The first description of typhus was probably given in 1083 at La Cava abbey near Salerno, Italy. In 1546, Girolamo Fracastoro, a Florentine physician, described typhus in his famous treatise on viruses and contagion, De Contagione et Contagiosis Morbis.Typhus was carried to mainland Europe by soldiers who had been fighting on Cyprus. The first reliable description of the disease appears during the siege of the Emirate of Granada by the Catholic Monarchs in 1489 during the Granada War. These accounts include descriptions of fever and red spots over arms, back and chest, progressing to delirium, gangrenous sores, and the stench of rotting flesh. During the siege, the Catholics lost 3,000 men to enemy action, but an additional 17,000 died of typhus.Typhus was also common in prisons (and in crowded conditions where lice spread easily), where it was known as Gaol fever or Jail fever. Gaol fever often occurs when prisoners are frequently huddled together in dark, filthy rooms. Imprisonment until the next term of court was often equivalent to a death sentence. Typhus was so infectious that prisoners brought before the court sometimes infected the court itself. Following the Black Assize of Oxford 1577, over 300 died from epidemic typhus, including Speaker Robert Bell, Lord Chief Baron of the Exchequer. The outbreak that followed, between 1577 and 1579, killed about 10% of the English population.During the Lent assize held at Taunton (1730), typhus caused the death of the Lord Chief Baron of the Exchequer, the High Sheriff of Somerset, the sergeant, and hundreds of other persons. During a time when there were 241 capital offences, more prisoners died from gaol fever than were put to death by all the public executioners in the realm. In 1759 an English authority estimated that each year a quarter of the prisoners had died from gaol fever. In London, typhus frequently broke out among the ill-kept prisoners of Newgate Gaol and moved into the general city population.

19th century
Epidemics occurred in the British Isles and throughout Europe, for instance, during the English Civil War, the Thirty Years War, and the Napoleonic Wars. Many historians believe that the typhus outbreak among Napoleons troops is the real reason why he stalled his military campaign into Russia, rather than starvation or the cold. A major epidemic occurred in Ireland between 1816 and 1819, and again in the late 1830s. Another major typhus epidemic occurred during the Great Irish Famine between 1846 and 1849. The Irish typhus spread to England, where it was sometimes called "Irish fever" and was noted for its virulence. It killed people of all social classes since lice were endemic and inescapable, but it hit particularly hard in the lower or "unwashed" social strata. It was carried to North America by the many Irish refugees who fled the famine. In Canada, the 1847 North American typhus epidemic killed more than 20,000 people, mainly Irish immigrants in fever sheds and other forms of quarantine, who had contracted the disease aboard coffin ships. As many as 900,000 deaths have been attributed to the typhus fever during the Crimean War in 1853–1856, and 270,000 to the 1868 Finnish typhus epidemic.In the United States, a typhus epidemic struck Philadelphia in 1837. The son of Franklin Pierce died in 1843 of a typhus epidemic in Concord, New Hampshire. Several epidemics occurred in Baltimore, Memphis, and Washington, D.C. between 1865 and 1873. Typhus fever was also a significant killer during the American Civil War, although typhoid fever was the more prevalent cause of US Civil War "camp fever." Typhoid is a completely different disease from typhus. Typically more men died on both sides of disease than wounds.Rudolph Carl Virchow, a physician, anthropologist, and historian attempted to control an outbreak of typhus in Upper Silesia and wrote a 190-page report about it. He concluded that the solution to the outbreak did not lie in individual treatment or by providing small changes in housing, food or clothing, but rather in widespread structural changes to directly address the issue of poverty. Virchows experience in Upper Silesia led to his observation that "Medicine is a social science". His report led to changes in German public health policy.

20th century
Typhus was endemic in Poland and several neighboring countries prior to World War I (1914–1918). During and shortly after the war, epidemic typhus caused up to three million deaths in Russia, and several million citizens also died in Poland and Romania. Since 1914, many troops, prisoners and even doctors were infected, and at least 150,000 died from typhus in Serbia, 50,000 of whom were prisoners. Delousing stations were established for troops on the Western Front, but the disease ravaged the armies of the Eastern Front. Fatalities were generally between 10 and 40 percent of those infected, and the disease was a major cause of death for those nursing the sick. During World War I and the Russian Civil War between the White and Red, the typhus epidemic caused 2–3 million deaths out of 20–30 million cases in Russia between 1918 and 1922.

Typhus caused hundreds of thousands of deaths during World War II. It struck the German Army during Operation Barbarossa, the invasion of Russia, in 1941. In 1942 and 1943 typhus hit French North Africa, Egypt and Iran particularly hard. Typhus epidemics killed inmates in the Nazi concentration camps and death camps such as Auschwitz, Dachau, Theresienstadt, and Bergen-Belsen. Footage shot at Bergen-Belsen concentration camp shows the mass graves for typhus victims. Anne Frank, at age 15, and her sister Margot both died of typhus in the camps. Even larger epidemics in the post-war chaos of Europe were averted only by the widespread use of the newly discovered DDT to kill lice on the millions of refugees and displaced persons.Following the development of a vaccine during World War II, Western Europe and North America have been able to prevent epidemics. These have usually occurred in Eastern Europe, the Middle East, and parts of Africa, particularly Ethiopia. Naval Medical Research Unit Five worked there with the government on research to attempt to eradicate the disease.In one of its first major outbreaks since World War II, epidemic typhus reemerged in 1995 in a jail in NGozi, Burundi. This outbreak followed the start of the Burundian Civil War in 1993, which caused the displacement of 760,000 people. Refugee camps were crowded and unsanitary, and often far from towns and medical services.

21st century
A 2005 study found seroprevalence of R. prowazekii antibodies in homeless populations in two shelters in Marseille, France. The study noted the "hallmarks of epidemic typhus and relapsing fever".

History of vaccines
Major developments for typhus vaccines started during World War I, as typhus caused high mortality, and threatened the health and readiness for soldiers on the battlefield. Vaccines for typhus, like other vaccines of the time, were classified as either living or killed vaccines. Live vaccines were typically an injection of live agent, and killed vaccines are live cultures of an agent that are chemically inactivated prior to use.Attempts to create a living vaccine of classical, louse-borne, typhus were attempted by French researchers but these proved unsuccessful. Researchers turned to murine typhus to develop a live vaccine. At the time, murine vaccine was viewed as a less severe alternative to classical typhus. Four versions of a live vaccine cultivated from murine typhus were tested, on a large scale, in 1934.While the French were making advancements with live vaccines, other European countries were working to develop killed vaccines. During World War II, there were three kinds of potentially useful killed vaccines. All three killed vaccines relied on the cultivation of Rickettsia prowazekii, the organism responsible for typhus. The first attempt at a killed vaccine was developed by Germany, using the Rickettsia prowazekii found in louse feces. The vaccine was tested extensively in Poland between the two world wars and used by the Germans for their troops during their attacks on the Soviet Union.A second method of growing Rickettsia prowazekii was discovered using the yolk sac of chick embryos. Germans tried several times to use this technique of growing Rickettsia prowazekii but no effort was pushed very far.The last technique was an extended development of the previously known method of growing murine typhus in rodents. It was discovered that rabbits could be infected, by a similar process, and contract classical typhus instead of murine typhus. Again, while proven to produce suitable Rickettsia prowazekii for vaccine development, this method was not used to produce wartime vaccines.During WWII, the two major vaccines available were the killed vaccine grown in lice and the live vaccine from France. Neither was used much during the war. The killed, louse-grown vaccine was difficult to manufacture in large enough quantities, and the French vaccine was not believed to be safe enough for use.The Germans worked to develop their own live vaccine from the urine of typhus victims. While developing a live vaccine, Germany used live Rickettsia prowazekii to test multiple possible vaccines capabilities. They gave live Rickettsia prowazekii to concentration camp prisoners, using them as a control group for the vaccine tests.The use of DDT as an effective means of killing lice, the main carrier of typhus, was discovered in Naples.

Society and culture
Biological weapon
Typhus was one of more than a dozen agents that the United States researched as potential biological weapons before President Richard Nixon suspended all non-defensive aspects of the U.S. biological weapons program in 1969.

Poverty and displacement
The CDC lists the following areas as active foci of human epidemic typhus: Andean regions of South America, some parts of Africa; on the other hand, the CDC only recognizes an active enzootic cycle in the United States involving flying squirrels (CDC). Though epidemic typhus is commonly thought to be restricted to areas of the developing world, serological examination of homeless persons in Houston found evidence for exposure to the bacterial pathogens that cause epidemic typhus and murine typhus.  A study involving 930 homeless people in Marseille, France, found high rates of seroprevalence to R. prowazekii and a high prevalence of louse-borne infections in the homeless.Typhus has been increasingly discovered in homeless populations in developed nations. Typhus among homeless populations is especially prevalent as these populations tend to migrate across states and countries, spreading the risk of infection with their movement. The same risk applies to refugees, who travel across country lines, often living in close proximity and unable to maintain necessary hygienic standards to avoid being at risk for catching lice possibly infected with typhus.Because the typhus-infected lice live in clothing, the prevalence of typhus is also affected by weather, humidity, poverty and lack of hygiene. Lice, and therefore typhus, are more prevalent during colder months, especially winter and early spring </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Progressive nodular histiocytosis and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Juvenile hyaline fibromatosis and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Camurati–Engelmann disease and explain in detail? [/INST] Camurati–Engelmann disease (CED) is a very rare autosomal dominant genetic disorder that causes characteristic anomalies in the skeleton. It is also known as progressive diaphyseal dysplasia. It is a form of dysplasia. Patients typically have heavily thickened bones, especially along the shafts of the long bones (called diaphyseal dysplasia).  The skull bones may be thickened so that the passages through the skull that carry nerves and blood vessels become narrowed, possibly leading to sensory deficits, blindness, or deafness.
This disease often appears in childhood and is considered to be inherited, however many patients have no previous history of CED within their family. The disease is slowly progressive and, while there is no cure, there is treatment.
It is named for M. Camurati and G. Engelmann.

Signs and symptoms
Patients with CED complain of chronic bone pain in the legs or arms, muscle weakness (myopathy) and experience a waddling gait. Other clinical problems associated with the disease include increased fatigue, weakness, muscle spasms, headache, difficulty gaining weight, and delay in puberty.  Some patients have an abnormal or absent tibia, may present with a flat foot, or scoliosis.This disease may also cause bones to become abnormally hardened which is referred to as sclerosis. This hardening may affect the bones at the base of the skull or those in the hands, feet, or jaw. This causes ongoing pain and aching within the body parts that are affected. The pain has been described as either a hot electric stabbing pain, an ever-increasing pressure sensation around the bones (especially before electrical storms) or as a constant ache that radiates through several long bones at once. Pain may also occur in the hips, wrists, knees and other joints as they essentially just lock-up (often becoming very stiff, immobile and sore), mostly when walking up or down staircases, writing for extended periods of time, or during the colder months of the year. Those with the disease tend to have a very characteristic walk medically diagnosed as a waddling gait. This is observed by the broad-based gait with a duck-like waddle to the swing phase, the pelvis drops to the side of the leg being raised, notable forward curvature of the lumbar spine and a marked body swing.The pain is especially severe during a flare-up, these can be unpredictable, exhausting and last anywhere from a few hours to several weeks. This is a common occurrence for several CED patients, often causing myopathy and extensive sleep deprivation from the chronic, severe and disabling pain. Patients may even require the use of a wheelchair (or additional carers help with getting dressed, showering, mobility/shopping, preparing meals or lifting heavy items) especially when bedridden or housebound for days or weeks at a time. Flare-ups may be attributed to, or exacerbated by growth spurts, stress, exhaustion, exercise, standing or walking for too long, illness, infection, being accidentally knocked/hurt or injured, after surgery/anaesthetics, cold weather, electrical storms, and sudden changes in barometric pressure.CED may also affect internal organs, the liver and spleen, which may become enlarged. A loss of vision and/or hearing can occur if bones are adversely affected by the hardening in the skull. Hence proactive specialist check-ups, X-rays, diagnostic tests/scans, and regular blood tests are recommended on an annual basis to monitor the CED bony growth and secondary medical issues that may arise from this condition.

Cause
Camurati-Engelmann disease is caused by autosomal dominant mutations in the gene TGFB1, localized at chromosome 19q13.

Diagnosis
Classification
There are two forms:

Type 1 is associated with TGFB1
Type 2 is not associated with TGFB1Type 1 Camurati-Engelmann Disease is associated with an error occurring in the TGFB1 protein.  Affected individuals shared a haplotype between D19S881 to D19S606.  TGFB1 protein is encoded by the TGF-B1 gene, which occurs on chromosome 19q13.1-13.3.  This protein is responsible for a multitude of functions, one of which includes regulating the function of osteoblasts and osteoclasts, which decreases bone resorption and increases bone formation.  These functions can be affected by a series of mutations that occur on exon 4, near the carboxyl terminus of the latency associated peptide, or LAP.  TGFB1 is expressed as a latent form, a mature form and a B1-LAP.  Mutations to R218H affect the association of the B1-LAP and the mature form of TGFB1 by conformational changes to B1-LAP.  These mutations can lead to a buildup of mature TGFB1, which accumulates in the mutant R218H fibroblasts.  Fibroblasts are a type of cell that creates collagen and the extracellular matrix.  This suggests that R218H mutation causes a disassociation between mature-TGFB1 and B1-LAP.  Mutations at the LLL12-13ins and Y81H regions decrease the secretion of TGFB1, which leads to intracellular buildup of TGFB1.Type 2 Camurati-Engelmann Disease is still speculative, with no distinct evidence to credit its existence.  There are many similarities between Type 2 CED and hyperostosis generalisata with striations of the bones (HGS), with some speculating they are two phenotypic variations of the same disease.

Treatment
Camurati–Engelmann disease is somewhat treatable. Glucocorticosteroids, which are anti-inflammatory and immunosuppressive agents, are used in some cases.  This form of medication helps in bone strength, however can have multiple side effects </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Alternating hemiplegia and explain in detail? [/INST] Alternating hemiplegia (also known as crossed hemiplegia) is a form of hemiplegia that has an ipsilateral cranial nerve palsies and contralateral hemiplegia or hemiparesis of extremities of the body. The disorder is characterized by recurrent episodes of paralysis on one side of the body. There are multiple forms of alternating hemiplegia, Webers syndrome, middle alternating hemiplegia, and inferior alternating hemiplegia.  This type of syndrome can result from a unilateral lesion in the brainstem affecting both upper motor neurons and lower motor neurons.  The muscles that would receive signals from these damaged upper motor neurons result in spastic paralysis.  With a lesion in the brainstem, this affects the majority of limb and trunk muscles on the contralateral side due to the upper motor neurons decussation after the brainstem.  The cranial nerves and cranial nerve nuclei are also located in the brainstem making them susceptible to damage from a brainstem lesion.  Cranial nerves III (Oculomotor), VI (Abducens), and XII (Hypoglossal) are most often associated with this syndrome given their close proximity with the pyramidal tract, the location which upper motor neurons are in on their way to the spinal cord.  Damages to these structures produce the ipsilateral presentation of paralysis or palsy due to the lack of cranial nerve decussation (aside from the trochlear nerve) before innervating their target muscles. The paralysis may be brief or it may last for several days, many times the episodes will resolve after sleep. Some common symptoms of alternating hemiplegia are mental impairment, gait and balance difficulties, excessive sweating and changes in body temperature.

Symptoms and signs
Superior alternating hemiplegia
Superior alternating hemiplegia (also known as Weber syndrome) has a few distinct symptoms: contralateral hemiparesis of limb and facial muscle accompanied by weakness in one or more muscles that control eye movement on the same side. Another symptom that appears is the loss of eye movement due to damage to the oculomotor nerve fibers. The upper and lower extremities have increased weakness.

Middle alternating hemiplegia
Middle alternating hemiplegia (also known as Foville Syndrome) typically constitutes weakness of the extremities accompanied by paralysis of the extraocular muscle specifically lateral rectus, on the opposite side of the affected extremities, which indicates a lesion in the caudal and medial pons involving the abducens nerve root (controls movement of the eye) and corticospinal fibers (carries motor commands from the brain to the spinal cord).

Inferior alternating hemiplegia
Inferior alternating hemiplegia (also known as medial medullary syndrome) typically involves a "weakness of the extremities accompanied by paralysis of muscles on the ipsilateral side of the tongue (seen as a deviation of the tongue on that side on protrusion).  These symptoms indicate a lesion in the medulla involving the corticospinal fibers in the pyramid and the exiting hypoglossal nerve roots.

Causes
Note that this description is focused on alternating hemiplegia of childhood. Similar syndromes may develop following a brainstem infarction.
The cause of alternating hemiplegia of childhood is the mutation of ATP1A3 gene. In a study of fifteen female and nine male patients with alternating hemiplegia, a mutation in ATP1A3 gene was present. Three patients showed heterozygous de-novo missense mutation. Six patients were found with de-novo missense mutation and one patient was identified with de-novo splice site mutation. De novo mutation is a mutation that occurs in the germ cell of one parent. Neither parent has the mutation, but it is passed to the child through the sperm or egg.

Diagnosis
There is no diagnostic test for alternating hemiplegia, which makes it very difficult to diagnose. Also, because alternating hemiplegia is extremely rare, it is frequently missed and the patient is often misdiagnosed. Proper diagnosis, however, is critical for early treatment of the disorder. There are many criteria that can help in the proper general diagnosis of alternating hemiplegia.

Criteria for diagnosis
First, the symptoms must be observed before the patient is 18 months of age. Second, there must be frequent episodes of hemiplegia, involving either side of the body. Third, other paroxysmal disorders including tonic attacks, dystonia, nystagmus, strabismus, dyspnoea, and other uncontrollable disorders are noticed to occur. Although common, the paroxysmal disorders involving the eye, nystagmus and strabismus, may not be apparent in older children and may not have been remembered in childhood so a lack of these symptoms does not rule out alternating hemiplegia. Fourth, all symptoms clear up directly after falling asleep and usually come back after waking during an attack.  This occurrence is very indicative of alternating hemiplegia and as such those who display this are usually diagnosed with probable alternating hemiplegia. Fifth, indications of developmental delays, learning disability, or neurological irregularities are present. These issues may not be obvious in very young patients; however, it appears in almost all older patients.: 777  The final criteria before a diagnosis of alternating hemiplegia can be made is that all of these symptoms must not be due to another disorder. If the symptoms can be attributed to another disease or disorder, then a definitive diagnosis is difficult to make.: 778

Diagnosis of Webers syndrome
Webers syndrome is the only form of alternating hemiplegia that is somewhat easy to diagnose beyond the general criteria. Although Webers syndrome is rare, a child born with the disorder typically has a port-wine stain on the face around the eye. While the port-wine stain does not necessarily mean the child has Webers syndrome, if the port-wine stain involves the ophthalmic division of the trigeminal nerve than the likelihood of it being webers syndrome greatly increases. If a port-wine stain around the eye is found, the patient should be screened for intracranial leptomeningeal angiomatosis </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Mastocytoma and explain in detail? [/INST] A mastocytoma or mast cell tumor is  a type of round-cell tumor consisting of mast cells.  It is found in humans and many animal species; it also can refer to an accumulation or nodule of mast cells that resembles a tumor.
Mast cells originate from the bone marrow and are normally found throughout the connective tissue of the body as normal components of the immune system. As they release histamine, they are associated with allergic reactions.  Mast cells also respond to tissue trauma.  Mast cell granules contain histamine, heparin, platelet-activating factor, and other substances.  Disseminated mastocytosis is rarely seen in young dogs and cats, while mast cell tumors are usually skin tumors in older dogs and cats. Although not always malignant, they do have the potential to be.  Up to 25 percent of skin tumors in dogs are mast cell tumors, with a similar number in cats.

Signs and symptoms
Humans
When mastocytomas affect humans, they are typically found in skin. They usually occur as a single lesion on the trunk or wrist. Although it is rare, mastocytomas are sometimes found in the lung. It can also affect children.

Other animals
Mast cell tumors are known among veterinary oncologists as the great pretenders because their appearance can be varied, from a wart-like nodule to a soft subcutaneous lump (similar on palpation to a benign lipoma) to an ulcerated skin mass.  Most mast cell tumors are small, raised lumps on the skin.  They may be hairless, ulcerated, or itchy.  They are usually solitary, but in about six percent of cases, there are multiple mast cell tumors (especially in Boxers and Pugs).Manipulation of the tumor may result in redness and swelling from release of mast cell granules, also known as Dariers sign, and prolonged local hemorrhage.  In rare cases, a highly malignant tumor is present, and signs may include loss of appetite, vomiting, diarrhea, and anemia.  The presence of these signs usually indicates mastocytosis, which is the spread of mast cells throughout the body.  Release of a large amount of histamine at one time can result in ulceration of the stomach and duodenum (present in up to 25 percent of cases) or disseminated intravascular coagulation.  When metastasis does occur, it is usually to the liver, spleen, lymph nodes and bone marrow.

Diagnosis
A needle aspiration biopsy of the tumor will typically show a large number of mast cells.   This is sufficient to make the diagnosis of a mast cell tumor, although poorly differentiated mast cells may have few granules and thus are difficult to identify.  The granules of the mast cell stain blue to dark purple with a Romanowsky stain, and the cells are medium-sized.  However, a surgical biopsy is required to find the grade of the tumor.  The grade depends on how well the mast cells are differentiated, mitotic activity, location within the skin, invasiveness, and the presence of inflammation or necrosis.
Grade I – well differentiated and mature cells with a low potential for metastasis
Grade II – intermediately differentiated cells with potential for local invasion and moderate metastatic behavior
Grade III – undifferentiated, immature cells with a high potential for metastasisHowever, there is a significant amount of discordance between veterinary pathologists in assigning grades to mast cell tumors due to imprecise criteria.The disease is also staged according to the WHO system:

Stage I - a single skin tumor with no spread to lymph nodes
Stage II - a single skin tumor with spread to lymph nodes in the surrounding area
Stage III - multiple skin tumors or a large tumor invading deep to the skin with or without lymph node involvement
Stage IV – a tumor with metastasis to the spleen, liver, or bone marrow, or with the presence of mast cells in the bloodX-rays, ultrasound, or lymph node, bone marrow, or organ biopsies may be necessary to stage the disease.

Treatment and prognosis
Removal of the mast cell tumor through surgery is the treatment of choice. Antihistamines, such as diphenhydramine, are given prior to surgery to protect against the effects of histamine released from the tumor. Wide margins (two to three centimeters) are required because of the tendency for the tumor cells to be spread out around the tumor. If complete removal is not possible due to the size or location, additional treatment, such as radiation therapy or chemotherapy, may be necessary. Prednisone is often used to shrink the remaining tumor portion. H2 blockers, such as cimetidine, protect against stomach damage from histamine. Vinblastine and lomustine are common chemotherapy agents used to treat mast cell tumors.Toceranib and masitinib, examples of receptor tyrosine kinase inhibitors, are used in the treatment of canine mast cell tumors. Both were recently approved by the U.S. Food and Drug Administration (FDA) as dog-specific anticancer drugs.Grade I or II mast cell tumors that can be completely removed have a good prognosis.  One study showed about 23 percent of incompletely removed grade II tumors recurred locally. Any mast cell tumor found in the gastrointestinal tract, paw, or on the muzzle has a guarded prognosis.  Previous beliefs that tumors in the groin or perineum carried a worse prognosis have been discounted. Tumors that have spread to the lymph nodes or other parts of the body have a poor prognosis. Any dog showing symptoms of mastocytosis or with a grade III tumor has a poor prognosis. Dogs of the Boxer breed have a better than average prognosis because of the relatively benign behavior of their mast cell tumors. Multiple tumors that are treated similarly to solitary tumors do not seem to have a worse prognosis.Mast cell tumors do not necessarily follow the histological prognosis. Further prognostic information can be provided by AgNOR stain of histological or cytological specimen. Even then, there is a risk of unpredictable behavior.

Other animals
Mast cell tumors are an uncommon occurrence in horses. They usually occur as benign, solitary masses on the skin of the head, neck, trunk, and legs. Mineralization of the tumor is common.  In pigs and cattle, mast cell tumors are rare. They tend to be solitary and benign in pigs and multiple and malignant in cattle </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Elastosis perforans serpiginosa and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Permanent junctional reciprocating tachycardia and explain in detail? [/INST] Permanent junctional reciprocating tachycardia (PJRT) is a rare cardiac arrhythmia. It is a supraventricular tachycardia, and a cause of atrioventricular reentrant tachycardia (AVRT) </s>