<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 Myocarditis and explain in detail? [/INST] Myocarditis, also known as inflammatory cardiomyopathy, is an acquired cardiomyopathy due to inflammation of the heart muscle. Symptoms can include shortness of breath, chest pain, decreased ability to exercise, and an irregular heartbeat. The duration of problems can vary from hours to months. Complications may include heart failure due to dilated cardiomyopathy or cardiac arrest.Myocarditis is most often due to a viral infection. Other causes include bacterial infections, certain medications, toxins and autoimmune disorders. A diagnosis may be supported by an electrocardiogram (ECG), increased troponin, heart MRI, and occasionally a heart biopsy. An ultrasound of the heart is important to rule out other potential causes such as heart valve problems.Treatment depends on both the severity and the cause. Medications such as ACE inhibitors, beta blockers, and diuretics are often used. A period of no exercise is typically recommended during recovery. Corticosteroids or intravenous immunoglobulin (IVIG) may be useful in certain cases. In severe cases an implantable cardiac defibrillator or heart transplant may be recommended.In 2013, about 1.5 million cases of acute myocarditis occurred. While people of all ages are affected, the young are most often affected. It is slightly more common in males than females. Most cases are mild. In 2015 cardiomyopathy, including myocarditis, resulted in 354,000 deaths up from 294,000 in 1990. The initial descriptions of the condition are from the mid-1800s.

Signs and symptoms
The signs and symptoms associated with myocarditis are varied, and relate either to the actual inflammation of the myocardium or to the weakness and dysfunction of the heart muscle that is secondary to the inflammation. While myocarditis may develop over periods ranging from hours to months, patients typically present with signs and symptoms that resemble heart failure, including the following:
Since myocarditis is often due to a viral illness, many patients experience symptoms consistent with a recent viral infection including a fever, rash, loss of appetite, abdominal pain, vomiting, diarrhea, joint pains, and easily becoming tired. Additionally, myocarditis is often associated with pericarditis, and many people with myocarditis present with signs and symptoms that suggest myocarditis and pericarditis at the same time.Children primarily present with the aforementioned symptoms associated with a viral infection. Since they overlap with many other illnesses, this can make it more challenging to diagnose myocarditis in younger patients.  Later stages of the illness can involve the respiratory system and lead to increased work of breathing. These are often mistaken for asthma.Myocarditis can be distinguished as either fulminant or acute based on the severity of symptoms on presentation, as well as the time course over which symptoms develop and persist. This categorization can help predict the treatment, outcomes, and complications of myocarditis.
Fulminant myocarditis is defined as sudden and severe myocarditis that is associated with signs and symptoms of heart failure while at rest. More specifically, fulminant myocarditis is characterized by a distinct, rapid onset of severe heart failure symptoms, such as shortness of breath and chest pain, that develop over the course of hours to days. Additionally, treatment requires the use of medications or mechanical devices to improve heart function.Acute non-fulminant myocarditis has a less distinct onset in contrast to fulminant myocarditis, and evolves over days to months. While the symptoms of acute myocarditis overlap with those of fulminant myocarditis, they do not typically occur at rest, and treatment does not require the use of mechanical circulatory support.

Causes
While many causes of myocarditis are known, there are many cases in which a causative agent cannot be identified. In Europe and North America, viruses are common culprits. Worldwide, however, the most common cause is Chagas disease, an illness endemic to Central and South America that results from infection with the protozoan Trypanosoma cruzi. Overall, myocarditis can be caused by infections, immune conditions, toxins, drug reactions, and physical injuries to the heart. These different etiologies are detailed below. Myocarditis is a rare adverse side effect from mRNA COVID-19 vaccines.

Infections
The most common causes of myocarditis are infectious organisms. Viral infections are the most common cause in developed countries, with a majority of cases being caused by those with single-stranded RNA genetic information such as Coxsackie viruses (especially Coxsackie B3 and B5). Globally, Chagas disease is the leading cause of myocarditis, which results from infection with the protozoan Trypanosoma cruzi. Bacteria can also result in myocarditis, although it is rare in patients with normal heart function and without a preexisting immunodeficiency. A list of the most relevant infectious organisms is below.

Viral: adenovirus, parvovirus B19, coxsackie virus, rubella virus, polio virus, Epstein-Barr virus, hepatitis C virus, and severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2, causing COVID-19)
Protozoan: Trypanosoma cruzi and Toxoplasma gondii (causing Chagas disease and toxoplasmosis, respectively)
Bacterial: Brucella, Corynebacterium diphtheriae, Neisseria gonorrhoeae, Haemophilus influenzae, Actinomyces, Tropheryma whipplei, Vibrio cholerae, Borrelia burgdorferi, Leptospira, Rickettsia, Mycoplasma pneumoniae
Fungal: Aspergillus
Parasitic: Ascaris, Echinococcus granulosus, Paragonimus westermani, Schistosoma, Taenia solium, Trichinella spiralis, visceral larva migrans, Wuchereria bancrofti

Immune conditions
Allergic reaction (e.g., to acetazolamide or amitriptyline)
Kawasaki disease
Autoimmunity (scleroderma, lupus, sarcoidosis, and systemic vasculitides)
Toxic shock syndrome

Drug reactions and toxins
Anthracyclines and other forms of chemotherapy
Antipsychotics including clozapine
Alcohol
Stimulants such as mephedrone and cocaine
Arsenic
Carbon monoxide
Snake venom
Heavy metals (copper or iron)

Vaccination
Myocarditis and pericarditis can be a rare side effect of some vaccines like the smallpox vaccine.
Some COVID-19 vaccination doses carry a very small risk (33 per million overall) of causing myocarditis and pericarditis, more so in young men at repeated administration. According to a meta-analysis that does not differentiate between the two mRNA-vaccines BNT162b2 and mRNA-1273, the risk is less than that associated with COVID-19 itself. In adolescent males aged 16 to 17 years the crude reporting rate of myocarditis was 105.9 per million doses of the BNT162b2 vaccine.

Physical injuries
Electric shock
Hyperpyrexia, and radiation

Mechanism
Most forms of myocarditis involve the infiltration of heart tissues by one or two types of pro-inflammatory blood cells, lymphocytes and macrophages plus two respective descendants of these cells, NK cells and macrophages. Eosinophilic myocarditis is a subtype of myocarditis in which cardiac tissue is infiltrated by another type of pro-inflammatory blood cell, the eosinophil. Eosinophilic myocarditis is further distinguished from non-eosinophilic myocarditis by having a different set of causes and recommended treatments. Coxsackie B, specifically B3 and B5, has been found to interact with coxsackievirus-adenovirus receptor (CAR) and decay-accelerating factor (DAF). However, other proteins have also been identified that allow Coxsackieviruses to bind to cardiac cells. The natural function of CAR and mechanism that the Coxsackievirus uses to infect the cardiac muscle is still unknown. The mechanism by which coxsackie B viruses (CBVs) trigger inflammation is believed to be through the recognition of CBV virions by Toll-like receptors.The binding of the SARS-CoV-2 virus through ACE2 receptors present in heart tissue may be responsible for direct viral injury leading to myocarditis. In a study done during the SARS outbreak,  SARS virus RNA  was ascertained in the autopsy of heart specimens in 35% of the patients who died due to SARS. It was also observed that an already diseased heart has increased expression of ACE2 receptor contrasted to healthy individuals. Hyperactive immune responses in COVID-19 Patients may lead to the initiation of the cytokine storm. This excess release of cytokines may lead to myocardial injury.

Diagnosis
Myocarditis refers to an underlying process that causes inflammation and injury of the heart.  It does not refer to inflammation of the heart as a consequence of some other insult.  Many secondary causes, such as a heart attack, can lead to inflammation of the myocardium and therefore the diagnosis of myocarditis cannot be made by evidence of inflammation of the myocardium alone.Myocardial inflammation can be suspected on the basis of electrocardiographic (ECG) results, elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR), and increased IgM (serology) against viruses known to affect the myocardium. Markers of myocardial damage (troponin or creatine kinase cardiac isoenzymes) are elevated.The ECG findings most commonly seen in myocarditis are diffuse T wave inversions; saddle-shaped ST-segment elevations may be present (these are also seen in pericarditis).The gold standard is the biopsy of the myocardium, in general done in the setting of angiography. A small tissue sample of the endocardium and myocardium is taken and investigated. The cause of the myocarditis can be only identified by a biopsy. Endomyocardial biopsy samples are assessed for histopathology (how the tissue looks like under the microscope): myocardial interstitium may show abundant edema and inflammatory infiltrate, rich in lymphocytes and macrophages. Focal destruction of myocytes explains the myocardial pump failure. In addition samples may be assessed with  immunohistochemistry to determine which types of immune cells are involved in the reaction and how they are distributed. Furthermore, PCR and/or RT-PCR may be performed to identify particular viruses. Finally, further diagnostic methods like microRNA assays and gene-expression profile may be performed.Cardiac magnetic resonance imaging (cMRI or CMR) has been shown to be very useful in diagnosing myocarditis by visualizing markers for inflammation of the myocardium. Consensus criteria for the diagnosis of myocarditis by CMR were published in 2009.

Treatment
While myocarditis has many etiologies and a variable constellation of signs and symptoms, there are few causes that are treatable and thus the main focus is on symptom management. In cases with biopsy-proven myocarditis, the causative cell type can indicate potentially beneficial treatments. These treatments typically consist of corticosteroids, or medications with known benefits in certain autoimmune and systemic conditions. In a majority of cases, the main therapies are used to support patients and are dependent on the severity of symptoms and the time course across which myocarditis develops. Supportive therapies can be divided into two broad categories, medications and mechanical support, since there has yet to be any demonstrated benefits from complementary therapies.

Medication
The specific medications that are used to support patients are directly related to the cause of the symptom or sign. Just as the symptoms of myocarditis mirror those of congestive heart failure, so too do the therapies. Additionally, the order in which  therapies are used depends on the degree of heart dysfunction, with stabilization of patient blood pressure and breathing taking highest priority when present. This can involve the use of inotropes, or medications that make the heart contract with greater force, as well as antiarrhythmic drugs such as adenosine or carvedilol. In patients that have stable and adequate heart function, further treatments are based on heart failure guidelines. ACE inhibitors can have a protective benefit to the heart, so they are typically used in any patient with symptomatic myocarditis. Simultaneously, beta blockers are used in patients that can tolerate their heart beating at a slower rate. Shortness of breath at rest and swelling can be relieved with diuretics such as furosemide, and the addition of aldosterone receptor blockers can augment the diuresis while preventing the excess loss of potassium. In patients with symptoms while resting, additional medications can be added such as digoxin.

Mechanical support
Mechanical support is used in cases of myocarditis in which medications alone do not lead to adequate heart function and the body requires additional support to achieve organ perfusion. Myocarditis cases that require mechanical circulatory support are categorized as fulminant by definition. People that require additional support with their heart function can benefit from the use of ventricular assist devices like intra-aortic balloon pumps. In people with myocarditis severe enough to cause cardiac arrest, extracorporeal membrane oxygenation (ECMO) is used to adequately pump blood and provide oxygen if needed. Both ventricular assist devices and ECMO can be used as bridge therapy until heart transplantation in patients that are candidates. Heart transplantation is reserved for those that do not respond to the aforementioned conventional medical therapies.

Prognosis
The prognosis associated with myocarditis is stratified by the severity and time course along which symptoms develop. In addition to symptom severity, there are also several indicators of heart function that can be used to predict patient outcomes, many of which are part of the standard evaluation of patients presenting with cardiovascular dysfunction.
An electrocardiogram is one of the most common screening tools used in cases of suspected cardiac pathology, such as myocarditis. The findings that correlate with poorer outcomes are non-specific and include widened QRS complexes and QT intervals, partial or complete atrial-ventricular heart block, and malignant ventricular arrhythmias like sustained ventricular tachycardia or ventricular fibrillation. Electrocardiogram findings of ST elevations with upward concavity and an early repolarization pattern, however, were associated with a better cardiovascular prognosis in general.In cases of acute myocarditis, cardiac magnetic resonance imaging can reveal several prognostic indicators that, similar to ECGs, are non-specific and reflect poorer cardiac physiology. Late gadolinium enhancement on cardiac MRI demonstrates perturbations in extracellular volume as a result of cell necrosis or edema, and is significantly associated with increases in all-cause mortality, cardiovascular mortality, and major adverse cardiovascular events. The association was strongest with any late gadolinium enhancement, but remained true for findings of anterolateral-specific enhancement. A similar relationship was found between a left ventricular ejection fraction < 50%, increased mortality, and increased major adverse cardiovascular events.Myocarditis has been reported to be a major cause of sudden cardiac death (SCD) in infants, adolescents, and young adults, but the reported rates show wide variation (1 to 14 percent) among young people depending on differences in SCD definition and classification/ definition of myocarditis post-mortem as well as inhomogeneity in the study populations. And one has also to distinguish between studies about myocarditis in general and fulminant myocarditis.

Epidemiology
The exact incidence of myocarditis is unknown since many cases are not associated with any symptoms. However, in series of routine autopsies, 1–9% of all patients had evidence of myocardial inflammation.
The prevalence rate of myocarditis is estimated to be about 22 cases per 100,000 persons annually. Fulminant myocarditis, the most severe subtype, has been shown to occur in up to 2.5% of known myocarditis presentations. When looking at different causes of myocarditis, viral infection is the most prevalent, especially in children; however, the prevalence rate of myocarditis is often underestimated since the condition is easily overlooked. Viral myocarditis being an outcome of viral infection depends heavily on genetic host factors and the pathogenicity unique to the virus. If one tests positive for an acute viral infection, clinical developments have discovered that 1-5% of said population may show some form of myocarditis.In regard to the population affected, myocarditis is more common in pregnant women, children, and those who are immunocompromised </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 Lymphomatoid papulosis 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 Hyperhidrosis and explain in detail? [/INST] Hyperhidrosis is a condition characterized by abnormally increased sweating, in excess of that required for regulation of body temperature. Although primarily a benign physical burden, hyperhidrosis can deteriorate quality of life from a psychological, emotional, and social perspective. This excess of sweat happens even if the person is not engaging in tasks that require muscular effort, and it does not depend on the exposure to heat. Common places to sweat can include underarms, face, neck, back, groin, feet, and hands. It has been called by some researchers the silent handicap.Both diaphoresis and hidrosis can mean either perspiration (in which sense they are synonymous with sweating) or excessive perspiration, in which case they refer to a specific, narrowly defined, clinical disorder.

Classification
Hyperhidrosis can either be generalized, or localized to specific parts of the body. Hands, feet, armpits, groin, and the facial area are among the most active regions of perspiration due to the high number of sweat glands (eccrine glands in particular) in these areas. When excessive sweating is localized (e.g. palms, soles, face, underarms, scalp) it is referred to as primary hyperhidrosis or focal hyperhidrosis. Excessive sweating involving the whole body is termed generalized hyperhidrosis or secondary hyperhidrosis.  It is usually the result of some other, underlying condition.
Primary or focal hyperhidrosis may be further divided by the area affected, for instance, palmoplantar hyperhidrosis (symptomatic sweating of only the hands or feet) or gustatory hyperhidrosis (sweating of the face or chest a few moments after eating certain foods).Hyperhidrosis can also be classified by onset, either congenital (present at birth) or acquired (beginning later in life). Primary or focal hyperhidrosis usually starts during adolescence or even earlier and seems to be inherited as an autosomal dominant genetic trait. It must be distinguished from secondary hyperhidrosis, which can start at any point in life. Secondary hyperhidrosis may be due to a disorder of the thyroid or pituitary glands, diabetes mellitus, tumors, gout, menopause, certain drugs, or mercury poisoning.One classification scheme uses the amount of skin affected. In this scheme, excessive sweating in an area of  100 square centimeters (16 square inches) or more is differentiated from sweating that affects only a small area.Another classification scheme is based on possible causes of hyperhidrosis.

Causes
The cause of primary hyperhidrosis is unknown. Anxiety or excitement can exacerbate the condition. A common complaint of patients is they get nervous because they sweat, then sweat more because they are nervous. Other factors can play a role, including certain foods and drinks, nicotine, caffeine, and smells.
Similarly, secondary (generalized) hyperhidrosis has many causes including certain types of cancer, disturbances of the endocrine system, infections, and medications.

Primary
Primary (focal) hyperhidrosis has many causes.

Idiopathic unilateral circumscribed hyperhidrosis
Reported association with:
Blue rubber bleb nevus
Glomus tumor
POEMS syndrome
Burning feet syndrome (Gopalans)
Trench foot
Causalgia
Pachydermoperiostosis
Pretibial myxedema
Gustatory sweating associated with:
Encephalitis
Syringomyelia
Diabetic neuropathies
Herpes zoster (shingles)
Parotitis
Parotid abscesses
Thoracic sympathectomy
Auriculotemporal or Freys syndrome
Miscellaneous
Lacrimal sweating (due to postganglionic sympathetic deficit, often seen in Raeders syndrome)
Harlequin syndrome
Emotional hyperhidrosis

Cancer
A variety of cancers have been associated with the development of secondary hyperhidrosis including lymphoma, pheochromocytoma, carcinoid tumors (resulting in carcinoid syndrome), and tumors within the thoracic cavity.

Endocrine
Certain endocrine conditions are also known to cause secondary hyperhidrosis including diabetes mellitus (especially when blood sugars are low), acromegaly, hyperpituitarism, pheochromocytoma (tumor of the adrenal glands, present in 71% of patients) and various forms of thyroid disease.

Medications
Use of selective serotonin reuptake inhibitors (e.g., sertraline) is a common cause of medication-induced secondary hyperhidrosis. Other medications associated with secondary hyperhidrosis include tricyclic antidepressants, stimulants, opioids, nonsteroidal anti-inflammatory drugs (NSAIDs), glyburide, insulin,  anxiolytic agents, adrenergic agonists, and cholinergic agonists.

Miscellaneous
In people with a history of spinal cord injuries
Autonomic dysreflexia
Orthostatic hypotension
Posttraumatic syringomyelia
Associated with peripheral neuropathies
Familial dysautonomia (Riley-Day syndrome)
Congenital autonomic dysfunction with universal pain loss
Exposure to cold, notably associated with cold-induced sweating syndrome
Associated with probable brain lesions
Episodic with hypothermia (Hines and Bannick syndrome)
Episodic without hypothermia
Olfactory
Associated with systemic medical problems
Parkinsons disease
Fibromyalgia
Congestive heart failure
Anxiety
Obesity
Menopausal state
Night sweats
Compensatory
Infantile acrodynia induced by chronic low-dose mercury exposure, leading to elevated catecholamine accumulation and resulting in a clinical picture resembling pheochromocytoma.
Febrile diseases
Vigorous exercise
A hot, humid environment

Diagnosis
Symmetry of excessive sweating in hyperhidrosis is most consistent with primary hyperhidrosis. To diagnose this condition, a dermatologist gives the patient a physical exam. This includes looking closely at the areas of the body that sweat excessively. A dermatologist also asks very specific questions. This helps the doctor understand why the patient has excessive sweating. Sometimes medical testing is necessary. Some patients require a test called the sweat test. This involves coating some of their skin with a powder that turns purple when the skin gets wet.
Excessive sweating affecting only one side of the body is more suggestive of secondary hyperhidrosis and further investigation for a neurologic cause is recommended.

Treatment
Antihydral cream is one of the solutions prescribed for hyperhidrosis for palms. Topical agents for hyperhidrosis therapy include formaldehyde lotion,  topical anticholinergics etc. These agents reduce perspiration by denaturing keratin, in turn occluding the pores of the sweat glands. They have a short-lasting effect.  Formaldehyde is classified as a probable human carcinogen. Contact sensitization is increased, especially with formalin. Aluminium chlorohydrate is used in regular antiperspirants. However, hyperhidrosis requires solutions or gels with a much higher concentration. These antiperspirant solutions or hyperhidrosis gels are especially effective for treatment of axillary or underarm regions. Normally it takes around three to five days to see improvement. The most common side-effect is skin irritation. For severe cases of plantar and palmar hyperhidrosis, there has been some success with conservative measures such as higher strength aluminium chloride antiperspirants. Treatment algorithms for hyperhidrosis recommend topical antiperspirants as the first line of therapy for hyperhidrosis. Both the International Hyperhidrosis Society and the Canadian Hyperhidrosis Advisory Committee have published treatment guidelines for focal hyperhidrosis that are said to be evidence-based.
Prescription medications called anticholinergics, often taken by mouth, are sometimes used in the treatment of both generalized and focal hyperhidrosis. Anticholinergics used for hyperhidrosis include propantheline, glycopyrronium bromide or glycopyrrolate, oxybutynin, methantheline, and benzatropine. Use of these drugs can be limited, however, by side-effects, including dry mouth, urinary retention, constipation, and visual disturbances such as mydriasis (dilation of the pupils) and cycloplegia. For people who find their hyperhidrosis is made worse by anxiety-provoking situations (public speaking, stage performances, special events such as weddings, etc.), taking an anticholinergic medicine before the event may be helpful.Several anticholinergic drugs can reduce hyperhidrosis. Oxybutynin (brand name Ditropan) is one that has shown promise,  although it can have side-effects, such as drowsiness, visual symptoms and dryness of the mouth and other mucous membranes. Glycopyrrolate is another drug sometimes used. It is said to be nearly as effective as oxybutynin, but has similar side-effects. In 2018, the U.S. Food and Drug Administration (FDA) approved a glycopyrronium bromide-containing disposable cloth (brand name Qbrexza) for the treatment of primary axillary hyperhidrosis.For peripheral hyperhidrosis, some chronic patients have found relief by simply ingesting crushed ice water. Ice water helps to cool excessive body heat during its transport through the blood vessels to the extremities, effectively lowering overall body temperature to normal levels within ten to thirty minutes.

Procedures
Injections of botulinum toxin type A can be used to block neural control of sweat glands. The effect can last from 3–9 months depending on the site of injections.  This use has been approved by the U.S. Food and Drug Administration (FDA). The duration of the beneficial effect in primary palmar hyperhidrosis has been found to increase with repetition of the injections. The Botox injections tend to be painful. Various measures have been tried to minimize the pain, one of which is the application of ice.
This was first demonstrated by Khalaf Bushara and colleagues as the first nonmuscular use of BTX-A in 1993. BTX-A has since been approved for the treatment of severe primary axillary hyperhidrosis (excessive underarm sweating of unknown cause), which cannot be managed by topical agents.A microwave-based device has been tried for excessive underarm perspiration and appears to show promise.Tap water iontophoresis as a treatment for palmoplantar hyperhidrosis was originally described in the 1950s. Studies showed positive results and good safety with tap water iontophoresis. One trial found it decreased sweating by about 80%.

Surgery
Sweat gland removal or destruction is one surgical option available for axillary hyperhidrosis (excessive underarm perspiration). There are multiple methods for sweat gland removal or destruction, such as sweat gland suction, retrodermal curettage, and axillary liposuction, Vaser, or Laser Sweat Ablation. Sweat gland suction is a technique adapted for liposuction.The other main surgical option is endoscopic thoracic sympathectomy (ETS), which cuts, burns, or clamps the thoracic ganglion on the main sympathetic chain that runs alongside the spine. Clamping is intended to permit the reversal of the procedure. ETS is generally considered a "safe, reproducible, and effective procedure and most patients are satisfied with the results of the surgery". Satisfaction rates above 80% have been reported, and are higher for children. The procedure brings relief from excessive hand sweating in about 85–95% of patients. ETS may be helpful in treating axillary hyperhidrosis, facial blushing and facial sweating, but failure rates in patients with facial blushing and/or excessive facial sweating are higher and such patients may be more likely to experience unwanted side effects.ETS side-effects have been described as ranging from trivial to devastating. The most common side-effect of ETS is compensatory sweating (sweating in different areas than prior to the surgery). Major problems with compensatory sweating are seen in 20–80% of patients undergoing the surgery. Most people find the compensatory sweating to be tolerable while 1–51% claim that their quality of life decreased as a result of compensatory sweating." Total body perspiration in response to heat has been reported to increase after sympathectomy. The original sweating problem may recur due to nerve regeneration, sometimes as early as 6 months after the procedure.Other possible side-effects include Horners Syndrome (about 1%), gustatory sweating (less than 25%) and excessive dryness of the palms (sandpaper hands). Some patients have experienced cardiac sympathetic denervation, which can result in a 10% decrease in heart rate both at rest and during exercise, resulting in decreased exercise tolerance.Percutaneous sympathectomy is a minimally invasive procedure similar to the botulinum method, in which nerves are blocked by an injection of phenol. The procedure provides temporary relief in most cases. Some physicians advocate trying this more conservative procedure before resorting to surgical sympathectomy, the effects of which are usually not reversible.

Prognosis
Hyperhidrosis can have physiological consequences such as cold and clammy hands, dehydration, and skin infections secondary to maceration of the skin. Hyperhidrosis can also have devastating emotional effects on ones individual life.Those with hyperhidrosis may have greater stress levels and more frequent depression.Excessive sweating or focal hyperhidrosis of the hands interferes with many routine activities, such as securely grasping objects </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 Entropion and explain in detail? [/INST] Entropion is a medical condition in which the eyelid (usually the lower lid) folds inward. It is very uncomfortable, as the eyelashes continuously rub against the cornea causing irritation. Entropion is usually caused by genetic factors. This is different from when an extra fold of skin on the lower eyelid causes lashes to turn in towards the eye (epiblepharon). In epiblepharons, the eyelid margin itself is in the correct position, but the extra fold of skin causes the lashes to be misdirected. Entropion can also create secondary pain of the eye (leading to self trauma, scarring of the eyelid, or nerve damage).  The upper or lower eyelid can be involved, and one or both eyes may be affected. When entropion occurs in both eyes, this is known as "bilateral entropion". Repeated cases of trachoma infection may cause scarring of the inner eyelid, which may cause entropion. In human cases, this condition is most common to people over 60 years of age.

Symptoms
Symptoms of entropion include:

Redness and pain around the eye
Sensitivity to light and wind
Sagging skin around the eye
Eye watering
Decreased vision, especially if the cornea is damaged

Causes
Congenital
Aging creating loose skin and stretched and loose ligaments and muscles (senile entropion).
Scarring (mechanical entropion)
Spasm
An eye infection called trachoma is still common in North Africa and South Asia and this can cause scarring of the inner eyelid, which may cause friction and entropion.

Treatment
Treatment is a relatively simple surgery in which excess skin of the outer lids is removed or tendons and muscles are shortened with one or two stitches. General anesthesia is sometimes used before local anesthetics are injected into the muscles around the eye.  Prognosis is excellent if surgery is performed before the cornea is damaged.

Entropion in other species
Entropion has been documented in most dog breeds, although there are some breeds (particularly purebreds) that are more commonly affected than others.  These include the Akita, Pug, Chow Chow, Shar Pei, St. Bernard, Cocker Spaniel, Boxer, English Springer Spaniel, Welsh Springer Spaniel, Labrador Retriever, Cavalier King Charles Spaniel, Neapolitan Mastiff, Bull Mastiff, Great Dane, Irish Setter, Shiba Inu, Rottweiler, Poodle and particularly Bloodhound. The condition is usually present by six months of age </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 Canine degenerative myelopathy and explain in detail? [/INST] Canine degenerative myelopathy, also known as chronic degenerative radiculomyelopathy, is an incurable, progressive disease of the canine spinal cord that is similar in many ways to amyotrophic lateral sclerosis (ALS). Onset is typically after the age of 7 years and it is seen most frequently in the German shepherd dog, Pembroke Welsh corgi, and boxer dog, though the disorder is strongly associated with a gene mutation in SOD1 that has been found in 43 breeds as of 2008, including the wire fox terrier, Chesapeake Bay retriever, Rhodesian ridgeback, and Cardigan Welsh corgi. Progressive weakness and incoordination of the rear limbs are often the first signs seen in affected dogs, with progression over time to complete paralysis. Myelin is an insulating sheath around neurons in the spinal cord.  One proposed cause of degenerative myelopathy is that the immune system attacks this sheath, breaking it down.  This results in a loss of communication between nerves in lower body of the animal and the brain.

Testing
The Orthopedic Foundation for Animals has a DNA saliva test to screen for the mutated gene that has been seen in dogs with degenerative myelopathy. Now that a test is available the disease can be bred out of breeds with a high preponderance. The test is only recommended for predisposed breeds, but can be performed on DNA from any dog on samples collected through swabbing the inside of the animals cheek with a sterile cotton swab or through venipuncture.
The test determines whether the mutated copy of SOD1 is present in the DNA sample submitted. It must be interpreted with caution by a veterinary clinician in combination with the animals clinical signs and other lab test results.
The results reported are:

Normal / Normal (N/N, or clear): The dog does not have the mutation and is extremely unlikely to develop degenerative myelopathy. There have been cases, however, in which dogs that tested clear were found to have DM upon necropsy.
Normal / Abnormal (N/A or carrier): The dog has one mutated copy of the gene (is heterozygous) and is a carrier but will not have degenerative myelopathy though there has now been some cases of heterozygous carriers developing DM. It will be possible for it to pass the mutation to offspring. A thorough examination of the dogs pedigree and DNA testing should be undertaken prior to breeding a dog with this result.
Abnormal / Abnormal (A/A or At Risk): The dog has two copies (is homozygous) for the mutation and is at risk for degenerative myelopathy.

Genetics
Breeding risks for degenerative myelopathy can be calculated using the Punnett Square:

If both parents are clear (N/N) then all of the puppies will be clear.
If one parent is a carrier (N/A) and one is clear (N/N) each puppy has a 50% chance of being clear and a 50% chance of being a carrier.
If both parents are carriers (N/A) each puppy has a 25% chance of being clear (N/N), 50% chance of being a carrier (N/A), and 25% chance of being affected and carrier (A/A)
If one parent is clear (N/N) and one parent is affected (A/A) then all puppies will be carriers (N/A)
If one parent is a carrier (N/A) and one is at risk (A/A) each puppy has a 50% chance of being a carrier(N/A) and 50% chance of being affected and carrier (A/A)
If both parents are at risk (A/A) then all puppies will be affected and carrier (A/A)

Symptoms
Degenerative myelopathy initially affects the back legs and causes muscle weakness and loss, and lack of coordination.  These cause a staggering affect that may appear to be arthritis. The dog may drag one or both rear paws when it walks. This dragging can cause the nails of one foot to be worn down.  The condition may lead to extensive paralysis of the back legs. As the disease progresses, the animal may display symptoms such as incontinence and has considerable difficulties with both balance and walking. If allowed to progress, the animal will show front limb involvement and extensive muscle atrophy and paralysis.  Eventually cranial nerve or respiratory muscle involvement necessitates euthanasia or long term palliative care.Progression of the disease is generally slow but highly variable. The animal could be crippled within a few months, or may survive as long as three years or more.

Causes
The etiology of this disease is unknown. Recent research has shown that a mutation in the SOD1 gene is a risk factor for developing degenerative myelopathy in several breeds. Mutations in SOD1 are also associated with familial amyotrophic lateral sclerosis (Lou Gehrigs disease) in people. More than 100 SOD1 gene mutations are involved in human familial amyotrophic lateral sclerosis (ALS), and the pathologic spinal lesions of ALS are similar to those of canine DM, making canine DM a potentially useful animal model of ALS.
Known causes of spinal cord dysfunction should be excluded before accepting the diagnosis of degenerative myelopathy;  disc disease (protrusions) or spinal cord tumors can cause compression of the spinal cord with similar signs to degenerative myelopathy.

Treatment
Degenerative myelopathy is an irreversible, progressive disease that cannot currently be cured. There are no treatments that have been clearly shown to stop or slow progression of DM.

Exercise
Exercise has been recommended to maintain the dogs ability to walk. Physiotherapy may prolong the length of time that the dog remains mobile and increase survival time. Canine hydrotherapy (swimming) may be more useful than walking. Use of a belly sling or hand-held harness allows the handler the ability to support the dogs hind legs for exercising or going up and down stairs. A 2-wheel dog cart, or "dog wheelchair" can allow the dog to remain active and maintain its quality of life once signs of weakness or paralysis of the hind limbs is detected.

Prognosis
The prognosis for the disease is generally poor. Aggressive therapy may be used to combat the disease, but even this puts the life expectancy at only around 14 months. It is recommended to put the dog to sleep at around 12 months, to prevent unnecessary suffering that comes from the disease. Some dogs have lived for many years with the disease, with one female boxer even living for 11 years. Without treatment, survival is around 3 months. The disease progresses rapidly without treatment, but this option arguably comes with less suffering. The dog begins to realize it is ill during the late stages </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 Hidrocystoma 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 Osteochondritis 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 Renal physiology and explain in detail? [/INST] Renal physiology (Latin rēnēs, "kidneys") is the study of the physiology of the kidney. This encompasses all functions of the kidney, including maintenance of acid-base balance; regulation of fluid balance; regulation of sodium, potassium, and other electrolytes; clearance of toxins; absorption of glucose, amino acids, and other small molecules;  regulation of blood pressure; production of various hormones, such as erythropoietin; and activation of vitamin D.
Much of renal physiology is studied at the level of the nephron, the smallest functional unit of the kidney. Each nephron begins with a filtration component that filters the blood entering the kidney. This filtrate then flows along the length of the nephron, which is a tubular structure lined by a single layer of specialized cells and surrounded by capillaries. The major functions of these lining cells are the reabsorption of water and small molecules from the filtrate into the blood, and the secretion of wastes from the blood into the urine.
Proper function of the kidney requires that it receives and adequately filters blood. This is performed at the microscopic level by many hundreds of thousands of filtration units called renal corpuscles, each of which is composed of a glomerulus and a Bowmans capsule. A global assessment of renal function is often ascertained by estimating the rate of filtration, called the glomerular filtration rate (GFR).

Formation of urine
The kidneys ability to perform many of its functions depends on the three fundamental functions of filtration, reabsorption, and secretion, whose sum is called renal clearance or renal excretion.  That is:

Urinary excretion rate = Filtration rate – Reabsorption rate + Secretion rateAlthough the strictest sense of the word excretion with respect to the urinary system is urination itself, renal clearance is also conventionally called excretion (for example, in the set term fractional excretion of sodium).

Filtration
The blood is filtered by nephrons, the functional units of the kidney. Each nephron begins in a renal corpuscle, which is composed of a glomerulus enclosed in a Bowmans capsule. Cells, proteins, and other large molecules are filtered out of the glomerulus by a process of ultrafiltration, leaving an ultrafiltrate that resembles plasma (except that the ultrafiltrate has negligible plasma proteins) to enter Bowmans space. Filtration is driven by Starling forces.

The ultrafiltrate is passed through, in turn, the proximal convoluted tubule, the loop of Henle, the distal convoluted tubule, and a series of collecting ducts to form urine.

Reabsorption
Tubular reabsorption is the process by which solutes and water are removed from the tubular fluid and transported into the blood. It is called reabsorption (and not absorption) both because these substances have already been absorbed once (particularly in the intestines) and because the body is reclaiming them from a postglomerular fluid stream that is well on its way to becoming urine (that is, they will soon be lost to the urine unless they are reclaimed).
Reabsorption is a two-step process beginning with the active or passive extraction of substances from the tubule fluid into the renal interstitium (the connective tissue that surrounds the nephrons), and then the transport of these substances from the interstitium into the bloodstream. These transport processes are driven by Starling forces, diffusion, and active transport.

Indirect reabsorption
In some cases, reabsorption is indirect. For example, bicarbonate (HCO3−) does not have a transporter, so its reabsorption involves a series of reactions in the tubule lumen and tubular epithelium. It begins with the active secretion of a hydrogen ion (H+) into the tubule fluid via a Na/H exchanger:

In the lumen
The H+ combines with HCO3− to form carbonic acid (H2CO3)
Luminal carbonic anhydrase enzymatically converts H2CO3 into H2O and CO2
CO2 freely diffuses into the cell
In the epithelial cell
Cytoplasmic carbonic anhydrase converts the CO2 and H2O (which is abundant in the cell) into H2CO3
H2CO3 readily dissociates into H+ and HCO3−
HCO3− is facilitated out of the cells basolateral membrane

Influence of hormones
Some key regulatory hormones for reabsorption include:

aldosterone, which stimulates active sodium reabsorption (and water as a result)
antidiuretic hormone, which stimulates passive water reabsorptionBoth hormones exert their effects principally on the collecting ducts.
Tubular secretion occurs simultaneously during reabsorption of filtrate. Substances, generally produced by body or the by-products of cell metabolism that can become toxic in high concentration, and some drugs (if taken). These all are secreted into the lumen of renal tubule. Tubular secretion can be either active or passive or co-transport.
Substances mainly secreted into renal tubule are; H+, K+, NH3, urea, creatinine, histamine and drugs like penicillin.
Tubular secretion occurs at Proximal Convoluted Tubule (PCT) and Distal Convoluted Tubule (DCT); for example, at proximal convoluted tubule, potassium is secreted by means of sodium-potassium pump, hydrogen ion is secreted by means of active transport and co-transport, i.e. antiporter, and ammonia diffuses into renal tubule.

Other functions
Hormone secretion
The kidneys secrete a variety of hormones, including erythropoietin, calcitriol, and renin. Erythropoietin is released in response to hypoxia (low levels of oxygen at tissue level) in the renal circulation. It stimulates erythropoiesis (production of red blood cells) in the bone marrow. Calcitriol, the activated form of vitamin D, promotes intestinal absorption of calcium and the renal reabsorption of phosphate.  Renin is an enzyme which regulates angiotensin and aldosterone levels.

Maintaining homeostasis
The kidney is responsible for maintaining a balance of the following substances:

The body is very sensitive to its pH. Outside the range of pH that is compatible with life, proteins are denatured and digested, enzymes lose their ability to function, and the body is unable to sustain itself. The kidneys maintain acid-base homeostasis by regulating the pH of the blood plasma. Gains and losses of acid and base must be balanced. Acids are divided into "volatile acids" and "nonvolatile acids". See also titratable acid.
The major homeostatic control point for maintaining this stable balance is renal excretion.  The kidney is directed to excrete or retain sodium via the action of aldosterone, antidiuretic hormone (ADH, or vasopressin), atrial natriuretic peptide (ANP), and other hormones. Abnormal ranges of the fractional excretion of sodium can imply acute tubular necrosis or glomerular dysfunction.

Acid-base
Two organ systems, the kidneys and lungs, maintain acid-base homeostasis, which is the maintenance of pH around a relatively stable value. The lungs contribute to acid-base homeostasis by regulating carbon dioxide (CO2) concentration.  The kidneys have two very important roles in maintaining the acid-base balance: to reabsorb and regenerate bicarbonate from urine, and to excrete hydrogen ions and fixed acids (anions of acids) into urine.

Osmolality
The kidneys help maintain the water and salt level of the body. Any significant rise in plasma osmolality is detected by the hypothalamus, which communicates directly with the posterior pituitary gland. An increase in osmolality causes the gland to secrete antidiuretic hormone (ADH), resulting in water reabsorption by the kidney and an increase in urine concentration. The two factors work together to return the plasma osmolality to its normal levels.
ADH binds to principal cells in the collecting duct that translocate aquaporins to the membrane, allowing water to leave the normally impermeable membrane and be reabsorbed into the body by the vasa recta, thus increasing the plasma volume of the body.
There are two systems that create a hyperosmotic medulla and thus increase the body plasma volume: Urea recycling and the single effect.
Urea is usually excreted as a waste product from the kidneys. However, when plasma blood volume is low and ADH is released the aquaporins that are opened are also permeable to urea. This allows urea to leave the collecting duct into the medulla, creating a hyperosmotic solution that "attracts" water. Urea can then re-enter the nephron and be excreted or recycled again depending on whether ADH is still present or not.
The single effect describes the fact that the ascending thick limb of the loop of Henle is not permeable to water but is permeable to sodium chloride. This allows for a countercurrent exchange system whereby the medulla becomes increasingly concentrated, but at the same time setting up an osmotic gradient for water to follow should the aquaporins of the collecting duct be opened by ADH.

Blood pressure
Although the kidney cannot directly sense blood, long-term regulation of blood pressure predominantly depends upon the kidney. This primarily occurs through maintenance of the extracellular fluid compartment, the size of which depends on the plasma sodium concentration </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 Retained placenta and explain in detail? [/INST] Retained placenta is a condition in which all or part of the placenta or membranes remain in the uterus during the third stage of labour. Retained placenta can be broadly divided into:

failed separation of the placenta from the uterine lining
placenta separated from the uterine lining but retained within the uterusA retained placenta is commonly a cause of postpartum haemorrhage, both primary and secondary.Retained placenta is generally defined as a placenta that has not undergone placental expulsion within 30 minutes of the baby’s birth where the third stage of labor has been managed actively.

Signs and symptoms
Risks of retained placenta include hemorrhage and infection </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 Viral pneumonia and explain in detail? [/INST] Viral pneumonia is a pneumonia caused by a virus. Pneumonia is an infection that causes inflammation in one or both of the lungs. The pulmonary alveoli fill with fluid or pus making it difficult to breathe. Pneumonia can be caused by bacteria, viruses, fungi or parasites. Viruses are the most common cause of pneumonia in children, while in adults bacteria are a more common cause.

Signs and symptoms
Symptoms of viral pneumonia include fever, non-productive cough, runny nose, and systemic symptoms (e.g. myalgia, headache). Different viruses cause different symptoms.

Diagnosis
Diagnosis, like with any infection, relies on the detection of the infectious cause. With viral pneumonia, samples are taken from the upper and/or lower respiratory tracts. The samples can then be run through polymerase chain reaction (PCR), allowing for amplification of the virus as that allows better detection if present in the sample. Other ways for a diagnosis to be obtained is by ordering a chest x-ray, blood tests, pulse oximetry, and a medical/family history to see if there are any known risks or previous exposures to a person with viral pneumonia. If the person is in serious condition and in the hospital there are more invasive studies that can be run to diagnosis the person.

Cause
Common causes of viral pneumonia are:

Influenza virus A and B
Respiratory syncytial virus (RSV)
Human parainfluenza viruses (in children)
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Rarer viruses that commonly result in pneumonia include:

Adenoviruses (in military recruits)
Metapneumovirus
Severe acute respiratory syndrome coronavirus (SARS-CoV)
Middle East respiratory syndrome virus (MERS-CoV)
HantavirusesViruses that primarily cause other diseases, but sometimes cause pneumonia include:

Herpes simplex virus (HSV), mainly in newborns or young children
Varicella-zoster virus (VZV)
Measles virus
Rubella virus
Cytomegalovirus (CMV), mainly in people with immune system problems
Smallpox virus
Dengue virusThe most commonly identified agents in children are respiratory syncytial virus, rhinovirus, human metapneumovirus, human bocavirus, and parainfluenza viruses.

History
In the pre-antibiotic age, pneumonias had been treated with specific anti-serums of highly variable therapeutic effect and undesirable side-effects (a practice eliminated by the advent of sulfamides in 1936 and the beginning availability of penicillin in the 1940s).
Viral pneumonia was first described by Hobart Reimann in 1938, in an article published by JAMA, An Acute Infection of the Respiratory Tract with Atypical Pneumonia: a disease entity probably caused by a filtrable virus. Reimann, Chairman of the Department of Medicine at Jefferson Medical College, had established the practice of routinely typing the pneumococcal organism in cases where pneumonia presented. Out of this work, the distinction between viral and bacterial strains was noticed.

Pathophysiology
Viruses must invade cells in order to reproduce. Typically, a virus will reach the lungs by traveling in droplets through the mouth and nose with inhalation. There, the virus invades the cells lining the airways and the alveoli. This invasion often leads to cell death either through direct killing by the virus or by self-destruction through apoptosis.
Further damage to the lungs occurs when the immune system responds to the infection. White blood cells, in particular lymphocytes, are responsible for activating a variety of chemicals (cytokines) which cause leaking of fluid into the alveoli. The combination of cellular destruction and fluid-filled alveoli interrupts the transportation of oxygen into the bloodstream.
In addition to the effects on the lungs, many viruses affect other organs and can lead to illness affecting many different bodily functions. Some viruses also make the body more susceptible to bacterial infection; for this reason, bacterial pneumonia often complicates viral pneumonia.

Prevention
The best prevention against viral pneumonia is vaccination against influenza, chickenpox (varicella zoster), herpes zoster, measles, respiratory syncytial virus vaccine (RSV), rubella, and adenovirus vaccine.  Besides vaccination there are no other ways to prevent viral pneumonia besides basic hygiene skills like covering the mouth when coughing or sneezing, staying home when sick, and washing your hands frequently.

Treatment
In cases of viral pneumonia where influenza A or B are thought to be causative agents, patients who are seen within 48 hours of symptom onset may benefit from treatment with oseltamivir, or zanamivir, or peramivir.  Respiratory syncytial virus (RSV) has no direct acting treatments, but ribavirin is indicated for severe cases </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 Cutaneous diphtheria infection 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 Diastasis recti and explain in detail? [/INST] Diastasis recti,  or rectus abdominis diastasis, is defined as a gap of about 2.7 cm or greater between the two sides of the rectus abdominis muscle. The distance between the right and left rectus abdominis muscles is created by the stretching of the linea alba, a connective collagen sheath created by the aponeurosis insertions of the transverse abdominis, internal oblique, and external oblique. This condition has no associated morbidity or mortality.Diastasis of the rectus abdominis muscle most frequently occurs in newborns and pregnant women; however, it may occur in any adult woman or man. In the newborn, the rectus abdominis is not fully developed and may not be sealed together at midline. Diastasis recti is more common in premature newborns. In pregnant or postpartum women, the condition is caused by the stretching of the rectus abdominis by the growing uterus. It is more common in multiparous women (women who have had multiple pregnancies) owing to repeated episodes of stretching. When the defect occurs during pregnancy, the uterus can sometimes be seen bulging through the abdominal wall beneath the skin. Non-pregnant women are more susceptible to develop diastasis recti when over the age of 35 or with high birth weight of child, multiple birth pregnancy, or multiple pregnancies. Additional causes can be attributed to excessive abdominal exercises after the first trimester of pregnancy.Strength training of all the core muscles, including the abdominis recti muscle, may or may not reduce the size of the gap in pregnant or postpartum women. Crunches may increase the diastasis recti separation. All corrective exercises should be in the form of pulling in the abdominal muscles rather than pushing them outwards. In extreme cases diastasis recti is corrected with a cosmetic surgery procedure known as an abdominoplasty by creating a plication, or folding, of the linea alba and suturing it together, which results in a tighter abdominal wall.

Presentation
A diastasis recti may appear as a ridge running down the midline of the abdomen, anywhere from the xiphoid process to the umbilicus. It becomes more prominent with straining and may disappear when the abdominal muscles are relaxed. The medial borders of the right and left halves of the muscle may be palpated during contraction of the rectus abdominis. The condition can be diagnosed by physical exam, and must be differentiated from an epigastric hernia or incisional hernia, if the patient has had abdominal surgery.  Hernias may be ruled out using ultrasound.In infants, they typically result from a minor defect of the linea alba between the rectus abdominis muscles. This allows tissue from inside the abdomen to herniate anteriorly. On infants, this may manifest as an apparent bubble under the skin of the belly between the umbilicus and xiphisternum (bottom of the breastbone).Examination is performed with the subject lying on the back, knees bent at 90° with feet flat, head slightly lifted placing chin on chest. With muscles tense, the examiner then places fingers in the ridge that is presented. Measurement of the width of separation is determined by the number of fingertips that can fit within the space between the left and right rectus abdominis muscles. Separation consisting of a width of 2 fingertips (approximately 1 1/2 centimeters) or more is the determining factor for diagnosing diastasis recti.

Diagnosis
Diastasis recti can be diagnosed by physical examination, which may include measuring the distance between the rectus abdominis muscles at rest and during contraction at several levels along the linea alba.
Abdominal ultrasonography provides objective evidence for the diagnosis, and also confirms that the bulge is not a hernia.
An abdominal CT scan is an acceptable alternative to an ultrasound.

Treatment
During pregnancy - No treatment is necessary for women while they are still pregnant.
After delivery - Typically the separation of the abdominal muscles will lessen in the mother within the first 8 weeks after childbirth; however, the connective tissue remains stretched for many. The weakening of the musculature may also cause lower back pain, weakened pelvic alignment, and altered posture.
In children - Complications include development of an umbilical or ventral hernia, which is rare and can be corrected with surgery. If an infant with the condition develops vomiting, or redness or pain in the abdominal area, medical attention should be sought.

Strength training
A systematic review of the evidence found that exercise may or may not reduce the size of the gap in pregnant or postpartum women. The authors looked at 8 studies totaling 336 women and concluded: "Due to the low number and quality of included articles, there is insufficient evidence to recommend that exercise may help to prevent or reduce DRAM," or diastasis of the rectus abdominis muscles, also stating that "non-specific exercise may or may not help to prevent or reduce DRAM during the ante- and postnatal periods."However, a study conducted by the Columbia University Program in Physical Therapy stated: "Ninety percent of non‐exercising pregnant women exhibited DRA while only 12.5% of exercising women had the condition. The mean DRA located 4.5 cm above the umbilicus was 9.6 mm (± 6.6) for the exercise group and 38.9 mm (± 17.8) for the non‐exercise group. The mean DRA located at the umbilicus was 11.4 mm (± 3.82) for the exercise group and 59.5 mm (± 23.6) for the non‐exercise group. The mean DRA located 4.5 cm below the umbilicus was 8.2 mm (± 7.4) for the exercise group and 60.4 (± 29.0) for the non‐exercise group."Nevertheless, the following exercises are often recommended to help build abdominal strength, which may or may not help reduce the size of diastasis recti:
Core contraction – In a seated position, place both hands on abdominal muscles. Take small controlled breaths. Slowly contract the abdominal muscles, pulling them straight back towards the spine. Hold the contraction for 30 seconds, while maintaining the controlled breathing. Complete 10 repetitions.
Seated squeeze - Again in a seated position, place one hand above the belly button, and the other below the belly button. With controlled breaths, with a mid-way starting point, pull the abdominals back toward the spine, hold for 2 seconds and return to the mid-way point. Complete 100 repetitions.
Head lift – In a lying down position, knees bent at 90° angle, feet flat, slowly lift the head, chin toward your chest, (concentrate on isolation of the abdominals to prevent hip-flexors from being engaged), slowly contract abdominals toward floor, hold for two seconds, lower head to starting position for 2 seconds. Complete 10 repetitions.
Upright push-up – A stand-up push-up against the wall, with feet together arms-length away from wall, place hands flat against the wall, contract abdominal muscles toward spine, lean body towards wall, with elbows bent downward close to body, pull abdominal muscles in further, with controlled breathing. Release muscles as you push back to starting position. Complete 20 repetitions.
Squat against the wall – Also known as a seated squat, stand with back against the wall, feet out in front of body, slowly lower body to a seated position so knees are bent at a 90° angle, contracting abs toward spine as you raise body back to standing position. Optionally, this exercise can also be done using an exercise ball placed against the wall and the lower back. Complete 20 repetitions.
Squat with squeeze – A variation to the "squat against the wall" is to place a small resistance ball between the knees, and squeeze the ball while lowering the body to the seated position </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 Optic neuropathy and explain in detail? [/INST] Optic neuropathy is damage to the optic nerve from any cause. The optic nerve is a bundle of millions of fibers in the retina that sends visual signals to the brain. [1].
Damage and death of these nerve cells, or neurons, leads to characteristic features of optic neuropathy. The main symptom is loss of vision, with colors appearing subtly washed out in the affected eye. A pale disc is characteristic of long-standing optic neuropathy. In many cases, only one eye is affected and patients may not be aware of the loss of color vision until the doctor asks them to cover the healthy eye.

Optic neuropathy is often called optic atrophy, to describe the loss of some or most of the fibers of the optic nerve.

Ischemic optic neuropathy
In ischemic optic neuropathies, there is insufficient blood flow (ischemia) to the optic nerve.  The anterior optic nerve is supplied by the short posterior ciliary artery and choroidal circulation, while the retrobulbar optic nerve is supplied intraorbitally by a pial plexus, which arises from the ophthalmic artery, internal carotid artery, anterior cerebral artery, and anterior communicating arteries. Ischemic optic neuropathies are classified based on the location of the damage and the cause of reduced blood flow, if known.
Anterior ischemic optic neuropathy (AION) includes diseases that affect the optic nerve head and cause swelling of the optic disc.  These diseases often cause sudden rapid visual loss in one eye.  Inflammatory diseases of the blood vessels, like giant-cell arteritis, polyarteritis nodosa, Churg–Strauss syndrome, granulomatosis with polyangiitis, and rheumatoid arthritis can cause arteritic AIONs (AAION).  The vast majority of AIONs are nonarteritic AIONs (NAION).  The most common acute optic neuropathy in patients over 50 years of age, NAION has an annual incidence of 2.3-10.2/100,000. NAION presents as a painless loss of vision, often when awakening, that occurs over hours to days.  Most patients lose the lower half of their visual field (an inferior altitudinal loss), though superior altitudinal loss is also common.  The pathophysiology of NAION is unknown, but it is related to poor circulation in the optic nerve head.  NAION is often associated with diabetes mellitus, elevated intraocular pressure (acute glaucoma, eye surgery), high cholesterol, hypercoagulable states, a drop in blood pressure (bleeding, cardiac arrest, peri-operative esp. cardiac and spine procedures), and sleep apnea.  Rarely, amiodarone, interferon-alpha, and erectile dysfunction drugs have been associated with this disease.
Posterior ischemic optic neuropathy is a syndrome of sudden visual loss with optic neuropathy without initial disc swelling with subsequent development of optic atrophy.  This can occur in patients who are predisposed to AAION and NAION as described above as well as those who had cardiac and spine surgery or serious episodes of hypotension.
Radiation optic neuropathy (RON) is also thought to be due to ischemia of the optic nerve that occurs 3 months to 8 or more years after radiation therapy to the brain and orbit.  It occurs most often around 1.5 years after treatment and results in irreversible and severe vision loss, which may also be associated with damage to the retina (radiation retinopathy). This is thought to be due to damage to dividing glial and vascular endothelial cells. RON can present with transient visual loss followed by acute painless visual loss in one or both eyes several weeks later.  The risk of RON is significantly increased with radiation doses over 50 Gy.

Optic neuritis
Optic neuritis is inflammation of the optic nerve, which is associated with swelling and destruction of the myelin sheath covering the optic nerve.  Young adults, usually females, are most commonly affected. Symptoms of optic neuritis in the affected eye include pain on eye movement, sudden loss of vision, and decrease in color vision (especially reds).  Optic neuritis, when combined with the presence of multiple demyelinating white matter brain lesions on MRI, is suspicious for multiple sclerosis.
Several causes and clinical courses are possible for the optic neuritis. It can be classified in:

Single isolated optic neuritis (SION)
relapsing isolated optic neuritis (RION)
chronic relapsing inflammatory optic neuropathy (CRION)
the neuromyelitis optica (NMO) spectrum disorder
multiple sclerosis associated optic neuritis (MSON)
unclassified optic neuritis (UCON) forms.Medical examination of the optic nerve with an ophthalmoscope may reveal a swollen optic nerve, but the nerve may also appear normal.  Presence of an afferent pupillary defect, decreased color vision, and visual field loss (often central) are suggestive of optic neuritis.  Recovery of visual function is expected within 10 weeks.  However, attacks may lead to permanent axonal loss and thinning of the retinal nerve fiber layer.

Compressive optic neuropathy
Tumors, infections, and inflammatory processes can cause lesions within the orbit and, less commonly, the optic canal.  These lesions may compress the optic nerve, resulting optic disc swelling and progressive visual loss.  Implicated orbital disorders include optic gliomas, meningiomas, hemangiomas, lymphangiomas, dermoid cysts, carcinoma, lymphoma, multiple myeloma, inflammatory orbital pseudotumor, and thyroid ophthalmopathy.  Patients often have bulging out of the eye (proptosis) with mild color deficits and almost normal vision with disc swelling.

Infiltrative optic neuropathy
The optic nerve can be infiltrated by a variety of processes, including tumors, inflammation, and infections.  Tumors that can infiltrate the optic nerve can be primary (optic gliomas, capillary hemangiomas, and cavernous hemangiomas) or secondary (metastatic carcinoma, nasopharyngeal carcinoma, lymphoma, and leukemia).  The most common inflammatory disorder that infiltrates the optic nerve is sarcoidosis.  Opportunistic fungi, viruses, and bacteria may also infiltrate the optic nerve.  The optic nerve may be elevated if the infiltration occurs in the proximal portion of the nerve.  The appearance of the nerve on examination depends on the portion of the nerve that is affected.

Traumatic optic neuropathy
The optic nerve can be damaged when exposed to direct or indirect injury.  Direct optic nerve injuries are caused by trauma to the head or orbit that crosses normal tissue planes and disrupts the anatomy and function of the optic nerve; e.g., a bullet or forceps that physically injures the optic nerve.  Indirect injuries, like blunt trauma to the forehead during a motor vehicle accident, transmit force to the optic nerve without transgressing tissue planes.  This type of force causes the optic nerve to absorb excess energy at the time of impact.  The most common site of injury of the optic nerve is the intracanalicular portion of the nerve.  Deceleration injuries from motor vehicle or bicycle accidents account for 17 to 63 percent of cases.  Falls are also a common cause, and optic neuropathy most commonly occurs when there is a loss of consciousness associated with multi-system trauma and serious brain injury.  In less than three percent of patients, an orbital hemorrhage after an injection behind the eye (retrobulbar block) can cause injury to the optic nerve, but this is readily manageable if it does not involve direct optic nerve injury and is caught early.  The role of high-dose steroids and orbital decompression in treating these patients is controversial and, if administered, must be done very soon after injury with minimal effects.  In patients with an orbital fracture, vomiting or nose blowing can force air into the orbit and possibly compromise the integrity of the optic nerve.

Mitochondrial optic neuropathies
Mitochondria play a central role in maintaining the life cycle of retinal ganglion cells because of their high energy dependence.  Mitochondria are made within the central somata of the retinal ganglion cell, transported down axons, and distributed where they are needed.  Genetic mutations in mitochondrial DNA, vitamin depletion, alcohol and tobacco abuse, and use of certain drugs can cause derangements in efficient transport of mitochondria, which can cause a primary or secondary optic neuropathy.

Nutritional optic neuropathies
A nutritional optic neuropathy may be present in a patient with obvious evidence of under-nutrition (weight loss and wasting). Months of depletion are usually necessary to deplete body stores of most nutrients. Undernourished patients often have many vitamin and nutrient deficiencies and have low serum protein levels. However, the optic neuropathy associated with pernicious anemia and vitamin B12 deficiency can even be seen in well-nourished individuals. Gastric bypass surgery may also cause a vitamin B12 deficiency from poor absorption.
Patients who have nutritional optic neuropathy may notice that colors are not as vivid or bright as before and that the color red is washed out. This normally occurs in both eyes at the same time and is not associated with any eye pain. They might initially notice a blur or fog, followed by a drop in vision. While vision loss may be rapid, progression to blindness is unusual. These patients tend to have blind spots in the center of their vision with preserved peripheral vision. In most cases, the pupils continue to respond normally to light.

Toxic optic neuropathies
The most recognized cause of toxic optic neuropathy is methanol poisoning.  This can be a life-threatening event that normally accidentally occurs when the person mistook or substituted, methanol for ethyl alcohol. The patient initially has nausea and vomiting, followed by respiratory distress, headache, and visual loss 18–48 hours after consumption.  Without treatment, patients can go blind, and their pupils will dilate and stop reacting to light.

Ethylene glycol, a component of automobile antifreeze, is a poison that is toxic to the whole body including the optic nerve. Consumption can be fatal, or recovery can occur with permanent neurologic and ophthalmologic deficits. While the visual loss is not very common, increased intracranial pressure can cause bilateral optic disc swelling from cerebral edema. A clue to the cause of intoxication is the presence of oxalate crystals in the urine. Like methanol intoxication, treatment is ethanol consumption.
Ethambutol, a drug commonly used to treat tuberculosis, is notorious for causing toxic optic neuropathy.  Patients with vision loss from ethambutol toxicity lose vision in both eyes equally. This initially presents with problems with colors (dyschromatopsia) and can leave central visual deficits. If vision loss occurs while using ethambutol, it would be best to discontinue this medication under a doctors supervision. Vision can improve slowly after discontinuing ethambutol but rarely returns to baseline.
Amiodarone is an antiarrhythmic medication commonly used for abnormal heart rhythms (atrial or ventricular tachyarrhythmias). Most patients on this medication get corneal epithelial deposits, but this medication has also been controversially associated with NAION. Patients on amiodarone with new visual symptoms should be evaluated by an ophthalmologist.
Tobacco exposure, most commonly through pipe and cigar smoking, can cause optic neuropathy. Middle-aged or elderly men are often affected and present with painless, slowly progressive, color distortion and visual loss in both eyes. The mechanism is unclear, but this has been reported to be more common in individuals who are already suffering from malnutrition.

Hereditary optic neuropathies
The inherited optic neuropathies typically manifest asa  symmetric bilateral central visual loss. Optic nerve damage in most inherited optic neuropathies is permanent and progressive.

Lebers hereditary optic neuropathy (LHON) is the most frequently occurring mitochondrial disease, and this inherited form of acute or subacute vision loss predominantly affects young males </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 Peritonitis and explain in detail? [/INST] Peritonitis is inflammation of the localized or generalized peritoneum, the lining of the inner wall of the abdomen and cover of the abdominal organs. Symptoms may include severe pain, swelling of the abdomen, fever, or weight loss. One part or the entire abdomen may be tender. Complications may include shock and acute respiratory distress syndrome.Causes include perforation of the intestinal tract, pancreatitis, pelvic inflammatory disease, stomach ulcer, cirrhosis, or a ruptured appendix. Risk factors include ascites (the abnormal build-up of fluid in the abdomen) and peritoneal dialysis. Diagnosis is generally based on examination, blood tests, and medical imaging.Treatment often includes antibiotics, intravenous fluids, pain medication, and surgery. Other measures may include a nasogastric tube or blood transfusion. Without treatment death may occur within a few days. About 20% of people with cirrhosis who are hospitalized have peritonitis.

Signs and symptoms
Abdominal pain
The main manifestations of peritonitis are acute abdominal pain, abdominal tenderness, abdominal guarding, rigidity, which are exacerbated by moving the peritoneum, e.g., coughing (forced cough may be used as a test), flexing ones hips, or eliciting the Blumberg sign (meaning that pressing a hand on the abdomen elicits less pain than releasing the hand abruptly, which will aggravate the pain, as the peritoneum snaps back into place). Rigidity is highly specific for diagnosing peritonitis (specificity: 76–100%). The presence of these signs in a person is sometimes referred to as peritonism. The localization of these manifestations depends on whether peritonitis is localized (e.g., appendicitis or diverticulitis before perforation), or generalized to the whole abdomen. In either case, pain typically starts as a generalized abdominal pain (with involvement of poorly localizing visceral innervation of the visceral peritoneal layer), and may become localized later (with involvement of the somatic innervation of the parietal peritoneal layer). Peritonitis is an example of an acute abdomen.

Other symptoms
Diffuse abdominal rigidity (abdominal guarding) is often present, especially in generalized peritonitis
Fever
Sinus tachycardia
Development of ileus paralyticus (i.e., intestinal paralysis), which also causes nausea, vomiting and bloating
Reduced or no passage of abdominal gas and bowel sound

Complications
Sequestration of fluid and electrolytes, as revealed by decreased central venous pressure, may cause electrolyte disturbances, as well as significant hypovolemia, possibly leading to shock and acute kidney failure.
A peritoneal abscess may form (e.g., above or below the liver, or in the lesser omentum)
Sepsis may develop, so blood cultures should be obtained.
Complicated peritonitis typically involves multiple organs.

Causes
Infection
Perforation of part of the gastrointestinal tract is the most common cause of peritonitis. Examples include perforation of the distal esophagus (Boerhaave syndrome), of the stomach (peptic ulcer, gastric carcinoma), of the duodenum (peptic ulcer), of the remaining intestine (e.g., appendicitis, diverticulitis, Meckel diverticulum, inflammatory bowel disease (IBD), intestinal infarction, intestinal strangulation, colorectal carcinoma, meconium peritonitis), or of the gallbladder (cholecystitis). Other possible reasons for perforation include abdominal trauma, ingestion of a sharp foreign body (such as a fish bone, toothpick or glass shard), perforation by an endoscope or catheter, and anastomotic leakage. The latter occurrence is particularly difficult to diagnose early, as abdominal pain and ileus paralyticus are considered normal in people who have just undergone abdominal surgery. In most cases of perforation of a hollow viscus, mixed bacteria are isolated; the most common agents include Gram-negative bacilli (e.g., Escherichia coli) and anaerobic bacteria (e.g., Bacteroides fragilis). Fecal peritonitis results from the presence of faeces in the peritoneal cavity.  It can result from abdominal trauma and occurs if the large bowel is perforated during surgery.
Disruption of the peritoneum, even in the absence of perforation of a hollow viscus, may also cause infection simply by letting micro-organisms into the peritoneal cavity. Examples include trauma, surgical wound, continuous ambulatory peritoneal dialysis, and intra-peritoneal chemotherapy. Again, in most cases, mixed bacteria are isolated; the most common agents include cutaneous species such as Staphylococcus aureus, and coagulase-negative staphylococci, but many others are possible, including fungi such as Candida.
Spontaneous bacterial peritonitis (SBP) is a peculiar form of peritonitis occurring in the absence of an obvious source of contamination. It occurs in people with ascites, including children.
Intra-peritoneal dialysis predisposes to peritoneal infection (sometimes named "primary peritonitis" in this context).
Systemic infections (such as tuberculosis) may rarely have a peritoneal localisation.
Pelvic inflammatory disease

Non-infection
Leakage of sterile body fluids into the peritoneum, such as blood (e.g., endometriosis, blunt abdominal trauma), gastric juice (e.g., peptic ulcer, gastric carcinoma), bile (e.g., liver biopsy), urine (pelvic trauma), menstruum (e.g., salpingitis), pancreatic juice (pancreatitis), or even the contents of a ruptured dermoid cyst. It is important to note that, while these body fluids are sterile at first, they frequently become infected once they leak out of their organ, leading to infectious peritonitis within 24 to 48 hours.
Sterile abdominal surgery, under normal circumstances, causes localised or minimal generalised peritonitis, which may leave behind a foreign body reaction or fibrotic adhesions. However, peritonitis may also be caused by the rare case of a sterile foreign body inadvertently left in the abdomen after surgery (e.g., gauze, sponge).
Much rarer non-infectious causes may include familial Mediterranean fever, TNF receptor associated periodic syndrome, porphyria, and systemic lupus erythematosus.

Risk factors
Previous history of peritonitis
History of alcoholism
Liver disease
Fluid accumulation in the abdomen
Weakened immune system
Pelvic inflammatory disease

Diagnosis
A diagnosis of peritonitis is based primarily on the clinical manifestations described above. Rigidity (involuntary contraction of the abdominal muscles) is the most specific exam finding for diagnosing peritonitis. If focal peritonitis is detected, further work-up should be done. If diffuse peritonitis is detected, then urgent surgical consultation should be obtained, and may warrant surgery without further investigations. Leukocytosis, hypokalemia, hypernatremia, and acidosis may be present, but they are not specific findings. Abdominal X-rays may reveal dilated, edematous intestines, although such X-rays are mainly useful to look for pneumoperitoneum, an indicator of gastrointestinal perforation. The role of whole-abdomen ultrasound examination is under study and is likely to expand in the future. Computed tomography (CT or CAT scanning) may be useful in differentiating causes of abdominal pain. If reasonable doubt still persists, an exploratory peritoneal lavage or laparoscopy may be performed. In people with ascites, a diagnosis of peritonitis is made via paracentesis (abdominal tap): More than 250 polymorphonuclear cells per μL is considered diagnostic. In addition, Gram stain is almost always negative, whereas culture of the peritoneal fluid can determine the microorganism responsible and determine their sensitivity to antimicrobial agents.

Pathology
In normal conditions, the peritoneum appears greyish and glistening; it becomes dull 2–4 hours after the onset of peritonitis, initially with scarce serous or slightly turbid fluid. Later on, the exudate becomes creamy and evidently suppurative; in people who are dehydrated, it also becomes very inspissated. The quantity of accumulated exudate varies widely. It may be spread to the whole peritoneum, or be walled off by the omentum and viscera </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 Ainhum and explain in detail? [/INST] Ainhum (from Portuguese, pronounced /aj.ˈɲũ/), also known as dactylolysis spontanea, is a painful constriction of the base of the fifth toe frequently followed by bilateral spontaneous autoamputation a few years later.

Signs and symptoms
The groove begins on the lower and internal side of the base of the fifth toe, usually according to the plantar-digital fold. The groove becomes gradually deeper and more circular. The rate of spread is variable, and the disease may progress to a full circle in a few months, or still be incomplete after years. In about 75 percent of cases both feet are affected, though not usually to the same degree. There is no case reported where it begins in any other toe than the fifth, while there is occasionally a groove on the fourth or third toe. The distal part of the toe swells and appears like a small potato. The swelling is due to lymphatic edema distal to the constriction. After a time crusts can appear in the groove which can be infected with staphylococcus.
While the groove becomes deeper, compression of tendons, vessels and nerves occurs. Bone is absorbed by pressure, without any evidence of infection. After a certain time all structures distal the stricture are reduced to an avascular cord. The toe’s connection to the foot becomes increasingly slender, and if it is not amputated, it spontaneously drops off without any bleeding. Normally it takes about five years for an autoamputation to occur.
Cole describes four stages of ainhum:

Pain is present in about 78% of cases. Slight pain is present in the earliest stage of ainhum, caused by pressure on the underlying nerves. Fracture of the phalanx or chronic sepsis is accompanied with severe pain.

Cause
The true cause of ainhum remains unclear. It is not due to infection by parasites, fungi, bacteria or virus, and it is not related to injury. Walking barefoot in childhood had been linked to this disease, but ainhum also occurs in patients who have never gone barefoot. Race seems to be one of the most predisposing factors and it may have a genetic component, since it has been reported to occur within families. Dent et al. discussed a genetically caused abnormality of the blood supply to the foot. It has been related to inadequate posterior tibial artery circulation and absence of plantar arch.

Diagnosis
Histolopathology
Histology shows a change in the prickle cell layer, and this is responsible for the laying down of condensed keratin causing the groove. The junctional tissue is reduced to a slender fibrous thread, almost avascular, and all the tissues beyond the constricting band is repressed by a fibro-fatty mass covered by hyperkeratotic integument.

Imaging
Soft tissue constriction on the medial aspect of the fifth toe is the most frequently presented radiological sign in the early stages. Distal swelling of the toe is considered to be a feature of the disease. In grade III lesions osteolysis is seen in the region of the proximal interphalangeal joint with a characteristic tapering effect. Dispersal of the head of the proximal phalanx is frequently seen. Finally, after autoamputation, the base of the proximal phalanx remains. Radiological examination allows early diagnosis and staging of ainhum. Early diagnosis is crucial to prevent amputation.
Doppler shows decreased blood flow in posterior tibial artery.

Differential diagnosis
Ainhum is an acquired and progressive condition, and thus differs from congenital annular constrictions. Ainhum has been much confused with similar constrictions caused by other diseases such as leprosy, diabetic gangrene, syringomyelia, scleroderma or Vohwinkel syndrome. In this case, it is called pseudo-ainhum, treatable with minor surgery or intralesional corticosteroids, as with ainhum. It has even been seen in psoriasis or it is acquired by the wrapping toes, penis or nipple with hairs, threads or fibers. Oral retinoids, such as tretinoin, and antifibrotic agents like tranilast have been tested for pseudo-ainhum. Impending amputation in Vohwinkel syndrome can sometimes be aborted by therapy with oral etretinate. It is rarely seen in the United States but often discussed in the international medical literature.

Prevention
Wearing shoes to protect barefoot trauma has shown decrease in incidence in ainhum. Congenital pseudoainhum cannot be prevented and can lead to serious birth defects.

Treatment
Incisions across the groove turned out to be ineffective. Excision of the groove followed by z-plasty could relieve pain and prevent autoamputation in Grade I and Grade II lesions. Grade III lesions are treated with disarticulating the metatarsophalangeal joint. This also relieves pain, and all patients have a useful and stable foot. Intralesional injection of corticosteroids is also helpful.

Epidemiology
Ainhum predominantly affects black people, living in West Africa, South America and India. In Nigeria it is a common disease with an incidence of 1.7 per thousand. In tropical and subtropical climates, its incidence has been reported as between 0.015 percent and 2.0 percent of the population </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 Paget–Schroetter disease and explain in detail? [/INST] Paget–Schroetter disease (also known as venous thoracic outlet syndrome) is a form of upper extremity deep vein thrombosis (DVT), a medical condition in which blood clots form in the deep veins of the arms. These DVTs typically occur in the axillary and/or subclavian veins.

Signs and symptoms
The condition is relatively rare </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 Flashing and explain in detail? [/INST]  </s>