<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 Idiopathic intracranial hypertension and explain in detail? [/INST] Idiopathic intracranial hypertension (IIH), previously known as pseudotumor cerebri and benign intracranial hypertension, is a condition characterized by increased intracranial pressure (pressure around the brain) without a detectable cause. The main symptoms are headache, vision problems, ringing in the ears, and shoulder pain. Complications may include vision loss.This condition is idiopathic, meaning there is no known cause. Risk factors include being overweight or a recent increase in weight. Tetracycline may also trigger the condition. The diagnosis is based on symptoms and a high opening pressure found during a lumbar puncture with no specific cause found on a brain scan.Treatment includes a healthy diet, salt restriction, and exercise. The medication acetazolamide may also be used along with the above measures. A small percentage of people may require surgery to relieve the pressure.About 2 per 100,000 people are newly affected per year. The condition most commonly affects women aged 20–50. Women are affected about 20 times more often than men. The condition was first described in 1897.

Signs and symptoms
The most common symptom of IIH is headache, which occurs in almost all (92–94%) cases. It is characteristically worse in the morning, generalized in character and throbbing in nature. It may be associated with nausea and vomiting. The headache can be made worse by any activity that further increases the intracranial pressure, such as coughing and sneezing. The pain may also be experienced in the neck and shoulders. Many have pulsatile tinnitus, a whooshing sensation in one or both ears (64–87%); this sound is synchronous with the pulse. Various other symptoms, such as numbness of the extremities, generalized weakness, loss of smell, and loss of coordination, are reported more rarely; none are specific for IIH. In children, numerous nonspecific signs and symptoms may be present.The increased pressure leads to compression and traction of the cranial nerves, a group of nerves that arise from the brain stem and supply the face and neck. Most commonly, the abducens nerve (sixth nerve) is involved. This nerve supplies the muscle that pulls the eye outward. Those with sixth nerve palsy therefore experience horizontal double vision which is worse when looking towards the affected side. More rarely, the oculomotor nerve and trochlear nerve (third and fourth nerve palsy, respectively) are affected; both play a role in eye movements. The facial nerve (seventh cranial nerve) is affected occasionally – the result is total or partial weakness of the muscles of facial expression on one or both sides of the face.The increased pressure leads to papilledema, which is swelling of the optic disc, the spot where the optic nerve enters the eyeball. This occurs in practically all cases of IIH, but not everyone experiences symptoms from this. Those who do experience symptoms typically report "transient visual obscurations", episodes of difficulty seeing that occur in both eyes but not necessarily at the same time. Long-term untreated papilledema leads to visual loss, initially in the periphery but progressively towards the center of vision.Physical examination of the nervous system is typically normal apart from the presence of papilledema, which is seen on examination of the eye with a small device called an ophthalmoscope or in more detail with a fundus camera. If there are cranial nerve abnormalities, these may be noticed on eye examination in the form of a squint (third, fourth, or sixth nerve palsy) or as facial nerve palsy. If the papilledema has been longstanding, visual fields may be constricted and visual acuity may be decreased. Visual field testing by automated (Humphrey) perimetry is recommended as other methods of testing may be less accurate. Longstanding papilledema leads to optic atrophy, in which the disc looks pale and visual loss tends to be advanced.

Causes
"Idiopathic" means of unknown cause. Therefore, IIH can only be diagnosed if there is no alternative explanation for the symptoms. Intracranial pressure may be increased due to medications such as high-dose vitamin A derivatives (e.g., isotretinoin for acne), long-term tetracycline antibiotics (for a variety of skin conditions) and hormonal contraceptives.
There are numerous other diseases, mostly rare conditions, that may lead to intracranial hypertension. If there is an underlying cause, the condition is termed "secondary intracranial hypertension". Common causes of secondary intracranial hypertension include obstructive sleep apnea (a sleep-related breathing disorder), systemic lupus erythematosus (SLE), chronic kidney disease, and Behçets disease.

Mechanism
The cause of IIH is not known. The Monro–Kellie rule states that the intracranial pressure is determined by the amount of brain tissue, cerebrospinal fluid (CSF) and blood inside the bony cranial vault. Three theories therefore exist as to why the pressure might be raised in IIH: an excess of CSF production, increased volume of blood or brain tissue, or obstruction of the veins that drain blood from the brain.The first theory, that of increased production of cerebrospinal fluid, was proposed in early descriptions of the disease. However, there is no experimental data that supports a role for this process in IIH.The second theory posits that either increased blood flow to the brain or increase in the brain tissue itself may result in the raised pressure. Little evidence has accumulated to support the suggestion that increased blood flow plays a role, but recently Bateman et al. in phase contrast MRA studies have quantified cerebral blood flow (CBF) in vivo and suggests that CBF is abnormally elevated in many people with IIH. Both biopsy samples and various types of brain scans have shown an increased water content of the brain tissue. It remains unclear why this might be the case.The third theory suggests that restricted venous drainage from the brain may be impaired resulting in congestion. Many people with IIH have narrowing of the transverse sinuses. It is not clear whether this narrowing is the pathogenesis of the disease or a secondary phenomenon. It has been proposed that a positive biofeedback loop may exist, where raised ICP (intracranial pressure) causes venous narrowing in the transverse sinuses, resulting in venous hypertension (raised venous pressure), decreased CSF resorption via arachnoid granulation and further rise in ICP.

Diagnosis
The diagnosis may be suspected on the basis of the history and examination. To confirm the diagnosis, as well as excluding alternative causes, several investigations are required; more investigations may be performed if the history is not typical or the person is more likely to have an alternative problem: children, men, the elderly, or women who are not overweight.

Investigations
Neuroimaging, usually with computed tomography (CT/CAT) or magnetic resonance imaging (MRI), is used to exclude any mass lesions. In IIH these scans typically appear to be normal, although small or slit-like ventricles, dilatation and buckling of the optic nerve sheaths and "empty sella sign" (flattening of the pituitary gland due to increased pressure) and enlargement of Meckels caves may be seen.
An MR venogram is also performed in most cases to exclude the possibility of venous sinus stenosis/obstruction or cerebral venous sinus thrombosis. A contrast-enhanced MRV (ATECO) scan has a high detection rate for abnormal transverse sinus stenoses. These stenoses can be more adequately identified and assessed with catheter cerebral venography and manometry. Buckling of the bilateral optic nerves with increased perineural fluid is also often noted on MRI imaging.
Lumbar puncture is performed to measure the opening pressure, as well as to obtain cerebrospinal fluid (CSF) to exclude alternative diagnoses. If the opening pressure is increased, CSF may be removed for transient relief (see below). The CSF is examined for abnormal cells, infections, antibody levels, the glucose level, and protein levels. By definition, all of these are within their normal limits in IIH. Occasionally, the CSF pressure measurement may be normal despite very suggestive symptoms. This may be attributable to the fact that CSF pressure may fluctuate over the course of the normal day. If the suspicion of problems remains high, it may be necessary to perform more long-term monitoring of the ICP by a pressure catheter.

Classification
The original criteria for IIH were described by Dandy in 1937.
They were modified by Smith in 1985 to become the "modified Dandy criteria". Smith included the use of more advanced imaging: Dandy had required ventriculography, but Smith replaced this with computed tomography. In a 2001 paper, Digre and Corbett amended Dandys criteria further. They added the requirement that the person is awake and alert, as coma precludes adequate neurological assessment, and require exclusion of venous sinus thrombosis as an underlying cause. Furthermore, they added the requirement that no other cause for the raised ICP is found.
In a 2002 review, Friedman and Jacobson propose an alternative set of criteria, derived from Smiths. These require the absence of symptoms that could not be explained by a diagnosis of IIH, but do not require the actual presence of any symptoms (such as headache) attributable to IIH. These criteria also require that the lumbar puncture is performed with the person lying sideways, as a lumbar puncture performed in the upright sitting position can lead to artificially high pressure measurements. Friedman and Jacobson also do not insist on MR venography for every person; rather, this is only required in atypical cases (see "diagnosis" above).

Treatment
The primary goal in treatment of IIH is the prevention of visual loss and blindness, as well as symptom control. IIH is treated mainly through the reduction of CSF pressure and. IIH may resolve after initial treatment, may go into spontaneous remission (although it can still relapse at a later stage), or may continue chronically.

Lumbar puncture
The first step in symptom control is drainage of cerebrospinal fluid by lumbar puncture. If necessary, this may be performed at the same time as a diagnostic LP (such as done in search of a CSF infection). In some cases, this is sufficient to control the symptoms, and no further treatment is needed.The procedure can be repeated if necessary, but this is generally taken as a clue that additional treatments may be required to control the symptoms and preserve vision. Repeated lumbar punctures are regarded as unpleasant by people, and they present a danger of introducing spinal infections if done too often. Repeated lumbar punctures are sometimes needed to control the ICP urgently if the persons vision deteriorates rapidly.

Medication
The best-studied medical treatment for intracranial hypertension is acetazolamide (Diamox), which acts by inhibiting the enzyme carbonic anhydrase, and it reduces CSF production by six to 57 percent. It can cause the symptoms of hypokalemia (low blood potassium levels), which include muscle weakness and tingling in the fingers. Acetazolamide cannot be used in pregnancy, since it has been shown to cause embryonic abnormalities in animal studies. Also, in human beings it has been shown to cause metabolic acidosis as well as disruptions in the blood electrolyte levels of newborn babies. The diuretic furosemide is sometimes used for a treatment if acetazolamide is not tolerated, but this drug sometimes has little effect on the ICP.Various analgesics (painkillers) may be used in controlling the headaches of intracranial hypertension. In addition to conventional agents such as paracetamol, a low dose of the antidepressant amitriptyline or the anticonvulsant topiramate have shown some additional benefit for pain relief.The use of steroids in the attempt to reduce the ICP is controversial. These may be used in severe papilledema, but otherwise their use is discouraged.

Venous sinus stenting
Venous sinus stenoses leading to venous hypertension appear to play a significant part in relation to raised ICP, and stenting of a transverse sinus may resolve venous hypertension, leading to improved CSF resorption, decreased ICP, cure of papilledema and other symptoms of IIH.A self-expanding metal stent is permanently deployed within the dominant transverse sinus across the stenosis under general anaesthesia. In general, people are discharged the next day. People require double antiplatelet therapy for a period of up to 3 months after the procedure and aspirin therapy for up to 1 year.
In a systematic analysis of 19 studies with 207 cases, there was an 87% improvement in overall symptom rate and 90% cure rate for treatment of papilledema. Major complications only occurred in 3/207 people (1.4%). In the largest single series of transverse sinus stenting there was an 11% rate of recurrence after one stent, requiring further stenting.Due to the permanence of the stent and small but definite risk of complications, most experts will recommend that person with IIH must have papilledema and have failed medical therapy or are intolerant to medication before stenting is undertaken.

Surgery
Two main surgical procedures exist in the treatment of IIH: optic nerve sheath decompression and fenestration and shunting. Surgery would normally only be offered if medical therapy is either unsuccessful or not tolerated. The choice between these two procedures depends on the predominant problem in IIH. Neither procedure is perfect: both may cause significant complications, and both may eventually fail in controlling the symptoms. There are no randomized controlled trials to guide the decision as to which procedure is best.Optic nerve sheath fenestration is an operation that involves the making of an incision in the connective tissue lining of the optic nerve in its portion behind the eye. It is not entirely clear how it protects the eye from the raised pressure, but it may be the result of either diversion of the CSF into the orbit or the creation of an area of scar tissue that lowers the pressure. The effects on the intracranial pressure itself are more modest. Moreover, the procedure may lead to significant complications, including blindness in 1–2%. The procedure is therefore recommended mainly in those who have limited headache symptoms but significant papilledema or threatened vision, or in those who have undergone unsuccessful treatment with a shunt or have a contraindication for shunt surgery.Shunt surgery, usually performed by neurosurgeons, involves the creation of a conduit by which CSF can be drained into another body cavity. The initial procedure is usually a lumboperitoneal (LP) shunt, which connects the subarachnoid space in the lumbar spine with the peritoneal cavity. Generally, a pressure valve is included in the circuit to avoid excessive drainage when the person is erect. LP shunting provides long-term relief in about half the cases; others require revision of the shunt, often on more than one occasion—usually due to shunt obstruction. If the lumboperitoneal shunt needs repeated revisions, a ventriculoatrial or ventriculoperitoneal shunt may be considered. These shunts are inserted in one of the lateral ventricles of the brain, usually by stereotactic surgery, and then connected either to the right atrium of the heart or the peritoneal cavity, respectively. Given the reduced need for revisions in ventricular shunts, it is possible that this procedure will become the first-line type of shunt treatment.It has been shown that in obese people, bariatric surgery (and especially gastric bypass surgery) can lead to resolution of the condition in over 95%.

Prognosis
It is not known what percentage of people with IIH will remit spontaneously, and what percentage will develop chronic disease.IIH does not normally affect life expectancy. The major complications from IIH arise from untreated or treatment-resistant papilledema. In various case series, the long-term risk of ones vision being significantly affected by IIH is reported to lie anywhere between 10 and 25%.

Epidemiology
On average, IIH occurs in about one per 100,000 people, and can occur in children and adults. The median age at diagnosis is 30. IIH occurs predominantly in women, especially in the ages 20 to 45, who are four to eight times more likely than men to be affected. Overweight and obesity strongly predispose a person to IIH: women who are more than ten percent over their ideal body weight are thirteen times more likely to develop IIH, and this figure goes up to nineteen times in women who are more than twenty percent over their ideal body weight. In men this relationship also exists, but the increase is only five-fold in those over 20 percent above their ideal body weight.Despite several reports of IIH in families, there is no known genetic cause for IIH. People from all ethnicities may develop IIH </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 Eustachian tube dysfunction and explain in detail? [/INST] Eustachian tube dysfunction (ETD) is a disorder where pressure abnormalities in the middle ear result in symptoms.

Signs and symptoms
Symptoms include aural fullness, ears popping, a feeling of pressure in the affected ear(s), a feeling that the affected ear(s) is clogged, crackling, ear pain, tinnitus, autophony, and muffled hearing.

Diagnosis
While Eustachian tube dysfunction can be hard to diagnose, due to the Eustachian tubes and the nasopharynx not being easily visible, usually a tympanometry is indicated, along with findings on an otoscopy </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 Ménières disease and explain in detail? [/INST] Ménières disease (MD) is a disease of the inner ear that is characterized by potentially severe and incapacitating episodes of vertigo, tinnitus, hearing loss, and a fullness in the ear. Typically, only one ear is affected initially, but over time, both ears may become involved. Episodes generally last from 20 minutes to a few hours. The time between episodes varies. The hearing loss and ringing in the ears can become constant over time.The cause of Ménières disease is unclear, but likely involves both genetic and environmental factors. A number of theories exist for why it occurs, including constrictions in blood vessels, viral infections, and autoimmune reactions. About 10% of cases run in families. Symptoms are believed to occur as the result of increased fluid buildup in the labyrinth of the inner ear. Diagnosis is based on the symptoms and a hearing test. Other conditions that may produce similar symptoms include vestibular migraine and transient ischemic attack.No cure is known. Attacks are often treated with medications to help with the nausea and anxiety. Measures to prevent attacks are overall poorly supported by the evidence. A low-salt diet, diuretics, and corticosteroids may be tried. Physical therapy may help with balance and counselling may help with anxiety. Injections into the ear or surgery may also be tried if other measures are not effective, but are associated with risks. The use of tympanostomy tubes, while popular, is not supported.Ménières disease was first identified in the early 1800s by Prosper Ménière. It affects between 0.3 and 1.9 per 1,000 people. It most often starts in people 40 to 60 years old. Females are more commonly affected than males. After 5 to 15 years of symptoms, the episodes of the world spinning sometimes stop and the person is left with loss of balance, poor hearing in the affected ear, and ringing or other sounds in the affected ear or ears.

Signs and symptoms
Ménières is characterized by recurrent episodes of vertigo, fluctuating hearing loss, and tinnitus; episodes may be preceded by a headache and a feeling of fullness in the ears. People may also experience additional symptoms related to irregular reactions of the autonomic nervous system. These symptoms are not symptoms of Menieres disease per se, but rather are side effects resulting from failure of the organ of hearing and balance, and include nausea, vomiting, and sweating, which are typically symptoms of vertigo, and not of Ménières. This includes a sensation of being pushed sharply to the floor from behind. Sudden falls without loss of consciousness (drop attacks) may be experienced by some people.

Causes
The cause of Ménières disease is unclear, but likely involves both genetic and environmental factors. A number of theories exist including constrictions in blood vessels, viral infections, and autoimmune reactions.

Mechanism
The initial triggers of Ménières disease are not fully understood, with a variety of potential inflammatory causes that lead to endolymphatic hydrops (EH), a distension of the endolymphatic spaces in the inner ear. EH, in turn, is strongly associated with developing MD, but not everyone with EH develops MD: "The relationship between endolymphatic hydrops and Menieres disease is not a simple, ideal correlation."Additionally, in fully developed MD, the balance system (vestibular system) and the hearing system (cochlea) of the inner ear are affected, but some cases occur where EH affects only one of the two systems enough to cause symptoms. The corresponding subtypes of MD are called vestibular MD, showing symptoms of vertigo, and cochlear MD, showing symptoms of hearing loss and tinnitus.The mechanism of MD is not fully explained by EH, but fully developed EH may mechanically and chemically interfere with the sensory cells for balance and hearing, which can lead to temporary dysfunction and even to death of the sensory cells, which in turn can cause the typical symptoms of MD – vertigo, hearing loss, and tinnitus.

Diagnosis
The diagnostic criteria as of 2015 define definite MD and probable MD as:
Definite
Two or more spontaneous episodes of vertigo, each lasting 20 minutes to 12 hours
Audiometrically documented low- to medium-frequency sensorineural hearing loss in the affected ear on at least one occasion before, during, or after one of the episodes of vertigo
Fluctuating aural symptoms (hearing, tinnitus, or fullness) in the affected ear
Not better accounted for by another vestibular diagnosisProbable

Two or more episodes of vertigo or dizziness, each lasting 20 minutes to 24 hours
Fluctuating aural symptoms (hearing, tinnitus, or fullness) in the reported ear
Not better accounted for by another vestibular diagnosis
A common and important symptom of MD is hypersensitivity to sounds. This hypersensitivity is easily diagnosed by measuring the loudness discomfort levels (LDLs).Symptoms of MD overlap with migraine-associated vertigo (MAV) in many ways, but when hearing loss develops in MAV, it is usually in both ears, and this is rare in MD, and hearing loss generally does not progress in MAV as it does in MD.People who have had a transient ischemic attack (TIA) or stroke can present with symptoms similar to MD, and in people at risk magnetic resonance imaging  should be conducted to exclude TIA or stroke.Other vestibular conditions that should be excluded include vestibular paroxysmia, recurrent unilateral vestibulopathy, vestibular schwannoma, or a tumor of the endolymphatic sac.

Management
No cure for Ménières disease is known, but medications, diet, physical therapy, and counseling, and some surgical approaches can be used to manage it.

Medications
During MD episodes, medications to reduce nausea are used, as are drugs to reduce the anxiety caused by vertigo. For longer-term treatment to stop progression, the evidence base is weak for all treatments. Although a causal relation between allergy and Ménières disease is uncertain, medication to control allergies may be helpful. To assist with vertigo and balance problems, glycopyrrolate has been found to be a useful vestibular suppressant in patients with Menieres disease.Diuretics, such as the thiazide-like diuretic chlortalidone, are widely used to manage MD on the theory that it reduces fluid buildup (pressure) in the ear. Based on evidence from multiple but small clinical trials, diuretics appear to be useful for reducing the frequency of episodes of dizziness but do not seem to prevent hearing loss.In cases where hearing loss and continuing severe episodes of vertigo occur, a chemical labyrinthectomy, in which a medication such as gentamicin is injected into the middle ear and kills parts of the vestibular apparatus, may be prescribed. This treatment has the risk of worsening hearing loss.

Diet
People with MD are often advised to reduce their sodium intake. Reducing salt intake, however, has not been well studied.Based on the assumption that MD is similar in nature to a migraine, some advise eliminating "migraine triggers" such as caffeine, but the evidence for this is weak. There is no high-quality evidence that changing diet by restricting salt, caffeine or alcohol improves symptoms.

Physical therapy
While use of physical therapy early after the onset of MD is probably not useful due to the fluctuating disease course, physical therapy to help retraining of the balance system appears to be useful to reduce both subjective and objective deficits in balance over the longer term.

Counseling
The psychological distress caused by the vertigo and hearing loss may worsen the condition in some people. Counseling may be useful to manage the distress, as may education and relaxation techniques.

Surgery
If symptoms do not improve with typical treatment, surgery may be considered. Surgery to decompress the endolymphatic sac is one option. A systematic review in 2015 found that three methods of decompression have been used – simple decompression, insertion of a shunt, and removal of the sac. It found some evidence that all three methods were useful for reducing dizziness, but that the level of evidence was low, as trials were not blinded nor were placebo controls used.Another 2015 review found that, on autopsy, shunts used in these surgeries often turn out to be displaced or misplaced, and recommended their use only in cases where the condition is uncontrolled and affecting both ears. A systematic review from 2014 found that in at least 75% of people, EL sac decompression was effective at controlling vertigo in the short term (>1 year of follow-up) and long term (>24 months).An estimated 30% of people with MD have Eustachian tube dysfunction. While a 2005 review found tentative evidence of benefit from tympanostomy tubes for improvement in the unsteadiness associated with the disease, a 2014 review concluded that their use is not supported.Destructive surgeries are irreversible and involve removing entire functionality of most, if not all, of the affected ear; as of 2013, almost no evidence existed with which to judge whether these surgeries are effective. The inner ear itself can be surgically removed via labyrinthectomy, although hearing is always completely lost in the affected ear with this operation. The surgeon can also cut the nerve to the balance portion of the inner ear in a vestibular neurectomy. The hearing is often mostly preserved; however, the surgery involves cutting open into the lining of the brain, and a hospital stay of a few days for monitoring is required.

Poorly supported
As of 2014, betahistine is often used as it is inexpensive and safe; but evidence does not justify its use in MD.
Transtympanic micropressure pulses were investigated in two systematic reviews. Neither found evidence to justify this technique.
Intratympanic steroids were investigated in three systematic reviews. The data were found to be insufficient to decide if this therapy has positive effects.
Evidence does not support the use of alternative medicine such as acupuncture or herbal supplements.

Prognosis
Ménières disease usually starts confined to one ear; it extends to both ears in about 30% of cases. People may start out with only one symptom, but in MD all three appear with time. Hearing loss usually fluctuates in the beginning stages and becomes more permanent in later stages. MD has a course of 5–15 years, and people generally end up with mild disequilibrium, tinnitus, and moderate hearing loss in one ear.

Epidemiology
From 3 to 11% of diagnosed dizziness in neuro-otological clinics are due to MD </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 Hirschsprungs disease and explain in detail? [/INST] Hirschsprungs disease (HD or HSCR) is a birth defect in which nerves are missing from parts of the intestine. The most prominent symptom is constipation. Other symptoms may include vomiting, abdominal pain, diarrhea and slow growth. Symptoms usually become apparent in the first two months of life. Complications may include enterocolitis, megacolon, bowel obstruction and intestinal perforation.The disorder may occur by itself or in association with other genetic disorders such as Down syndrome or Waardenburg syndrome. About half of isolated cases are linked to a specific genetic mutation, and about 20% occur within families. Some of these occur in an autosomal dominant manner. The cause of the remaining cases is unclear. If otherwise normal parents have one child with the condition, the next child has a 4% risk of being affected. The condition is divided into two main types, short-segment and long-segment, depending on how much of the bowel is affected. Rarely, the small bowel may be affected, as well. Diagnosis is based on symptoms and confirmed by biopsy.Treatment is generally by surgery to remove the affected section of bowel. The surgical procedure most often carried out is known as a "pull through". Occasionally, an intestinal transplantation may be recommended. Hirschsprungs disease occurs in about one in 5,000 of newborns. Males are more often affected than females. The condition is believed to have first been described in 1691 by Dutch anatomist Frederik Ruysch and is named after Danish physician Harald Hirschsprung following his description in 1888.

Signs and symptoms
Typically, Hirschsprung disease is diagnosed shortly after birth, although it may develop well into adulthood,  because of the presence of megacolon, or because the baby fails to pass the first stool (meconium) within 48 hours of delivery.  Normally, 90% of babies pass their first meconium within 24 hours, and 99% within 48 hours.Other symptoms include symptoms of bowel perforation such as vomiting, constipation, poor feeding, lethargy, and diarrhea. Symptoms of bowel obstruction would include vomiting of bile and abdominal distension. Those who pass stools after 36 to 48 hours after birth should raise suspicion of Hirschsprung disease. Such suspicion can also be risen if there is only passage of stools after suppository, rectal exam, or enema. Children who do not respond to constipation treatment for six months should also raise suspicion of such disease. Enterocolitis, an acute complication of Hirschsprung disease, is characterised by sudden onset of fever, abdominal distension, vomiting, passage of bloody stools or release of explosive gas or stools after rectal examination.Some cases are diagnosed later, into childhood, but usually before age 10. The child may experience fecal retention, constipation, or abdominal distention.

Associated syndromes
Hirschsprungs disease can also present as part of multi system disorders, such as:
Bardet–Biedl syndrome
Cartilage–hair hypoplasia
Congenital central hypoventilation syndrome
MEN2
Mowat–Wilson syndrome
Smith–Lemli–Opitz syndrome
Trisomy 21 (Down syndrome)
Some forms of Waardenburg syndrome

Cause
The disorder may occur by itself or in association with other genetic disorders such as Down syndrome. About half of isolated cases are linked to a specific genetic mutation and about 20% occur within families. Some of these occur in an autosomal dominant manner. The cause of the remaining cases is unclear. If otherwise normal parents have one child with the condition, the next child has a 4% risk of being affected.

Genetics
Several genes and specific regions on chromosomes (loci) have been shown or suggested to be associated with Hirschsprungs disease:
The RET proto-oncogene accounts for the highest proportion of both familial and sporadic cases, with a wide range of mutations scattered along its entire coding region. A proto-oncogene  can cause cancer if it is mutated or overexpressed.

RET proto-oncogene
RET is a gene that codes for proteins that assist cells of the neural crest in their movement through the digestive tract during the development of the embryo.  Those neural crest cells eventually form bundles of nerve cells called ganglions. EDNRB codes for proteins that connect these nerve cells to the digestive tract. Thus, mutations in these two genes could directly lead to the absence of certain nerve fibers in the colon. Research suggests that several genes are associated with Hirschsprungs disease. Also, new research suggests that mutations in genomic sequences involved in regulating EDNRB have a bigger impact on Hirschsprungs disease than previously thought.RET can mutate in many ways and is associated with Down syndrome.  Since Down syndrome is comorbid in 2% of Hirschsprungs cases, a likelihood exists that RET is involved heavily in both Hirschsprungs disease and Down syndrome.  RET is also associated with medullary thyroid cancer and neuroblastoma, which is a type of cancer common in children.  Both of these disorders are more common in Hirschsprungs patients than in the general population.  One function that RET controls is the travel of the neural crest cells through the intestines in the developing fetus. The earlier the RET mutation occurs in Hirschsprungs disease, the more severe the disorder becomes.

Other genes
Common and rare DNA variations in the neuregulin 1 (NRG1) and NRG3 (NRG3) were first shown to be associated with the disease in Chinese patients through a Genome Wide Association Study by the Hong Kong team in 2009  and 2012, respectively Subsequent studies in both Asian and Caucasian patients confirmed the initial findings by the University of Hong Kong. Both rare and common variants in these two genes have been identified in additional Chinese, Thai, Korean, Indonesian, and Spanish patients. These two genes are known to play a role in the formation of the enteric nervous system; thus, they are likely to be involved in the pathology of Hirschsprungs disease, at least in some cases.Another gene associated with this condition is NADPH oxidase, EF-hand calcium binding domain 5 (NOX5). This gene is located on the long arm of chromosome 15 (15q23).

Pathophysiology
During normal prenatal development, cells from the neural crest migrate into the large intestine (colon) to form the networks of nerves called the myenteric plexus (Auerbach plexus) (between the smooth muscle layers of the gastrointestinal tract wall) and the submucosal plexus (Meissner plexus) (within the submucosa of the gastrointestinal tract wall). In Hirschsprung disease, the migration is not complete and part of the colon lacks these nerve bodies that regulate the activity of the colon. The affected segment of the colon cannot relax and pass stool through the colon, creating an obstruction.The most accepted theory of the cause of Hirschsprung is a defect in the craniocaudal migration of neuroblasts originating from the neural crest that occurs during the first 12 weeks of gestation.  Defects in the differentiation of neuroblasts into ganglion cells and accelerated ganglion cell destruction within the intestine may also contribute to the disorder.This lack of ganglion cells in the myenteric and submucosal plexus is well documented in Hirschsprungs disease. With Hirschsprungs disease, the segment lacking neurons (aganglionic) becomes constricted, causing the normal, proximal section of bowel to become distended with feces. This narrowing of the distal colon and the failure of relaxation in the aganglionic segment are thought to be caused by the lack of neurons containing nitric oxide synthase.The most cited feature is absence of ganglion cells: notably in males, 75% have none in the end of the colon (rectosigmoid) and 8% lack ganglion cells in the entire colon. The enlarged section of the bowel is found proximally, while the narrowed, aganglionic section is found distally, closer to the end of the bowel. The absence of ganglion cells results in a persistent overstimulation of nerves in the affected region, resulting in contraction.The equivalent disease in horses is lethal white syndrome.

Diagnosis
Definitive diagnosis is made by suction biopsy of the distally narrowed segment. A histologic examination of the tissue would show a lack of ganglionic nerve cells. Diagnostic techniques involve anorectal manometry, barium enema, and rectal biopsy.
The suction rectal biopsy is considered the current international gold standard in the diagnosis of Hirschsprungs disease.Radiologic findings may also assist with diagnosis. Cineanography (fluoroscopy of contrast medium passing anorectal region) assists in determining the level of the affected intestines.

Treatment
Treatment of Hirschsprungs disease consists of surgical removal (resection) of the abnormal section of the colon, followed by reanastomosis.

Colostomy
The first stage of treatment used to be a reversible colostomy.  In this approach, the healthy end of the large intestine is cut and attached to an opening created on the front of the abdomen. The contents of the bowel are discharged through the hole in the abdomen and into a bag.  Later, when the patients weight, age, and condition are right, the "new" functional end of the bowel is connected with the anus. The first surgical treatment involving surgical resection followed by reanastomosis without a colostomy occurred as early as 1933 by Doctor Baird in Birmingham on a one-year-old boy.

Other procedures
The Swedish-American surgeon Orvar Swenson (1909–2012), who discovered the cause of Hirschsprungs, first performed its surgical treatment, the pull-through surgery, in 1948. The pull-through procedure repairs the colon by connecting the functioning portion of the bowel to the anus. The pull-through procedure is the typical method for treating Hirschsprungs in younger patients. Swenson devised the original procedure, and the pull-through surgery has been modified many times.
Currently,  several different surgical approaches are used, which include the Swenson, Soave, Duhamel, and Boley procedures. The Swenson procedure leaves a small portion of the diseased bowel. The Soave procedure, named after the Italian pediatric surgeon, Franco Soave (1917–1984), leaves the outer wall of the colon unaltered. The Boley procedure, pioneered by the American surgeon, Scott Boley (b. 1941), is a small modification of the Soave procedure, so the term "Soave-Boley" procedure is sometimes used.  The Duhamel procedure, named for the French pediatric surgeon Bernard Duhamel (1917–1996), uses a surgical stapler to connect the good and bad bowel.For the 15% of children who do not obtain full bowel control, other treatments are available. Constipation may be remedied by laxatives or a high-fiber diet. In those patients, serious dehydration can play a major factor in their lifestyles. A lack of bowel control may be addressed by an ileostomy – similar to a colostomy, but uses the end of the small intestine rather than the colon. The Malone antegrade colonic enema (ACE) is also an option. In a Malone ACE, a tube goes through the abdominal wall to the appendix, or if available, to the colon. The bowel is then flushed daily. Children as young as 6 years of age may administer this daily flush on their own.If the affected portion of the lower intestine is restricted to the lower portion of the rectum, other surgical procedures may be performed, such as a posterior rectal myectomy. The prognosis is good in 70% of cases. Chronic postoperative constipation is present in 7 to 8% of the operated cases. Postoperative enterocolitis, a severe manifestation, is present in the 10–20% of operated patients.

Epidemiology
According to a 1984 study conducted in Maryland, Hirschsprungs disease appears in 18.6 per 100,000 live births.  In Japan, it occurs at a similar rate of about one in 5,000 births (20 per 100,000). It is more common in male than female (4.32:1) and in white rather than nonwhite.  Nine percent of the Hirschsprung cases were also diagnosed as having Down syndrome </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Rib fracture and explain in detail? [/INST] A rib fracture is a break in a rib bone. This typically results in chest pain that is worse with inspiration. Bruising may occur at the site of the break. When several ribs are broken in several places a flail chest results. Potential complications include a pneumothorax, pulmonary contusion, and pneumonia.Rib fractures usually occur from a direct blow to the chest such as during a motor vehicle collision or from a crush injury. Coughing or metastatic cancer may also result in a broken rib. The middle ribs are most commonly fractured. Fractures of the first or second ribs are more likely to be associated with complications. Diagnosis can be made based on symptoms and supported by medical imaging.Pain control is an important part of treatment. This may include the use of paracetamol (acetaminophen), NSAIDs, or opioids. A nerve block may be another option. While fractured ribs can be wrapped, this may increase complications. In those with a flail chest, surgery may improve outcomes. They are a common injury following trauma.

Signs and symptoms
This typically results in chest pain that is worse with inspiration. Bruising may occur at the site of the break.

Complications
When several ribs are broken in several places a flail chest results. Potential complications include a pneumothorax, pulmonary contusion, and pneumonia.

Causes
Rib fractures can occur with or without direct trauma during recreational activity. Cardiopulmonary resuscitation (CPR) has also been known to cause thoracic injury, including but not limited to rib and sternum fractures. They can also occur as a consequence of diseases such as cancer or rheumatoid arthritis. While for elderly individuals a fall can cause a rib fracture, in adults automobile accidents are a common event for such an injury.

Diagnosis
Signs of a broken rib may include:
Pain on inhalation
Swelling in chest area
Bruise in chest area
Increasing shortness of breath
Coughing up blood (rib may have damaged lung)Plain X-rays often pick up displaced fractures but often miss undisplaced fractures. CT scanning is generally able to pick up both types of fractures.Because children have more flexible chest walls than adults do, their ribs are more likely to bend than to break; therefore the presence of rib fractures in children is evidence of a significant amount of force and may indicate severe thoracic injuries such as pulmonary contusion </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 Thromboangiitis obliterans and explain in detail? [/INST] Thromboangiitis obliterans, also known as Buerger disease (English ; German: [ˈbʏʁɡɐ]), is a recurring progressive inflammation and thrombosis (clotting) of small and medium arteries and veins of the hands and feet. It is strongly associated with use of tobacco products, primarily from smoking, but is also associated with smokeless tobacco.

Signs and symptoms
There is a recurrent acute and chronic inflammation and thrombosis of arteries and veins of the hands and feet. The main symptom is pain in the affected areas, at rest and while walking (claudication). The impaired circulation increases sensitivity to cold. Peripheral pulses are diminished or absent. There are color changes in the extremities. The colour may range from cyanotic blue to reddish blue. Skin becomes thin and shiny. Hair growth is reduced. Ulcerations and gangrene in the extremities are common complications, often resulting in the need for amputation of the involved extremity.

Pathophysiology
There are characteristic pathologic findings of acute inflammation and thrombosis (clotting) of arteries and veins of the hands and feet (the lower limbs being more common). The mechanisms underlying Buergers disease are still largely unknown, but smoking and tobacco consumption are major factors associated with it. It has been suggested that the tobacco may trigger an immune response in susceptible persons or it may unmask a clotting defect, either of which could incite an inflammatory reaction of the vessel wall. This eventually leads to vasculitis and ischemic changes in distal parts of limbs.A possible role for Rickettsia in this disease has been proposed.

Diagnosis
A concrete diagnosis of thromboangiitis obliterans is often difficult as it relies heavily on exclusion of other conditions. The commonly followed diagnostic criteria are outlined below although the criteria tend to differ slightly from author to author. Olin (2000) proposes the following criteria:
Typically between 20 and 40 years old and male, although recently females have been diagnosed.
Current (or recent) history of tobacco use.
Presence of distal extremity ischemia (indicated by claudication, pain at rest, ischemic ulcers or gangrene) documented by noninvasive vascular testing such as ultrasound.
Exclusion of other autoimmune diseases, hypercoagulable states, and diabetes mellitus by laboratory tests.
Exclusion of a proximal source of emboli by echocardiography and arteriography.
Consistent arteriographic findings in the clinically involved and noninvolved limbs.Buergers disease can be mimicked by a wide variety of other diseases that cause diminished blood flow to the extremities. These other disorders must be ruled out with an aggressive evaluation, because their treatments differ substantially from that of Buergers disease, for which there is no treatment known to be effective.Some diseases with which Buergers disease may be confused include atherosclerosis (build-up of cholesterol plaques in the arteries), endocarditis (an infection of the lining of the heart), other types of vasculitis, severe Raynauds phenomenon associated with connective tissue disorders (e.g., lupus or scleroderma), clotting disorders or the production of clots in the blood.Angiograms of the upper and lower extremities can be helpful in making the diagnosis of Buergers disease. In the proper clinical setting, certain angiographic findings are diagnostic of Buergers. These findings include a "corkscrew" appearance of arteries that result from vascular damage, particularly the arteries in the region of the wrists and ankles. Collateral circulation gives "tree root" or "spider leg" appearance. Angiograms may also show occlusions (blockages) or stenosis (narrowings) in multiple areas of both the arms and legs. Distal plethysmography also yields useful information about circulatory status in digits.
To rule out other forms of vasculitis (by excluding involvement of vascular regions atypical for Buergers), it is sometimes necessary to perform angiograms of other body regions (e.g., a mesenteric angiogram).Skin biopsies of affected extremities are rarely performed because of the frequent concern that a biopsy site near an area poorly perfused with blood will not heal well.

Prevention
The cause of the disease is thought to be autoimmune in nature and heavily linked to tobacco use in patients with Buergers as primary disease.

Treatment
Smoking cessation has been shown to slow the progression of the disease and decrease the severity of amputation in most patients, but does not halt the progression.
In acute cases, drugs and procedures which cause vasodilation are effective in reducing pain experienced by patient. For example, prostaglandins like Limaprost are vasodilators and give relief of pain, but do not help in changing the course of disease. Epidural anesthesia and hyperbaric oxygen therapy also have vasodilator effect.  There is moderate certainty evidence that intravenous iloprost (prostacyclin analogue) is more effective than aspirin for relieving rest pain and healing ischemic ulcers. No difference have been detected between iloprost or clinprost (prostacyclin) and alprostadil (prostaglandin analogue) for relieving pain and healing ulcers.In chronic cases, lumbar sympathectomy may be occasionally helpful. It reduces vasoconstriction and increases blood flow to limb. It aids in healing and giving relief from pain of ischemic ulcers. Bypass can sometimes be helpful in treating limbs with poor perfusion secondary to this disease.  Use of vascular growth factor and stem cell injections have been showing promise in clinical studies. There may be a benefit of using bone marrow-derived stem cells in healing ulcers and improving pain-free walking distance, but larger, high-quality trials are needed. Debridement is done in necrotic ulcers. In gangrenous digits, amputation is frequently required. Below-knee and above-knee amputation is rarely required.Streptokinase has been proposed as adjuvant therapy in some cases.Despite the clear presence of inflammation in this disorder, anti-inflammatory agents such as corticosteroids have not been shown to be beneficial in healing, but do have significant anti-inflammatory and pain relief qualities in low dosage intermittent form. Similarly, strategies of anticoagulation have not proven effective.
physical therapy: interferential current therapy to decrease inflammation.

Prognosis
Buergers is not immediately fatal.  Amputation is common and major amputations (of limbs rather than fingers/toes) are almost twice as common in patients who continue to smoke. Prognosis markedly improves if a person quits smoking.  Female patients tend to show much higher longevity rates than men. The only known way to slow the progression of the disease is to abstain from all tobacco products.

Epidemiology
Buergers is more common among men than women </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 Dyshidrosis and explain in detail? [/INST] Dyshidrosis is a type of dermatitis that is characterized by itchy blisters on the palms of the hands and bottoms of the feet. Blisters are generally one to two millimeters in size and heal over three weeks. However, they often recur. Redness is not usually present. Repeated attacks may result in fissures and skin thickening.The cause is unknown. Triggers may include allergens, physical or mental stress, frequent hand washing, or metals. Diagnosis is typically based on what it looks like and the symptoms. Allergy testing and culture may be done to rule out other problems. Other conditions that produce similar symptoms include pustular psoriasis and scabies.Avoiding triggers may be useful, as may a barrier cream. Treatment is generally with steroid cream. High strength steroid creams may be required for the first week or two. Antihistamines may be used to help with the itch. If this is not effective steroid pills, tacrolimus, or psoralen plus ultraviolet A (PUVA) may be tried.About 1 in 2,000 people are affected in Sweden. Males and females appear to be affected equally. It explains about one in five cases of hand dermatitis. The first description was in 1873. The name comes from the word "dyshidrotic", meaning "difficult sweating", as problems with sweating was once believed to be the cause.

Signs and symptoms
Dyshidrosis has been described as having the following characteristics:

Itchiness of the palms or soles, followed by the sudden development of intensely itchy small blisters on the sides of the fingers, the palms or the feet.
These blisters are often described as having a "tapioca pudding" appearance.
After a few weeks, the small blisters eventually disappear as the top layer of skin falls off.
These eruptions do not occur elsewhere on the body.
The eruptions may be symmetrical.

Causes
The exact causes of dyshidrosis are unknown. Food allergens may be involved in certain 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 Testicular torsion and explain in detail? [/INST] Testicular torsion occurs when the spermatic cord (from which the testicle is suspended) twists, cutting off the blood supply to the testicle. The most common symptom in children is sudden, severe testicular pain. The testicle may be higher than usual in the scrotum and vomiting may occur. In newborns, pain is often absent and instead the scrotum may become discolored or the testicle may disappear from its usual place.Most of those affected have no obvious prior underlying health problems. Testicular tumor or prior trauma may increase risk. Other risk factors include a congenital malformation known as a "bell-clapper deformity" wherein the testis is inadequately attached to the scrotum allowing it to move more freely and thus potentially twist. Cold temperatures may also be a risk factor. The diagnosis should usually be made based on the presenting symptoms, but requires timely diagnosis and treatment to avoid testicular loss. An ultrasound can be useful when the diagnosis is unclear.Treatment is by physically untwisting the testicle, if possible, followed by surgery. Pain can be treated with opioids. Outcome depends on time to correction. If successfully treated within six hours onset, it is often good. However, if delayed for 12 or more hours the testicle is typically not salvageable. About 40% of people require removal of the testicle.It is most common just after birth and during puberty. It occurs in about 1 in 4,000 to 1 in 25,000 males under 25 years of age each year. Of children with testicular pain of rapid onset, testicular torsion is the cause of about 10% of cases. Complications may include an inability to have children. The condition was first described in 1840 by Louis Delasiauve.

Signs and symptoms
Testicular torsion usually presents with severe testicular pain or pain in the groin and lower abdomen. Pain generally begins suddenly and typically involves only one side. There is often associated nausea and vomiting. The testicle may lie higher in the scrotum due to twisting and subsequent shortening of the spermatic cord or may be positioned in a horizontal orientation. Mild warmth and redness of the overlying area may be present. Elevation of the testicle may worsen the pain. Urinary symptoms, such as pain or increased frequency of urination are also typically absent. Symptom onset often follows physical activity or trauma to the testes or scrotum. Children with testicular torsion may awaken with testicular or abdominal pain in the middle of the night or in the morning. There may be a history of previous, similar episodes of scrotal pain due to prior transient testicular torsion with spontaneous resolution.

Complications
Testicular infarction: Testicular damage occurs as a consequence of decreased blood flow, and therefore decreased oxygen and nutrient supply, to the testicle. If the testicle is not viable during surgical exploration, it must be removed to prevent further necrosis, or tissue death.
Infertility: The impact of testicular torsion on long-term fertility is not yet fully understood. However, testicular torsion may cause abnormal sperm function on semen analysis, although these abnormalities are more likely to be found in adolescents and in adults. Torsion does not seem to affect long-term sperm function in neonates. The cause of abnormal sperm function is thought to be due to the following mechanisms:
Immunological theory, also known as "sympathetic orchidopathia": It is thought that following injury to the testicle, the bodys immune system is activated to clean up damaged cells. In the process, it creates anti-testicular cell antibodies, or proteins that cross the injured blood-testis barrier and damage both the affected and contralateral testicles.
Abnormalities in microcirculation within the testicle
Reperfusion injury: This type of injury is seen in tissues that have been deprived of blood supply for a prolonged period.
Gangrene, or a type of tissue damage caused by lack of blood supply, of the testis.
Sepsis, in extremely rare cases (0,03%), if not treated for a long period of time, it could lead to sepsis and cause severe life-threatening infections and injuries through the blood and organs, which could lead to death.
Recurrence of torsion may occur even after surgical fixation, although this is very unlikely.
Psychological impact of losing a testicle.

Risk factors
Most of those affected with testicular torsion have no prior underlying health problems or predisposing conditions. However, there are certain factors that may increase risk of testicular torsion. A larger testicle either due to normal variation or testicular tumor increases the risk of torsion. Similarly, the presence of a mass or malignancy involving the spermatic cord can also predispose to torsion.Age is also an important risk factor for torsion. Torsion most commonly occurs either in the newborn or just before or during puberty. Testicular torsion often occurs before or during puberty, prior to complete testicular descent. Epididymitis is more commonly a postpubertal condition.Several congenital anatomic malformations or variations in the testicle or the surrounding structures may allow for increased scrotal rotation and increase the risk of testicular torsion. A congenital malformation of the processus vaginalis known as "bell-clapper deformity" accounts for 90% of all cases. In this condition, rather than the testes attaching posteriorly to the inner lining of the scrotum by the mesorchium, the mesorchium terminates early and the testis is free floating in the tunica vaginalis. Other anatomic risk factors include horizontal lie of the testicle or a spermatic cord with a long intrascrotal portion. Cryptorchidisim is also a risk factor for torsion with some studies proposing a 10-fold higher risk.
Testicular torsion may also be caused by trauma to the scrotum or exercise (in particular, bicycle riding), however only about 4-8% of cases are the result of trauma. There is thought to be a possible genetic basis for predisposition to torsion, based on multiple published reports of familial testicular torsion. There is controversy whether cold weather months are associated with an increased risk.

Pathophysiology
Testicular torsion occurs when there is mechanical twisting of the spermatic cord, which suspends the testicle within the scrotum and contains the testicular artery and vein. Twisting of the cord reduces or eliminates blood flow to the testicle. The degree of arterial and venous obstruction depends on the duration and severity of the torsion event. Typically, venous blood flow is compromised first. The increase in venous pressure subsequently causes decreased arterial blood flow, leading to decreased oxygen supply to the testicle, and if untreated, testicular infarction.It is also believed that torsion occurring during fetal development can lead to so-called neonatal torsion or vanishing testis, and is one of the causes of an infant being born with monorchism (one testicle).

Intermittent testicular torsion
Intermittent testicular torsion (ITT) is a less serious but chronic variant of torsion. It is characterized by intermittent scrotal or testicular pain, followed by eventual spontaneous detorsion and resolution of pain. Nausea and vomiting may also occur.: 150  Though less pressing, such individuals are at significant risk of complete torsion and possible subsequent orchiectomy and the recommended treatment is elective bilateral orchiopexy.  Ninety-seven percent of patients who undergo such surgery experience complete relief from their symptoms.: 316

Extravaginal testicular torsion
Torsion occurring outside of the tunica vaginalis, when the testis and gubernaculum can rotate freely, is termed an extravaginal testicular torsion. This type occurs exclusively in newborns, however, newborns can be affected by other testicular torsion variants as well. Neonates experiencing such a torsion typically present with painless scrotal swelling, discoloration, and a firm, painless mass in the scrotum. Such testes are usually necrotic from birth and must be removed surgically.: 315  The exact cause of or specific risk factors for extravaginal torsion in this population remain unclear.

Intravaginal testicular torsion
Intravaginal testicular torsion occurs when the testicle rotates on the spermatic cord within the tunica vaginalis. This variant more commonly occurs in older children and adults. The "bell-clapper deformity," in which there is inappropriately high attachment of the tunica vaginalis over the spermatic cord and failure of the normal posterior attachment of the testicle to the inner scrotum, which allows the testicle to move freely within the tunica vaginalis and predisposes to intravaginal testicular torsion.

Torsion of the testicular appendix
The testicular appendix is located in the upper pole of the testicle. It is an embryonic remnant that has no known function, but is at risk for torsion events. This type of torsion is the most common cause of acute scrotal pain in boys ages 7–14. Its appearance is similar to that of testicular torsion but the onset of pain is typically more gradual. Palpation reveals a small firm nodule on the upper portion of the testis which displays a characteristic "blue dot sign".  This is the appendix of the testis which has become discolored and is noticeably blue through the skin. Unlike other torsions, however, the cremasteric reflex is still active.  Typical treatment involves the use of over-the-counter analgesics and the condition resolves within 2–3 days.: 316

Torsion of the undescended testicle
The undescended testis is at increased risk of testicular torsion. The mechanism for torsion in the undescended testicle is not fully understood, though it may be due to abnormal contractions of the cremaster muscle, which covers the testicle and spermatic cord and is responsible for raising and lowering the testicle to regulate scrotal temperature. The undescended testicle is also at higher risk for testicular tumor, which due to the increased weight and size compared to a healthy testicle can predispose to torsion.

Diagnosis
The diagnosis should generally be made based on the presenting symptoms. An ultrasound can be useful when the diagnosis is unclear. However, imaging should not delay surgical intervention as complications develop with prolonged ischemia. Immediate surgery is recommended regardless of imaging findings if there is a high degree of suspicion based on history and physical examination.Given the treatment implications of testicular torsion, it is important to distinguish testicular torsion from other causes of testicular pain, such as epididymitis, which can present similarly. While both conditions can cause testicular pain, the pain of epididymitis is typically localized to the epididymis at the rear pole of the testicle. Epididymitis may also be characterized by discoloration and swelling of the testis, and fever. The cremasteric reflex in epididymitis is usually present. Testicular torsion, or more probably impending testicular infarction, can also produce a low-grade fever. There is often an absent or decreased cremasteric reflex.

Clinical exam
The absence of the cremasteric reflex in an acutely painful testicle is most indicative of testicular torsion (the twisting of the spermatic cord of the testicle makes reflexive responses all but impossible). The cremasteric reflex normally causes elevation of the testicle by stroking the inner thigh. Absence is especially common in children, but its presence does not exclude a diagnosis of testicular torsion.On physical examination, the testis can be swollen, tender, high-riding, and with an abnormal transverse lie.Prehns sign, a classic physical exam finding, has not been reliable in distinguishing torsion from other causes of testicular pain such as epididymitis. The individual will not usually have a fever, though nausea is common.

Imaging
A doppler ultrasound scan of the scrotum can identify the absence of blood flow in the twisted testicle and is nearly 90% accurate in diagnosis. It can also help distinguish torsion from epididymitis.Radionuclide scanning (scintigraphy) of the scrotum is the most accurate imaging technique, but it is not routinely available, particularly with the urgency that might be required. The agent of choice for this purpose is technetium-99m pertechnetate. Initially it provides a radionuclide angiogram, followed by a static image after the radionuclide has perfused the tissue. In the healthy patient, initial images show symmetric flow to the testes, and delayed images show uniformly symmetric activity. In testicular torsion, the images may show heterogenous activity within the affected testicle.

Treatment
Testicular torsion is a surgical emergency that requires immediate intervention to restore the flow of blood to the testicle. If treated either manually or surgically within six hours, there is a high chance (approximately 90%) of saving the testicle. At 12 hours the rate decreases to 50%; at 24 hours it drops to 10%, and after 24 hours the ability to save the testicle approaches 0, although salvage of the testicle has been reported beyond 24 hours </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 Pelvic inflammatory disease and explain in detail? [/INST] Pelvic inflammatory disease, also known as pelvic inflammatory disorder (PID), is an infection of the upper part of the female reproductive system, namely the uterus, fallopian tubes, and ovaries, and inside of the pelvis. Often, there may be no symptoms. Signs and symptoms, when present, may include lower abdominal pain, vaginal discharge, fever, burning with urination, pain with sex, bleeding after sex, or irregular menstruation. Untreated PID can result in long-term complications including infertility, ectopic pregnancy, chronic pelvic pain, and cancer.The disease is caused by bacteria that spread from the vagina and cervix. Infections by Neisseria gonorrhoeae or Chlamydia trachomatis are present in 75 to 90 percent of cases. Often, multiple different bacteria are involved. Without treatment, about 10 percent of those with a chlamydial infection and 40 percent of those with a gonorrhea infection will develop PID. Risk factors are generally similar to those of sexually transmitted infections and include a high number of sexual partners and drug use. Vaginal douching may also increase the risk. The diagnosis is typically based on the presenting signs and symptoms. It is recommended that the disease be considered in all women of childbearing age who have lower abdominal pain. A definitive diagnosis of PID is made by finding pus involving the fallopian tubes during surgery. Ultrasound may also be useful in diagnosis.Efforts to prevent the disease include not having sex or having few sexual partners and using condoms. Screening women at risk for chlamydial infection followed by treatment decreases the risk of PID. If the diagnosis is suspected, treatment is typically advised. Treating a womans sexual partners should also occur. In those with mild or moderate symptoms, a single injection of the antibiotic ceftriaxone along with two weeks of doxycycline and possibly metronidazole by mouth is recommended. For those who do not improve after three days or who have severe disease, intravenous antibiotics should be used.Globally, about 106 million cases of chlamydia and 106 million cases of gonorrhea occurred in 2008. The number of cases of PID, however, is not clear. It is estimated to affect about 1.5 percent of young women yearly. In the United States, PID is estimated to affect about one million people each year. A type of intrauterine device (IUD) known as the Dalkon shield led to increased rates of PID in the 1970s. Current IUDs are not associated with this problem after the first month.

Signs and symptoms
Symptoms in PID range from none to severe. If there are symptoms, fever, cervical motion tenderness, lower abdominal pain, new or different discharge, painful intercourse, uterine tenderness, adnexal tenderness, or irregular menstruation may be noted.Other complications include endometritis, salpingitis, tubo-ovarian abscess, pelvic peritonitis, periappendicitis, and perihepatitis.

Complications
PID can cause scarring inside the reproductive system, which can later cause serious complications, including chronic pelvic pain, infertility, ectopic pregnancy (the leading cause of pregnancy-related deaths in adult females), and other complications of pregnancy. Occasionally, the infection can spread to the peritoneum causing inflammation and the formation of scar tissue on the external surface of the liver (Fitz-Hugh–Curtis syndrome).

Cause
Chlamydia trachomatis and Neisseria gonorrhoeae are usually the main cause of PID. Data suggest that PID is often polymicrobial. Isolated anaerobes and facultative microorganisms have been obtained from the upper genital tract. N. gonorrhoeae has been isolated from fallopian tubes, facultative and anaerobic organisms were recovered from endometrial tissues.The anatomical structure of the internal organs and tissues of the female reproductive tract provides a pathway for pathogens to ascend from the vagina to the pelvic cavity thorough the infundibulum. The disturbance of the naturally occurring vaginal microbiota associated with bacterial vaginosis increases the risk of PID.N. gonorrhoea and C. trachomatis are the most common organisms. The least common were infections caused exclusively by anaerobes and facultative organisms. Anaerobes and facultative bacteria were also isolated from 50 percent of the patients from whom Chlamydia and Neisseria were recovered; thus, anaerobes and facultative bacteria were present in the upper genital tract of nearly two-thirds of the PID patients. PCR and serological tests have associated extremely fastidious organism with endometritis, PID, and tubal factor infertility.  Microorganisms associated with PID are listed below.Rarely cases of PID have developed in people who have stated they have never had sex.

Bacteria
Diagnosis
Upon a pelvic examination, cervical motion, uterine, or adnexal tenderness will be experienced.  Mucopurulent cervicitis and or urethritis may be observed. In severe cases more testing may be required such as laparoscopy, intra-abdominal bacteria sampling and culturing, or tissue biopsy.Laparoscopy can visualize "violin-string" adhesions, characteristic of Fitz-Hugh–Curtis perihepatitis and other abscesses that may be present.Other imaging methods, such as ultrasonography, computed tomography (CT), and magnetic imaging (MRI), can aid in diagnosis. Blood tests can also help identify the presence of infection: the erythrocyte sedimentation rate (ESR), the C-reactive protein (CRP) level, and chlamydial and gonococcal DNA probes.Nucleic acid amplification tests (NAATs), direct fluorescein tests (DFA), and enzyme-linked immunosorbent assays (ELISA) are highly sensitive tests that can identify specific pathogens present. Serology testing for antibodies is not as useful since the presence of the microorganisms in healthy people can confound interpreting the antibody titer levels, although antibody levels can indicate whether an infection is recent or long-term.Definitive criteria include histopathologic evidence of endometritis, thickened filled Fallopian tubes, or laparoscopic findings. Gram stain/smear becomes definitive in the identification of rare, atypical and possibly more serious organisms. Two thirds of patients with laparoscopic evidence of previous PID were not aware they had PID, but even asymptomatic PID can cause serious harm.
Laparoscopic identification is helpful in diagnosing tubal disease; a 65 percent to 90 percent positive predictive value exists in patients with presumed PID.Upon gynecologic ultrasound, a potential finding is tubo-ovarian complex, which is edematous and dilated pelvic structures as evidenced by vague margins, but without abscess formation.

Differential diagnosis
A number of other causes may produce similar symptoms including appendicitis, ectopic pregnancy, hemorrhagic or ruptured ovarian cysts, ovarian torsion, and endometriosis and gastroenteritis, peritonitis, and bacterial vaginosis among others.Pelvic inflammatory disease is more likely to reoccur when there is a prior history of the infection, recent sexual contact, recent onset of menses, or an IUD (intrauterine device) in place or if the partner has a sexually transmitted infection.Acute pelvic inflammatory disease is highly unlikely when recent intercourse has not taken place or an IUD is not being used. A sensitive serum pregnancy test is typically obtained to rule out ectopic pregnancy. Culdocentesis will differentiate hemoperitoneum (ruptured ectopic pregnancy or hemorrhagic cyst) from pelvic sepsis (salpingitis, ruptured pelvic abscess, or ruptured appendix).Pelvic and vaginal ultrasounds are helpful in the diagnosis of PID. In the early stages of infection, the ultrasound may appear normal. As the disease progresses, nonspecific findings can include free pelvic fluid, endometrial thickening, uterine cavity distension by fluid or gas. In some instances the borders of the uterus and ovaries appear indistinct. Enlarged ovaries accompanied by increased numbers of small cysts correlates with PID.Laparoscopy is infrequently used to diagnose pelvic inflammatory disease since it is not readily available.  Moreover, it might not detect subtle inflammation of the fallopian tubes, and it fails to detect endometritis.  Nevertheless, laparoscopy is conducted if the diagnosis is not certain or if the person has not responded to antibiotic therapy after 48 hours.No single test has adequate sensitivity and specificity to diagnose pelvic inflammatory disease. A large multisite U.S. study found that cervical motion tenderness as a minimum clinical criterion increases the sensitivity of the CDC diagnostic criteria from 83 percent to 95 percent. However, even the modified 2002 CDC criteria do not identify women with subclinical disease.

Prevention
Regular testing for sexually transmitted infections is encouraged for prevention. The risk of contracting pelvic inflammatory disease can be reduced by the following:

Using barrier methods such as condoms; see human sexual behaviour for other listings.
Seeking medical attention if you are experiencing symptoms of PID.
Using hormonal combined contraceptive pills also helps in reducing the chances of PID by thickening the cervical mucosal plug & hence preventing the ascent of causative organisms from the lower genital tract.
Seeking medical attention after learning that a current or former sex partner has, or might have had a sexually transmitted infection.
Getting a STI history from your current partner and strongly encouraging they be tested and treated before intercourse.
Diligence in avoiding vaginal activity, particularly intercourse, after the end of a pregnancy (delivery, miscarriage, or abortion) or certain gynecological procedures, to ensure that the cervix closes.
Reducing the number of sexual partners.
Sexual monogamy.
Abstinence

Treatment
Treatment is often started without confirmation of infection because of the serious complications that may result from delayed treatment. Treatment depends on the infectious agent and generally involves the use of antibiotic therapy although there is no clear evidence of which antibiotic regimen is more effective and safe in the management of PID. If there is no improvement within two to three days, the patient is typically advised to seek further medical attention. Hospitalization sometimes becomes necessary if there are other complications.  Treating sexual partners for possible STIs can help in treatment and prevention.For women with PID of mild to moderate severity, parenteral and oral therapies appear to be effective.  It does not matter to their short- or long-term outcome whether antibiotics are administered to them as inpatients or outpatients. Typical regimens include cefoxitin or cefotetan plus doxycycline, and clindamycin plus gentamicin. An alternative parenteral regimen is ampicillin/sulbactam plus doxycycline. Erythromycin-based medications can also be used. A single study suggests superiority of azithromycin over doxycycline. Another alternative is to use a parenteral regimen with ceftriaxone or cefoxitin plus doxycycline </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 Yersinia and explain in detail? [/INST] Yersinia is a genus of bacteria in the family Yersiniaceae. Yersinia species are Gram-negative, coccobacilli bacteria, a few micrometers long and fractions of a micrometer in diameter, and are facultative anaerobes. Some members of Yersinia are pathogenic in humans; in particular, Y. pestis is the causative agent of the plague. Rodents are the natural reservoirs of Yersinia; less frequently, other mammals serve as the host. Infection may occur either through blood (in the case of Y. pestis) or in an alimentary fashion, occasionally via consumption of food products (especially vegetables, milk-derived products, and meat) contaminated with infected urine or feces.
Speculations exist as to whether or not certain Yersinia can also be spread by  protozoonotic mechanisms, since Yersinia species are known to be facultative intracellular parasites; studies and discussions of the possibility of amoeba-vectored (through the cyst form of the protozoan) Yersinia propagation and proliferation are now in progress.

Microbial physiology
An interesting feature peculiar to some of the Yersinia bacteria is the ability to not only survive, but also to actively proliferate at temperatures as low as 1–4 °C (e.g., on cut salads and other food products in a refrigerator). Yersinia bacteria are relatively quickly inactivated by oxidizing agents such as hydrogen peroxide and potassium permanganate solutions.

Genetics
Database
The creation of YersiniaBase, a data and tools collection for the reporting and comparison of Yersinia species genome sequence data, was reported in January 2015.  The provisional representation of species addressed by the resource has been indicated in the TaxBox on this page by a superscript yb beside the species name.  Development of YersiniaBase was funded by the University of Malaya and the Ministry of Education, Malaysia.

Pathogenesis
Y. pestis is the causative agent of plague </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 Post-nasal drip and explain in detail? [/INST] Post-nasal drip (PND), also known as upper airway cough syndrome (UACS), occurs when excessive mucus is produced by the nasal mucosa. The excess mucus accumulates in the back of the nose, and eventually in the throat once it drips down the back of the throat. It can be caused by rhinitis, sinusitis, gastroesophageal reflux disease (GERD), or by a disorder of swallowing (such as an esophageal motility disorder). Other causes can be allergy, cold, flu, and side effects from medications.
However, some researchers argue that the flow of mucus down the back of the throat from the nasal cavity is a normal physiologic process that occurs in all healthy individuals. Some researchers challenge post-nasal drip as a syndrome and instead view it as a symptom, also taking into account variation across different societies. Furthermore, this rebuttal is reinforced because of the lack of an accepted definition, pathologic tissue changes, and available biochemical tests.

Signs and symptoms
PND may present itself through the constant presence of discomfort in the upper airways. It is classically described as the sensation of a substance "dripping down the throat" and may also present with rhinorrhea, constant throat clearing, and cough, although its symptoms can be very nonspecific.  PND is one of the most common etiologies for chronic cough, defined as a cough persisting beyond 8 weeks.GERD is often associated with a high prevalence of upper-respiratory symptoms similar to those of PND, such as coughing, throat clearing, hoarseness and change in voice. Reflux causes throat irritation, leading to a sensation of increased mucus in the throat, which is believed to aggravate and, in some cases, cause post-nasal drip.Post-nasal drip can be a cause of laryngeal inflammation and hyperresponsiveness, leading to symptoms of vocal cord dysfunction.

Causes
There are multiple causes of PND, which can be acute or chronic.

Allergic rhinitis
Allergic rhinitis (AR) is a common condition where exposure to allergens results in the release of inflammatory mediators, such as histamine, that causes sneezing, rhinorrhea, itchy eyes, and nasal congestion. The increased rhinorrhea and mucus production can result in PND.

Non-allergic rhinitis
Non-allergic rhinitis (NAR) is a condition in which there are symptoms of rhinitis, including rhinorrhea and nasal obstruction, but with negative skin and serum allergy testing results. It can be further categorized into:
Non-allergic rhinitis with eosinophilia (NARES)
Hormonal rhinitis (such as during pregnancy)
Medication-induced rhinitis
Atrophic rhinitis
Irritant and occupational rhinitis (including tobacco smoke, cleaning supplies, etc.)
Idiopathic nonallergic rhinitis

Rhinosinusitis
Rhinosinusitis is inflammation or infection of the sinus cavities. Acute rhinosinusitis has symptoms lasting less than four weeks, while chronic rhinosinusitis lasts greater than 12 weeks. This persistent irritation can lead to increased mucus production as a result of pro-inflammatory pathways, producing symptoms of PND.

Mechanism
The exact mechanism of PND depends on its etiology, but usually involves increased production of mucus from the nasal mucosa. In addition to providing sense of smell, the nasal cavity serves to filter and regulate the temperature and humidity of inspired air. The nasal mucosa can produce secretions, or mucus, that provides lubrication and protection for the nasal cavity. This mucus production is activated by the autonomic nervous system; specifically, cholinergic neuropeptides are responsible for increasing mucus production. Excess mucus can drain posteriorly into the upper and lower airways, which, along with other physical and chemical irritants, can activate receptors in the respiratory tract that results in a protective physiological cough.

Diagnosis
Diagnosis of PND depends on both a detailed history and clinical examination to help determine its etiology. The history may begin with feelings of obstructed nasal breathing or "stuffy nose" with or without nasal discharge. If allergic rhinitis is suspected, a family history of allergic conditions as well as a personal history of other associated conditions such as food allergy, asthma, and atopic dermatitis can be evaluated.  Allergic rhinitis classically has more symptoms of sneezing attacks, itchy eyes, and respiratory problems, although it is difficult to distinguish the different types of rhinitis by symptomology alone. Visual inspection can reveal mouth breathing, which is suggestive of nasal obstruction, or a horizontal crease across the nose (caused by the "allergic salute").In the absence of any specific diagnostic tests, it may be difficult to diagnose PND from history of symptoms alone, as the etiology is broad and the symptoms may be very general. As such, suggestive procedures that highlight rhinitis and mucopurulent secretions, such as nasoendoscopy, may instead be utilized because of the vague nature of information available to directly attribute specific symptoms to the syndrome.

Treatment
Treatment options depend on the nature of an individual’s post-nasal drip and its cause </s>