<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 Epilepsia partialis continua and explain in detail? [/INST] Epilepsia partialis continua is a rare type of brain disorder in which a patient experiences recurrent motor epileptic seizures that are focal (hands and face), and recur every few seconds or minutes for extended periods (days to years). It is sometimes called Kozhevnikovs epilepsia named after Russian psychiatrist Aleksei Yakovlevich Kozhevnikov who first described this type of epilepsy.

Signs and symptoms
During these seizures, there is repetitive focal myoclonus or Jacksonian march.
After a seizure has subsided, Todds phenomenon may be observed, which includes transient unilateral weakness.

Causes
There are numerous causes for this kind of seizure and they differ depending somewhat on the age at which the seizures begin. Epilepsy most often occurs at the extremes of life – in childhood or in very old age – but can develop at any time throughout ones life.
Although these seizures are usually due to large, acute brain lesions resulting from strokes in adults and focal cortical inflammatory processes in children (Rasmussens encephalitis), possibly caused by chronic viral infections, edema, or autoimmune processes.
They are very medication and therapy-resistant, and the primary therapeutic goal is to stop secondary generalization. There are also many other reasons why these seizures occur. For example, they could be due to genetics, infections, or problems with brain development. Commonly the cause is unknown.
Genetic background determines such features as height, eye color, and potential to develop certain diseases like diabetes, but it also determines all the chemicals and structures that make up the brain, therefore playing a role in epilepsia partialis continua. The chemicals and structures that make up the brain have similarities across different people, but they vary in certain enzymes and receptors. These variations are not usually enough to cause a problem, but occasionally they do. For example, if a person has a mutation in a gene that creates the sodium channel (a part of the neuron required for firing) it makes it easier for neuronal firing to get out of control.
An infection of the brain (encephalitis) can also be a contributing factor. Although this sort of infection is uncommon it can be due to a virus, bacterium, or (very rarely) fungus. If a seizure happens during the infection itself, the person most likely doesnt have epilepsy but has "symptomatic seizures" or seizures occurring because of a known injury to the brain. Once the infection is stopped the seizures will stop. Another more common infection is "meningitis", infection of the membranes surrounding the brain </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 Greig cephalopolysyndactyly syndrome and explain in detail? [/INST] Greig cephalopolysyndactyly syndrome is a disorder that affects development of the limbs, head, and face. The features of this syndrome are highly variable, ranging from very mild to severe. People with this condition typically have one or more extra fingers or toes (polydactyly) or an abnormally wide thumb or big toe (hallux).

Presentation
The skin between the fingers and toes may be fused (cutaneous syndactyly). This disorder is also characterized by widely spaced eyes (ocular hypertelorism), an abnormally large head size (macrocephaly), and a high, prominent forehead. Rarely, affected individuals may have more serious medical problems including seizures and developmental delay.

Pathophysiology
Greig cephalopolysyndactyly syndrome is a chromosomal condition related to chromosome 7. Mutations in the GLI3 gene cause Greig cephalopolysyndactyly syndrome. The GLI3 gene provides instructions for making a protein that controls gene expression, which is a process that regulates whether genes are turned on or off in particular cells. By interacting with certain genes at specific times during development, the GLI3 protein plays a role in the normal shaping (patterning) of many organs and tissues before birth.Different genetic changes involving the Gli3 gene can cause Greig cephalopolysyndactyly syndrome. In some cases, the condition results from a chromosomal abnormality, such as a large deletion or translocation of genetic material, in the region of chromosome 7 that contains the GLI3 gene. In other cases, a mutation in the GLI3 gene itself is responsible for the disorder. Each of these genetic changes prevents one copy of the gene in each cell from producing any functional protein. It remains unclear how a reduced amount of this protein disrupts early development and causes the characteristic features of Greig cephalopolysyndactyly syndrome.This condition is inherited in an autosomal dominant pattern, which means the defective gene is located on an autosome, and only one copy of the defective GLI3 gene is sufficient to cause the disorder. In cases of dominant inheritance, an affected person inherits the genetic mutation or chromosomal abnormality from one affected parent.Rare instances of this disorder are sporadic, and occur in people with no history of the condition in their family.

Diagnosis
The disease is not easily definable. The main form of diagnosis is presumptive, if the person has the usual triad of preaxial polydactyly with cutaneous syndactyly of at least one limb, macrocephaly, and  hypertelorism. However, a definitive diagnosis can be made if there is a phenotype that is caused by a Gcps and a Gli3 gene mutation. It can also be made if the person has a family member or relative with the disease </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 Iridodialysis and explain in detail? [/INST] Iridodialysis is a localized separation or tearing away of the iris from its attachment to the ciliary body.

Symptoms and signs
Those with small iridodialyses may be asymptomatic and require no treatment, but those with larger dialyses may have corectopia or polycoria and experience monocular diplopia, glare, or photophobia. Iridodialyses often accompany angle recession and may cause glaucoma or hyphema. Hypotony may also occur.

Complications
Those with traumatic iridodialyses (particularly by blunt trauma) are at high risk for angle recession, which may cause glaucoma. This is typically seen about 100 days after the injury, and as such is sometimes  called "100-day glaucoma" </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 Fibromatosis colli and explain in detail? [/INST] Fibromatosis colli (FMC), also termed sternocleidomastoid tumor of infancy, pseudotumor of infancy, and infancy sternocleidomastoid pseudotumor, is an uncommon (incidence: 0.4%-1.3% of live births), congenital tumor in one of the two sternocleidomastoid neck muscles although rare cases have presented with a FMC tumor in both sternocleidomastoid muscles. A tumor is here defined as a growth of tissue that is not coordinated with the normal surrounding tissue and persists in growing even if the original trigger for its growth is removed. FMC tumors are benign growths that may cause disfigurements but are not cancers and do not metastasize (i.e. spread) to distant tissues.As judged by microscopic cytology analyses, fibromatosis colli tumors consist of spindle-shaped fibroblasts (i.e. the most common cell type in connective tissue) located in a background of collagen fibers, decomposing skeletal muscle fibers, and, in some cases, regenerating skeletal muscle fibers. The fibroblasts have a completely normal appearance with no evidence suggesting that they are malignant. The World Health Organization, 2020, classified fibromatosis colli as in the category of benign fibroblastic and myofibroblastic tumors.In the majority of cases, FMC tumors decrease in size and completely resolve by the newborns second year. If left untreated, however, a significant percentage of cases progress to, and are the most frequent cause of, congenital muscular torticollis, i.e. an abnormal, asymmetrical head or neck position commonly called wry neck. Untreated FMC tumors may also progress to facial asymmetry, plagiocephaly (i.e. flattened head), permanent loss of neck mobility, scoliosis (i.e. sidewise curvature of the spine), or other structural disfigurements that result from compensatory mechanisms.

Presentation
FMC tumors most commonly present as slow-growing, firm, mobile, nontender, spindle-shaped masses in the lower two-thirds of the sternocleidomastoid muscle of infants within 8 weeks (average: 24 days) of delivery. At diagnosis, these infants heads may tilt toward the side with the mass while their chins tilt to the opposite, uninvolved side. This tilting is due to sternocleidomastoid muscle contracture. FMC tumors are more common in males and the right sternocleidomastoid muscle  although very rare cases present with bilateral tumors. Untreated, the masses may continue to grow for weeks after birth but then stabilize, start regressing after 4–8 months of life, and over the ensuing 1–2 years typically fully resolve. In three studies, >25%, >50% and >80% of these infants have had difficult deliveries such as a breech birth, delivery requiring forceps, primigravida birth (i.e. mothers first child), prolonged, difficult labor, or delivery by Caesarean section. From 6-20% of newborns with fibromatosis colli also present with other congenital lesions such as hip dysplasia or, less commonly, facial asymmetry.

Pathology
Microscopic histopathological analyses of biopsied FMC tumor tissues typically find benign-appearing, spindle-shaped fibroblasts, decomposing skeletal muscle fibers, and, in some cases, regenerating skeletal muscle fibers in a collagen fiber-containing background. If necessary, these tumors are typically diagnosed by microscopic examination of fine-needle aspiration samples rather than the more invasive approach of tumor biopsy sampling. The asperates show scant to moderately cellular, scattered, oval-shaped to spindle-shaped fibroblasts, naked nuclei (i.e. cell nuclei virtually devoid of other cell elements such as the cytoplasm), wisps of collagen, atrophic, degenerating muscle fibers, regenerating muscle fibers, and intact skeletal muscle cells containing multiple nuclei. There is no evidence of inflammation, hemorrhage, cell necrosis, or rapidly dividing and/or proliferating cells.

Etiology
It has been postulated that the FMC tumor mass itself is a remnant of a hematoma caused by tissue injury occurring during delivery. However, there are no features of hematomas (e.g. hemosiderin released by dying red blood cells) in theses lesions at diagnosis and no evidence of trauma (e.g. overlying skin changes or discolorations) at birth in infants who later present with FMC tumors. It has also been suggested that venous outflow obstruction occurring in the fetus while in the uterus or during delivery leads to degeneration of sternocleidomastoid muscle fibers and subsequent fibrosis of the damaged areas. Finally, it has been suggested that an injury due to poor fetal head positioning in the uterus produces a compartment syndrome-like pressure-induced injury to the sternocleidomastoid muscle that results in muscle cell death followed by tissue fibrosis and the usual pathology of FMC tumors.

Diagnosis
The recommended first step after clinically detecting a sternocleidomastoid mass in a newborn infant is Doppler ultrasonography combined with duplex ultrasonography. This method commonly reveals diagnostic (up to 100% sensitivity rates) findings of diffuse or focal enlargement of sternocleidomastoid muscle that has no cysts or other ultrasonography-detected abnormalities </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 Open fracture and explain in detail? [/INST] An open fracture, also  called a compound fracture, is a type of bone fracture in orthopedics that is frequently caused by high energy trauma. It is a bone fracture associated with a break in the skin continuity which can cause complications such as infection, malunion, and nonunion. Gustilo open fracture classification is the most commonly used method to classify open fractures, to guide treatment and to predict clinical outcomes. Advanced trauma life support is the first line of action in dealing with open fractures and to rule out other life-threatening condition in cases of trauma. Cephalosporins are generally the first line of antibiotics. The antibiotics are continued for 24 hours to minimize the risk of infections. Therapeutic irrigation, wound debridement, early wound closure and bone fixation are the main management of open fractures. All these actions aimed to reduce the risk of infections.

Causes
Open fractures can occur due to direct impacts such as high-energy physical forces (trauma), motor vehicular accidents, firearms, and falls from height.  Indirect mechanisms include twisting (torsional injuries) and falling from a standing position. These mechanisms are usually associated with substantial degloving of the soft-tissues, but can also have a subtler appearance with a small poke hole and accumulation of clotted blood in the tissues. Depending on the nature of the trauma, it can cause different types of fractures:

Common fractures
Result from significant trauma to the bone. This trauma can come from a variety of forces – a direct blow, axial loading, angular forces, torque, or a mixture of these.

Pathological fractures
Result from minor trauma to diseased bone. These preexisting processes include metastatic lesions, bone cysts, advanced osteoporosis, etc.

Fracture-dislocations
Severe injury in which both fracture and dislocation take place simultaneously.

Gunshot wounds
Caused by high-speed projectiles, they cause damage as they go through the tissue, through secondary shock wave and cavitation.

Diagnosis
The initial evaluation for open fractures is to rule out any other life-threatening injuries. Advanced Trauma Life Support (ATLS) is the initial protocol to rule out such injuries. Once the patient is stabilised, orthopedic injuries can be evaluated. Mechanism of injury is important to know the amount energy that is transferred to the patient and the level of contamination. Every limb should be exposed to evaluate any other hidden injuries. Characteristics of the wound should be noted in detail. Neurology and the vascular status of the affected limb are important to rule out any nerve or blood vessels injuries. High index of suspicion of compartment syndrome should be maintained for leg and forearm fractures.There are a number of classification systems attempting to categorise open fractures such as Gustilo open fracture classification, Tscherne classification, and Müller AO Classification of fractures. However, Gustilo open fracture classification is the most commonly used classification system. Gustilo system grades the fracture according to energy of injury, soft tissue damage, level of contamination, and comminution of fractures. The higher the grade, the worse the outcome of the fracture.
However, Gustilo system is not without its limitations. The system has limited interobserver reliability at 50% to 60%. The size of injury on the skin surface does not necessarily reflect the extent of deep underlying soft tissue injury. Therefore, the true grading of Gustilo can only be done in operating theatre.

Management
Acute management
Urgent interventions, including therapeutic irrigation and wound debridement, are often necessary to clean the area of injury and minimize the risk of infection. Other risks of delayed intervention include long-term complications, such as deep infection, vascular compromise and complete limb loss. After wound irrigation, dry or wet gauze should be applied to the wound to prevent bacterial contamination. Taking photographs of the wound can help to reduce the need of multiple examinations by different doctors, which could be painful. Limb should be reduced and placed in a well-padded splint for immobilization of fractures. Pulses should be documented before and after reduction.Wound cultures are positive in 22% of pre-debridement cultures and 60% of post-debridement cultures of infected cases. Therefore, pre-operative cultures no longer recommended. The value of post-operative cultures is unknown. Tetanus prophylaxis is routinely given to enhance immune response against Clostridium tetani. Anti-tetanus immunoglobulin is only indicated for those with highly contaminated wounds with uncertain vaccination history. Single intramuscular dose of 3000 to 5000 units of tetanus immunoglobulin is given to provide immediate immunity.Another important clinical decision during acute management of open fractures involves the effort to avoid preventable amputations, where functional salvage of the limb is clearly desirable. Care must be taken to ensure this decision is not solely based on an injury severity tool score, but rather a decision made following a full discussion of options between doctors and the person, along with their family and care team.

Antibiotics
Administration of antibiotics as soon as possible is necessary to reduce the risk of infection. However, antibiotics may not provide necessary benefits in open finger fractures and low velocity firearms injury. First generation cephalosporin (cefazolin) is recommended as first line antibiotics for the treatment of open fractures. The antibiotic is useful against gram positive cocci and gram negative rods such as Escherichia coli, Proteus mirabilis, and Klebsiella pneumoniae. To extend the coverage of antibiotics against more bacteria in Type III Gustilo fractures, combination of first generation cephalosporin and aminoglycoside (gentamicin or tobramycin) or a third generation cephalosporin is recommended to cover against nosocomial gram negative bacilli such as Pseudomonas aeruginosa. Adding penicillin to cover for gas gangrene caused by anaerobic bacteria Clostridium perfringens is a controversial practice. Studies has shown that such practice may not be necessary as the standard antibiotic regimen is enough to cover for Clostridial infections. Antibiotic impregnated devices such as tobramycin impregnated Poly(methyl methacrylate) (PMMA) beads and antibiotic bone cement are helpful in reducing rates of infection. The use of absorbable carriers with implant coatings at the time of surgical fixation is also an effective means of delivering local antibiotics.There has been no agreement on the optimal duration of antibiotics. Studies has shown that there is no additional benefits of risk of infection when giving antibiotics for one day, when compared to giving antibiotics for three days or five days. However, at present, there is only low to moderate evidence for this and more research is needed. Some authors recommended that antibiotics to be given for three doses for Gustilo Grade I fractures, for one day after wound closure in Grade II fractures, three days in Grade IIIA fractures, and three days after wound closure for Grade IIIB and IIIC.

Wound irrigation
There has been no agreement for the optimal solution for wound irrigation. Studies found out that there is no difference in infection rates by using normal saline or other various forms of water (distilled, boiled, or tap). There is also no difference in infection rates when using normal saline with castile soap compared with normal saline together with bacitracin in irrigating wounds. Studies also have shown that there is no difference in infection rates using low pressure pulse lavage (LPPL) when compared to high pressure pulse lavage (HPPL) in irrigating wounds. Optimal amount of fluid for irrigation also has not been established. It is recommended that the amount of irrigation solution to be determined by the severity of the fracture, with 3 litres for type I fractures, 6 litres for type II fractures, and 9 litres for type III fractures.

Wound debridement
The purpose of wound debridement is to remove all contaminated and non-viable tissues including skin, subcutaneous fat, muscles and bones. Viability of bones and soft tissues are determined by their capacity to bleed. Meanwhile, the viability of muscles is determined by colour, contractility, consistency, and their capacity to bleed. The optimal timing of performing wound debridement and closure is debated and dependent on the severity of the injury, resources and antibiotics available, and individual needs. Debridement time can vary from 6 to 72 hours, and closure time can be immediate (less than 72 hours) or delayed (72 hours to up to 3 months). There is no difference in infection rates for performing surgery within 6 hours of injury when compared to until 72 hours after injury.

Surgical management
Early fracture immobilisation and fixation helps to prevent further soft tissue injury and promotes wound and bone healing. This is especially important in the treatment of intraarticular fractures where early fixation allows early joint motion to prevent joint stiffness. Fracture management depends on the persons overall well-being, fracture pattern and location, and the extent of soft tissue injury. Both reamed and unreamed intramedullary nailing are accepted surgical treatments for open tibial fracture. Both techniques have similar rates of postoperative healing, postoperative infection, implant failure and compartment syndrome. Unreamed intramedullary nailing is advantageous because it has a lower incidence of superficial infection and malunion compared to external fixation.  However, unreamed intramedullary nailing can result in high rates of hardware failure if a persons weight bearing after surgery is not closely controlled.  Compared to external fixation, unreamed intramedullary nailing has similar rates of deep infection, delayed union and nonunion following surgery </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 Vibratory angioedema 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 Familial nasal acilia 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 Idiopathic pneumonia syndrome 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 Inguinal lymphadenopathy and explain in detail? [/INST] Inguinal lymphadenopathy causes swollen lymph nodes in the groin area. It can be a symptom of infective or neoplastic processes.
Infective aetiologies include Tuberculosis, HIV, non-specific or reactive lymphadenopathy to recent lower limb infection or groin infections </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 Hypoparathyroidism and explain in detail? [/INST] Hypoparathyroidism is decreased function of the parathyroid glands with underproduction of parathyroid hormone (PTH). This can lead to low levels of calcium in the blood, often causing cramping and twitching of muscles or tetany (involuntary muscle contraction), and several other symptoms. It is a very rare disease. The condition can be inherited, but it is also encountered after thyroid or parathyroid gland surgery, and it can be caused by immune system-related damage as well as a number of rarer causes. The diagnosis is made with blood tests, and other investigations such as genetic testing depending on the results. The primary treatment of hypoparathyroidism is calcium and vitamin D supplementation. Calcium replacement or vitamin D can ameliorate the symptoms but can increase the risk of kidney stones and chronic kidney disease. Additionally, injectable medications such as recombinant human parathyroid hormone or teriparatide may be given by injection to replace the missing hormone.

Signs and symptoms
The main symptoms of hypoparathyroidism are the result of the low blood calcium level, which interferes with normal muscle contraction and nerve conduction. As a result, people with hypoparathyroidism can experience paresthesia, an unpleasant tingling sensation around the mouth and in the hands and feet, as well as muscle cramps and severe spasms known as "tetany" that affect the hands and feet. Many also report a number of subjective symptoms such as fatigue, headaches, bone pain and insomnia. Crampy abdominal pain may occur. Physical examination of someone with hypocalcemia may show tetany, but it is also possible to provoke tetany of the facial muscles by tapping on the facial nerve (a phenomenon known as Chvosteks sign) or by using the cuff of a sphygmomanometer to temporarily obstruct the blood flow to the arm (a phenomenon known as Trousseaus sign of latent tetany).A number of medical emergencies can arise in people with low calcium levels. These are seizures, severe irregularities in the normal heart beat, as well as spasm of the upper part of the airways or the smaller airways known as the bronchi (both potentially causing respiratory failure).

Related conditions
Causes
Hypoparathyroidism can have the following causes:
Removal of, or trauma to, the parathyroid glands due to thyroid surgery (thyroidectomy), parathyroid surgery (parathyroidectomy) or other surgical interventions in the central part of the neck (such as operations on the larynx and/or pharynx) is a recognized cause. It is the most common cause of hypoparathyroidism. Although surgeons generally make attempts to spare normal parathyroid glands at surgery, inadvertent injury to the glands or their blood supply is still common. When this happens, the parathyroids may cease functioning. This is usually temporary but occasionally long term (permanent).
Kenny-Caffey Syndrome
Autoimmune invasion and destruction is the most common non-surgical cause. It can occur as part of autoimmune polyendocrine syndromes.
Hemochromatosis can lead to iron accumulation and consequent dysfunction of a number of endocrine organs, including the parathyroids.
Absence or dysfunction of the parathyroid glands is one of the components of chromosome 22q11 microdeletion syndrome (other names: DiGeorge syndrome, Schprintzen syndrome, velocardiofacial syndrome).
Magnesium deficiency
A defect in the calcium receptor leads to a rare congenital form of the disease
Idiopathic (of unknown cause)
Occasionally due to other hereditary causes (e.g. Barakat syndrome (HDR syndrome) a genetic development disorder resulting in hypoparathyroidism, sensorineural deafness, and kidney disease)

Mechanism
The parathyroid glands are so named because they are usually located behind the thyroid gland in the neck. They arise during fetal development from structures known as the third and fourth pharyngeal pouch. The glands, usually four in number, contain the parathyroid chief cells that sense the level of calcium in the blood through the calcium-sensing receptor and secrete parathyroid hormone. Magnesium is required for PTH secretion. Under normal circumstances, the parathyroids secrete PTH to maintain a calcium level within normal limits, as calcium is required for adequate muscle and nerve function (including the autonomic nervous system). PTH acts on several organs to increase calcium levels. It increases calcium absorption in the bowel, while in the kidney it prevents calcium excretion and increases phosphate release and in bone it increases calcium through bone resorption.

Diagnosis
Diagnosis is by measurement of calcium, serum albumin (for correction) and PTH in blood </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 White sponge nevus and explain in detail? [/INST] White sponge nevus (WSN) is an autosomal dominant condition of the oral mucosa (the mucous membrane lining of the mouth). It is caused by a mutations in certain genes coding for keratin, which causes a defect in the normal process of keratinization of the mucosa. This results in lesions which are thick, white and velvety on the inside of the cheeks within the mouth. Usually, these lesions are present from birth or develop during childhood </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 Brain herniation and explain in detail? [/INST] Brain herniation is a potentially deadly side effect of very high pressure within the skull that occurs when a part of the brain is squeezed across structures within the skull. The brain can shift across such structures as the falx cerebri, the tentorium cerebelli, and even through the foramen magnum (the hole in the base of the skull through which the spinal cord connects with the brain).  Herniation can be caused by a number of factors that cause a mass effect and increase intracranial pressure (ICP): these include traumatic brain injury, intracranial hemorrhage, or brain tumor.Herniation can also occur in the absence of high ICP when mass lesions such as hematomas occur at the borders of brain compartments. In such cases local pressure is increased at the place where the herniation occurs, but this pressure is not transmitted to the rest of the brain, and therefore does not register as an increase in ICP.Because herniation puts extreme pressure on parts of the brain and thereby cuts off the blood supply to various parts of the brain, it is often fatal. Therefore, extreme measures are taken in hospital settings to prevent the condition by reducing intracranial pressure, or decompressing (draining) a hematoma which is putting local pressure on a part of the brain.

Signs and symptoms
Brain herniation frequently presents with abnormal posturing, a characteristic positioning of the limbs indicative of severe brain damage. These patients have a lowered level of consciousness, with Glasgow Coma Scores of three to five. One or both pupils may be dilated and fail to constrict in response to light. Vomiting can also occur due to compression of the vomiting center in the medulla oblongata. Severe headaches and seizures as a result of increased intracranial pressure are not uncommon. Cardiovascular and pulmonary symptoms may also be present as the brain loses function, but might also be associated with bleeding. They can include: hypertension, respiratory depression, arrhythmia and in severe cases cardiac arrest.

Causes
Causes of brain herniation include:
Brain edema
Hematoma
Stroke
Tumour
Infection

Classification
The tentorium is an extension of the dura mater that separates the cerebellum from the cerebrum. There are two major classes of herniation: supratentorial and infratentorial. Supratentorial refers to herniation of structures normally found above the tentorial notch, and infratentorial refers to structures normally found below it.
Supratentorial herniation1) Uncal (transtentorial)
2) Central
3) Cingulate (subfalcine/transfalcine)
4) Transcalvarial
5) Tectal (posterior)

Infratentorial herniation6) Upward (upward cerebellar or upward transtentorial)
7) Tonsillar (downward cerebellar)

Uncal herniation
In uncal herniation, a common subtype of transtentorial herniation, the innermost part of the temporal lobe, the uncus, can be squeezed so much that it moves towards the tentorium and puts pressure on the brainstem, most notably the midbrain. The tentorium is a structure within the skull formed by the dura mater of the meninges.  Tissue may be stripped from the cerebral cortex in a process called decortication.The uncus can squeeze the oculomotor nerve (a.k.a. CN III), which may affect the parasympathetic input to the eye on the side of the affected nerve, causing the pupil of the affected eye to dilate and fail to constrict in response to light as it should. Pupillary dilation often precedes the somatic motor effects of CN III compression called oculomotor nerve palsy or third nerve palsy. This palsy presents as deviation of the eye to a "down and out" position due to loss of innervation to all ocular motility muscles except for the lateral rectus (innervated by abducens nerve (a.k.a. CN VI) and the superior oblique (innervated by trochlear nerve a.k.a. CN IV). The symptoms occur in this order because the parasympathetic fibers surround the motor fibers of CN III and are hence compressed first.Compression of the ipsilateral posterior cerebral artery will result in ischemia of the ipsilateral primary visual cortex and contralateral visual field deficits in both eyes (contralateral homonymous hemianopsia).
Another important finding is a false localizing sign, the so-called Kernohans notch, which results from compression of the contralateral cerebral crus containing descending corticospinal and some corticobulbar tract fibers. This leads to Ipsilateral hemiparesis in reference to the herniation and contralateral hemiparesis with reference to the cerebral crus.With increasing pressure and progression of the hernia there will be distortion of the brainstem leading to Duret hemorrhages (tearing of small vessels in the parenchyma) in the median and paramedian zones of the mesencephalon and pons. The rupture of these vessels leads to linear or flamed shaped hemorrhages. The disrupted brainstem can lead to decorticate posture, respiratory center depression and death. Other possibilities resulting from brain stem distortion include lethargy, slow heart rate, and pupil dilation.Uncal herniation may advance to central herniation. The sliding uncus syndrome represents uncal herniation without alteration in the level of consciousness and other sequelae mentioned above.

Central herniation
In central herniation, the diencephalon and parts of the temporal lobes of both of the cerebral hemispheres are squeezed through a notch in the tentorium cerebelli.  Transtentorial herniation can occur when the brain moves either up or down across the tentorium, called ascending and descending transtentorial herniation respectively; however descending herniation is much more common.  Downward herniation can stretch branches of the basilar artery (pontine arteries), causing them to tear and bleed, known as a Duret hemorrhage. The result is usually fatal. Other symptoms of this type of herniation include small, fixed pupils with paralysis of upward eye movement giving the characteristic appearance of "sunset eyes". Also found in these patients, often as a terminal complication is the development of diabetes insipidus due to the compression of the pituitary stalk.  Radiographically, downward herniation is characterized by obliteration of the suprasellar cistern from temporal lobe herniation into the tentorial hiatus with associated compression on the cerebral peduncles.  Upwards herniation, on the other hand, can be radiographically characterized by obliteration of the quadrigeminal cistern. Intracranial hypotension syndrome has been known to mimic downwards transtentorial herniation.

Cingulate herniation
In cingulate or subfalcine herniation, the most common type, the innermost part of the frontal lobe is scraped under part of the falx cerebri, the dura mater at the top of the head between the two hemispheres of the brain. Cingulate herniation can be caused when one hemisphere swells and pushes the cingulate gyrus by the falx cerebri. This does not put as much pressure on the brainstem as the other types of herniation, but it may interfere with blood vessels in the frontal lobes that are close to the site of injury (anterior cerebral artery), or it may progress to central herniation.  Interference with the blood supply can cause dangerous increases in ICP that can lead to more dangerous forms of herniation.  Symptoms for cingulate herniation are not well defined.  Usually occurring in addition to uncal herniation, cingulate herniation may present with abnormal posturing and coma.  Cingulate herniation is frequently believed to be a precursor to other types of herniation.

Transcalvarial herniation
In transcalvarial herniation, the brain squeezes through a fracture or a surgical site in the skull. Also called "external herniation", this type of herniation may occur during craniectomy, surgery in which a flap of skull is removed, the protruding brain region preventing the piece of skull from being replaced during the operation.

Upward herniation
Increased pressure in the posterior fossa can cause the cerebellum to move up through the tentorial opening in upward, or cerebellar herniation.  The midbrain is pushed through the tentorial notch upward. This is also known as ascending transtentorial herniation since it occurs across the tentorium cerebelli.

Tonsillar herniation
In tonsillar herniation, also called downward cerebellar herniation, transforaminal herniation, or "coning", the cerebellar tonsils move downward through the foramen magnum possibly causing compression of the lower brainstem and upper cervical spinal cord as they pass through the foramen magnum. Increased pressure on the brainstem can result in dysfunction of the centers in the brain responsible for controlling respiratory and cardiac function. The most common signs are intractable headache, head tilt, and neck stiffness due to tonsillar impaction. The level of consciousness may decrease and also give rise to flaccid paralysis. Blood pressure instability is also evident in these patients.Congenital tonsillar herniation of the cerebellum is also known as a Chiari malformation (CM),  or previously an Arnold-Chiari malformation (ACM).  There are four types of Chiari malformation, and they represent very different disease processes with different symptoms and prognosis.  These conditions can be found in asymptomatic patients as an incidental finding, or can be so severe as to be life-threatening.  This condition is now being diagnosed more frequently by radiologists, as more patients undergo MRI scans of their heads, especially upright MRI, which is more than twice as sensitive for detecting this condition.  Cerebellar tonsillar ectopia (CTE) is a term used by radiologists to describe cerebellar tonsils that are "low lying" but that do not meet the radiographic criteria for definition as a Chiari malformation.  The currently accepted radiographic definition for a Chiari malformation is that cerebellar tonsils lie at least 5mm below the level of the foramen magnum.  Some clinicians have reported that some patients appear to experience symptoms consistent with a Chiari malformation without radiographic evidence of tonsillar herniation </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 Thanatophoric dysplasia and explain in detail? [/INST] Thanatophoric dysplasia is a severe skeletal disorder characterized by a disproportionately small ribcage, extremely short limbs and folds of extra skin on the arms and legs.

Symptoms and signs
Infants with this condition have disproportionately short arms and legs with extra folds of skin. Other signs of the disorder include a narrow chest, small ribs, underdeveloped lungs, and an enlarged head with a large forehead and prominent, wide-spaced eyes.
Thanatophoric dysplasia is a lethal skeletal dysplasia divided into two subtypes. Type I is characterized by extreme rhizomelia, bowed long bones, narrow thorax, a relatively large head, normal trunk length and absent cloverleaf skull. The spine shows platyspondyly, the cranium has a short base, and, frequently, the foramen magnum is decreased in size. The forehead is prominent, and hypertelorism and a saddle nose may be present. Hands and feet are normal, but fingers are short. Type II is characterized by short, straight long bones and cloverleaf skull.
It presents with typical telephone-handle shaped long bones and H-shaped vertebrae.

Causes
It can be associated with missense mutations in fibroblast growth factor receptor-3. It is inherited in an autosomal dominant manner.

Diagnosis
Classification
Infants with type 1 thanatophoric dysplasia also have curved thigh bones, flattened bones of the spine (platyspondyly) and shortened thoracic ribs. Note: Prenatal ultra-sound images of the ribs sometimes appear asymmetrical when in fact they are not </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 Retinal vasculitis 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 Macronychia 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 Neisseria gonorrhoeae and explain in detail? [/INST] Neisseria gonorrhoeae, also known as gonococcus (singular), or gonococci (plural), is a species of Gram-negative diplococci bacteria isolated by Albert Neisser in 1879. It causes the sexually transmitted genitourinary infection gonorrhea as well as other forms of gonococcal disease including disseminated gonococcemia, septic arthritis, and gonococcal ophthalmia neonatorum.
It is oxidase positive and aerobic, and it survives phagocytosis and grows inside neutrophils. Culturing it requires carbon dioxide supplementation and enriched agar (chocolate agar) with various antibiotics (Thayer–Martin). It exhibits antigenic variation through genetic recombination of its pili and surface proteins that interact with the immune system.Sexual transmission is through vaginal, anal, or oral sex. Sexual transmission may be prevented through the use of barrier protection. Perinatal transmission may occur during childbirth, and may be prevented by antibiotic treatment of the mother before birth and the application of antibiotic eye gel on the eyes of the newborn. After an episode of gonococcal infection, infected persons do not develop immunity to future infections. Reinfection is possible due to N. gonorrhoeaes ability to evade the immune system by varying its surface proteins.N. gonorrhoeae can cause infection of the genitals, throat, and eyes. Asymptomatic infection is common in males and females. Untreated infection may spread to the rest of the body (disseminated gonorrhea infection), especially the joints (septic arthritis). Untreated infection in women may cause pelvic inflammatory disease and possible infertility due to the resulting scarring. Diagnosis is through culture, Gram stain, or nucleic acid tests, such as polymerase chain reaction, of a urine sample, urethral swab, or cervical swab. Chlamydia co-testing and testing for other STIs is recommended due to high rates of co-infection.

Microbiology
Neisseria species are fastidious, Gram-negative cocci that require nutrient supplementation to grow in laboratory cultures. Neisseria spp. are facultatively intracellular and typically appear in pairs (diplococci), resembling the shape of coffee beans. Neisseria is non-spore-forming, capable of moving using twitching motility, and an obligate aerobe (requires oxygen to grow). Of the 11 species of Neisseria that colonize humans, only two are pathogens. N. gonorrhoeae is the causative agent of gonorrhea and N. meningitidis is one cause of bacterial meningitis.

Culture and identification
N. gonorrhoeae is usually isolated on Thayer–Martin agar (or VPN) agar in an atmosphere enriched with 3-7% carbon dioxide. Thayer–Martin agar is a chocolate agar plate (heated blood agar) containing nutrients and antimicrobials (vancomycin, colistin, nystatin, and trimethoprim). This agar preparation facilitates the growth of Neisseria species while inhibiting the growth of contaminating bacteria and fungi. Martin Lewis and New York City agar are other types of selective chocolate agar commonly used for Neisseria growth. N. gonorrhoeae is oxidase positive (possessing cytochrome c oxidase) and catalase positive (able to convert hydrogen peroxide to oxygen). When incubated with the carbohydrates lactose, maltose, sucrose, and glucose, N. gonorrhoeae will oxidize only the glucose.

Surface molecules
On its surface, N. gonorrhoeae bears hair-like pili, surface proteins with various functions, and sugars called lipooligosaccharides.  The pili mediate adherence, movement, and DNA exchange. The Opa proteins interact with the immune system, as do the porins. Lipooligosaccharide (LOS) is an endotoxin that provokes an immune response. All are antigenic and all exhibit antigenic variation (see below). The pili exhibit the most variation.  The pili, Opa proteins, porins, and even the LOS have mechanisms to inhibit the immune response, making asymptomatic infection possible.Dynamic polymeric protein filaments called type IV pili allow N. gonorrhoeae to adhere to and move along surfaces. To enter the host the bacteria uses the pili to adhere to and penetrate mucosal surfaces. The pili are a necessary virulence factor for N. gonorrhoeae; without them, the bacterium is unable to cause infection. To move, individual bacteria use their pili like a grappling hook: first, they are extended from the cell surface and attach to a substrate. Subsequent pilus retraction drags the cell forward. The resulting movement is referred to as twitching motility. N. gonorrhoeae is able to pull 100,000 times its own weight, and the pili used to do so are amongst the strongest biological motors known to date, exerting one nanonewton. The PilF and PilT ATPase proteins are responsible for powering the extension and retraction of the type IV pilus, respectively. The adhesive functions of the gonococcal pilus play a role in microcolony aggregation and biofilm formation.
Surface proteins called Opa proteins can be used to bind to receptors on immune cells and prevent an immune response. At least 12 Opa proteins are known and the many permutations of surface proteins make recognizing N. gonorrhoeae and mounting a defense by immune cells more difficult.Lipooligosaccharide (LOS) is a low-weight version of lipopolysaccharide present on the surfaces of most other Gram-negative bacteria. It is a sugar (saccharide) side chain attached to lipid A (thus "lipo-") in the outer membrane coating the cell wall of the bacteria. The root "oligo" refers to the fact that it is a few sugars shorter than the typical lipopolysaccharide. As an endotoxin, LOS provokes inflammation. The shedding of LOS by the bacteria is responsible for local injury in, for example, pelvic inflammatory disease. Although its main function is as an endotoxin, LOS may disguise itself with host sialic acid and block initiation of the complement cascade.

Antigenic variation
N. gonorrhoeae evades the immune system through a process called antigenic variation. This process allows N. gonorrhoeae to recombine its genes and alter the antigenic determinants (sites where antibodies bind), such as the Type IV pili, that adorn its surface. Simply stated, the chemical composition of molecules is changed due to changes at the genetic level. N. gonorrhoeae is able to vary the composition of its pili, and LOS; of these, the pili exhibit the most antigenic variation due to chromosomal rearrangement. The PilS gene is an example of this ability to rearrange as its combination with the PilE gene is estimated to produce over 100 variants of the PilE protein. These changes allow for adjustment to the differences in the local environment at the site of infection, evasion of recognition by targeted antibodies, and contribute to the lack of an effective vaccine.In addition to the ability to rearrange the genes it already has, it is also naturally competent to acquire new DNA (via plasmids), via its type IV pilus, specifically proteins Pil Q and Pil T. These processes allow N. gonorrhoeae to acquire/spread new genes, disguise itself with different surface proteins, and prevent the development of immunological memory – an ability which has led to antibiotic resistance and has also impeded vaccine development.

Phase variation
Phase variation is similar to antigenic variation, but instead of changes at the genetic level altering the composition of molecules, these genetic changes result in the turning on or off of a gene. Phase variation most often arises from a frameshift in the expressed gene. The Opacity, or Opa, proteins of N. gonorrhoeae rely strictly on phase variation. Every time the bacteria replicate, they may switch multiple Opa proteins on or off through slipped-strand mispairing. That is, the bacteria introduce frameshift mutations that bring genes in or out of frame. The result is that different Opa genes are translated every time. Pili are varied by antigenic variation, but also phase variation. Frameshifts occur in both the pilE and pilC genes, effectively turning off the expression of pili in situations when they are not needed, such as after colonization when N. gonorrhoeae survives within cells as opposed to on their surfaces.

Survival of gonococci
After gonococci invade and transcytose the host epithelial cells, they land in the submucosa, where neutrophils promptly consume them. The pili and Opa proteins on the surface may interfere with phagocytosis, but most gonococci end up in neutrophils. The exudates from infected individuals contain many neutrophils with ingested gonococci. Neutrophils release an oxidative burst of reactive oxygen species in their phagosomes to kill the gonococci. However, a significant fraction of the gonococci can resist killing through the action of their catalase which breaks down reactive oxygen species and is able to reproduce within the neutrophil phagosomes.Stohl and Seifert showed that the bacterial RecA protein, which mediates repair of DNA damage, plays an important role in gonococcal survival. Michod et al. have suggested that N. gonorrhoeae may replace DNA damaged in neutrophil phagosomes with DNA from neighboring gonococci. The process in which recipient gonococci integrate DNA from neighboring gonococci into their genome is called transformation.

Genome
The genomes of several strains of N. gonorrhoeae have been sequenced. Most of them are about 2.1 Mb in size and encode 2,100 to 2,600 proteins (although most seem to be in the lower range). For instance, strain NCCP11945 consists of one circular chromosome (2,232,025 bp) encoding 2,662 predicted open reading frames (ORFs) and one plasmid (4,153 bp) encoding 12 predicted ORFs. The estimated coding density over the entire genome is 87%, and the average G+C content is 52.4%, values that are similar to those of strain FA1090. The NCCP11945 genome encodes 54 tRNAs and four copies of 16S-23S-5S rRNA operons.

Horizontal gene transfer
In 2011, researchers at Northwestern University found evidence of a human DNA fragment in a N. gonorrhoeae genome, the first example of horizontal gene transfer from humans to a bacterial pathogen.

Disease
Symptoms of infection with N. gonorrhoeae differ depending on the site of infection and many infections are asymptomatic independent of sex. In symptomatic men, the primary symptom of genitourinary infection is urethritis – burning with urination (dysuria), increased urge to urinate, and a pus-like (purulent) discharge from the penis. The discharge may be foul smelling. If untreated, scarring of the urethra may result in difficulty urinating. Infection may spread from the urethra in the penis to nearby structures, including the testicles (epididymitis/orchitis), or to the prostate (prostatitis). Men who have had a gonorrhea infection have a significantly increased risk of having prostate cancer. In symptomatic women, the primary symptoms of genitourinary infection are increased vaginal discharge, burning with urination (dysuria), increased urge to urinate, pain with intercourse, or menstrual abnormalities. Pelvic inflammatory disease results if N. gonorrhoeae ascends into the pelvic peritoneum (via the cervix, endometrium, and fallopian tubes). The resulting inflammation and scarring of the fallopian tubes can lead to infertility and increased risk of ectopic pregnancy. Pelvic inflammatory disease develops in 10 to 20% of the females infected with N. gonorrhoeae. It is important to note that depending on the route of transmission, N. gonorrhoeae may cause infection of the throat (pharyngitis) or infection of the anus/rectum (proctitis).In perinatal infection, the primary manifestation is infection of the eye (neonatal conjunctivitis or ophthalmia neonatorum) when the newborn is exposed to N. gonorrhoeae in the birth canal.  The eye infection can lead to corneal scarring or perforation, ultimately resulting in blindness. If the newborn is exposed during birth, conjunctivitis occurs within 2–5 days after birth and is severe. Gonococcal ophthalmia neonatorum, once common in newborns, is prevented by the application of erythromycin (antibiotic) gel to the eyes of babies at birth as a public health measure. Silver nitrate is no longer used in the United States.Disseminated gonococcal infections can occur when N. gonorrhoeae enters the bloodstream, often spreading to the joints and causing a rash (dermatitis-arthritis syndrome). Dermatitis-arthritis syndrome results in joint pain (arthritis), tendon inflammation (tenosynovitis), and painless non-pruritic (non-itchy) dermatitis. Disseminated infection and pelvic inflammatory disease in women tend to begin after menses due to reflux during menses, facilitating spread. In rare cases, disseminated infection may cause infection of the meninges of the brain and spinal cord (meningitis) or infection of the heart valves (endocarditis).

Transmission
N. gonorrhoeae is transmitted through vaginal, oral, or anal sex; nonsexual transmission is unlikely in adult infection. It can also be transmitted to the newborn during passage through the birth canal if the mother has untreated genitourinary infection. Given the high rate of asymptomatic infection, all pregnant women should be tested for gonorrhea infection. However, communal baths, towels or fabric, rectal thermometers and caregivers hands have been implicated as means of transmission in the pediatric setting. Kissing has also been implicated as a theoretical means of transmission in the gay male population, based on a newer study.Traditionally, the bacterium was thought to move attached to spermatozoa, but this hypothesis did not explain female to male transmission of the disease. A recent study suggests that rather than "surf" on wiggling sperm, N. gonorrhoeae bacteria use pili to anchor onto proteins in the sperm and move through coital liquid.

Infection
For N. gonorrhoeae, the first step after successful transmission is adherence to the epithelial cells found at the mucosal site that is infected. The bacterium relies on type IV pili that attach and retract, pulling N. gonorrhoeae toward the epithelial membrane where its surface proteins, such as opacity proteins, can interact directly. After adherence, N. gonorrhoeae replicates itself and forms microcolonies. While colonizing, N. gonorrhoeae has the potential to transcytose across the epithelial barrier and work its way in to the bloodstream. During growth and colonization, N. gonorrhoeae stimulates the release of cytokines and chemokines from host immune cells that are pro-inflammatory. These pro-inflammatory molecules result in the recruitment of macrophages and neutrophils. These phagocytic cells typically take in foreign pathogens and destroy them, but N. gonorrhoeae has evolved many mechanisms that allow it to survive within these immune cells and thwart the attempts at elimination.

Prevention
Transmission is reduced by using latex barriers (e.g. condoms or dental dams) during sex and by limiting sexual partners. Condoms and dental dams should be used during oral and anal sex, as well. Spermicides, vaginal foams, and douches are not effective for prevention of transmission.

Treatment
The current treatment recommended by the CDC is an injected single dose of ceftriaxone (a third-generation cephalosporin). Sexual partners (defined by the CDC as sexual contact within the past 60 days) should also be notified, tested, and treated. It is important that if symptoms persist after receiving treatment of N. gonorrhoeae infection, a reevaluation should be pursued.

Antibiotic resistance
Antibiotic resistance in gonorrhea has been noted beginning in the 1940s. Gonorrhea was treated with penicillin, but doses had to be progressively increased to remain effective. By the 1970s, penicillin- and tetracycline-resistant gonorrhea emerged in the Pacific Basin. These resistant strains then spread to Hawaii, California, the rest of the United States, Australia and Europe. Fluoroquinolones were the next line of defense, but soon resistance to this antibiotic emerged, as well. Since 2007, standard treatment has been third-generation cephalosporins, such as ceftriaxone, which are considered to be our "last line of defense".Recently, a high-level ceftriaxone-resistant strain of gonorrhea called H041 was discovered in Japan. Lab tests found it to be resistant to high concentrations of ceftriaxone, as well as most of the other antibiotics tested. Within N. gonorrhoeae, genes exist that confer resistance to every single antibiotic used to cure gonorrhea, but thus far they do not coexist within a single gonococcus. However, because of N. gonorrhoeaes high affinity for horizontal gene transfer, antibiotic-resistant gonorrhea is seen as an emerging public health threat.

Serum resistance
As a Gram negative bacteria, N. gonorrhoeae requires defense mechanisms to protect itself against the complement system (or complement cascade), whose components are found with human serum. There are three different pathways that activate this system however, they all result in the activation of complement protein 3 (C3). A cleaved portion of this protein, C3b, is deposited on pathogenic surfaces and results in opsonization as well as the downstream activation of the membrane attack complex. N. gonorrhoeae has several mechanisms to avoid this action. As a whole, these mechanisms are referred to as serum resistance.

History
Name origin
Neisseria gonorrhoeae is named for Albert Neisser, who isolated it as the causative agent of the disease gonorrhea in 1878. Galen (130 AD) coined the term "gonorrhea" from the Greek gonos which means "seed" and rhoe which means "flow". Thus, gonorrhea means "flow of seed", a description referring to the white penile discharge, assumed to be semen, seen in male infection.

Discovery
In 1878, Albert Neisser isolated and visualized N. gonorrhoeae diplococci in samples of pus from 35 men and women with the classic symptoms of genitourinary infection with gonorrhea – two of whom also had infections of the eyes </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 Cheilitis and explain in detail? [/INST] Cheilitis is a medical condition characterized by inflammation of the lips. The inflammation may include the perioral skin (the skin around the mouth), the vermilion border, or the labial mucosa. The skin and the vermilion border are more commonly involved, as the mucosa is less affected by inflammatory and allergic reactions.Cheilitis is a general term, and there are many recognized types and different causes. According to its onset and course, cheilitis can be either acute or chronic. Most cheilitis is caused by exogenous factors such as dryness (chapping) and acute sun exposure. Allergic tests may identify allergens that cause cheilitis.

Chapped lips
Chapped lips (also known as cheilitis simplex or common cheilitis) is characterized by the cracking, fissuring, and peeling of the skin of the lips, and is one of the most common types of cheilitis. While both lips may be affected, the lower lip is the most common site. There may also be burning or the formation of large, painful cracks when the lips are stretched. Chronic cheilitis simplex can progress to crusting and bleeding.

Counterintuitively, constant licking of the lips causes drying and irritation, and eventually the mucosa splits or cracks. The lips have a greater tendency to dry out in cold, dry weather. Digestive enzymes present in the saliva may also irritate the lips, and the evaporation of the water in saliva saps moisture from them.

Some children have a habit of sucking and chewing on the lower lip, producing a combination of cheilitis and a sharply demarcated perioral erythema.Treatment is usually successful with barrier lubricants, such as lip salve or Vaseline. Medical grade (USP) lanolin accelerates repair of the lips, and is used in some lip repair products.
Sometimes the term "cheilitis simplex" is used interchangeably with cheilitis in general; however, exfoliative cheilitis is also sometimes stated to be the equivalent of chapped lips.

Actinic cheilitis
Also termed "solar cheilosis", actinic cheilitis is the result of chronic over-exposure to ultraviolet radiation in sunlight. It usually occurs on the lower lip, which is dry, scaling, and wrinkled grey-white in appearance. It is especially common in people with light skin types who live in sunny climates (e.g., Australians of European ancestry), and in persons who spend a lot of time outdoors. There is a small risk that actinic cheilitis can develop into squamous cell carcinoma in the long term, but lip cancer is usually noticed early and hence has a good prognosis compared to oral cancer generally.

Angular cheilitis
Angular cheilitis (angular stomatitis, also known as cheilosis) is inflammation of one or both of the corners (angles) of the mouth. It is a fairly common condition, and often affects elderly people.
There are many possible causes, including nutritional deficiencies (iron, B vitamins, folate), contact allergies, infections (Candida albicans, Staphylococcus aureus or β-hemolytic streptococci) and edentulism (often with overclosure of the mouth and concomitant denture-related stomatitis), and others.

Eczematous cheilitis
Also termed "lip dermatitis", eczematous cheilitis is a diverse group of disorders which often have an unknown cause. Chronic eczematous reactions account for the majority of chronic cheilitis cases.It is divided into endogenous (due to an inherent characteristic of the individual), and exogenous (where it is caused by an external agent). The main cause of endogenous eczematous cheilitis is atopic cheilitis (atopic dermatitis), and the main causes of exogenous eczematous cheilitis is irritant contact cheilitis (e.g., caused by a lip-licking habit) and allergic contact cheilitis. The latter is characterized by a dryness, fissuring, edema, and crusting. It affects females more commonly than males, in a ratio of about 9:1.

The most common causes of allergic contact cheilitis is lip cosmetics, including lipsticks and lip balm, followed by toothpastes. A lipstick allergy can be difficult to diagnose in some cases as it is possible that cheilitis can develop without the person even wearing lipstick. Instead, small exposure such as kissing someone who is wearing lipstick is enough to cause the condition.Allergy to Balsam of Peru can manifest as cheilitis.  Allergies to metal, wood, or other components can cause cheilitis reactions in musicians, especially players of woodwind and brass instruments, e.g., the so-called "clarinetists cheilitis", or "flutists cheilitis".  "Pigmented contact cheilitis" is one type of allergic cheilitis in which a brown-black discoloration of the lips develops. Patch testing is used to identify the substance triggering allergic contact cheilitis.

Infectious cheilitis
Infectious cheilitis refers to cheilitis caused by infectious disease. The terms "Candidal cheilitis" and "bacterial cheilitis" are sometimes used, denoting the involvement of Candida organisms and bacterial species respectively. The term "cheilocandidiasis" describes exfoliative (flaking) lesions of the lips and the skin around the lips, and is caused by a superficial candidal infection due to chronic lip licking. Impetigo (caused by Streptococcus pyogenes and/or Staphylococcus aureus), can manifest as an exfoliative cheilitis-like appearance.Herpes labialis (cold sore) is a common cause of infectious cheilitis. A lesion caused by recurrence of a latent herpes simplex infection can occur in the corner of the mouth, and be mistaken for other causes of angular cheilitis. In fact this is herpes labialis, and is sometimes termed "angular herpes simplex".

Granulomatous cheilitis
Orofacial granulomatosis is enlargement of lips due to the formation of non-caseating granulomatous inflammation, which obstruct lymphatic drainage of the orofacial soft tissues, causing lymphedema. Essentially, granulomatous cheilitis refers to the lip swelling that accompanies this condition. "Median cheilitis" may be seen, which is fissuring in the midline of the lips due to the enlargement of the lips. Angular cheilitis may also be associated with orofacial granulomatosis.
A related condition is Melkersson–Rosenthal syndrome, a triad of facial palsy, chronic lip edema, and fissured tongue. "Mieschers cheilitis", and "granulomatous macrocheilitis", are synonyms of granulomatous cheilitis.

Drug-related cheilitis
Common causes of drug-related cheilitis include Etretinate, Indinavir, Protease inhibitors, Vitamin A and Isotretinoin (a retinoid drug). Uncommon causes include Atorvastatin, Busulphan, Clofazimine, Clomipramine, Cyancobalamin, Gold, Methyldopa, Psoralens, Streptomycin, Sulfasalazine and Tetracycline. A condition called "drug-induced ulcer of the lip" is described as being characterized by painful or tender, well-defined ulcerations of the lip without induration. It is the result of oral administration of drugs, and the condition resolves when the drugs are stopped.

Exfoliative cheilitis
Also termed "cheilitis exfoliativa" or "tic de levres", is an uncommon inflammatory condition of the vermilion zone of the lips, which become painful and crusted. There  is continuous production and desquamation (shedding) of thick, brown scales of keratin. The keratin layer of the epidermis of the lips experiences a faster growth and death rate than normal and desquamates. When these scales are removed, a lip of normal appearance is revealed beneath, although  there may be associated erythema and edema. The condition has not yet been attributed to any particular cause. Rarely are infections to blame. In some individuals, there is an association with stress, anxiety, depression or personality disorders. In one report, 87% of individuals had some form of psychiatric disturbance, and 47% had thyroid dysfunction, which in turn can cause psychiatric conditions like depression.Some cases of exfoliative cheilitis are thought to represent factitious damage, termed "factitious cheilitis" or "artifactual cheilitis", and are related to repetitive lip picking or licking habits. This appears as crusting and ulceration caused by repetitive chewing and sucking of the lips. Some consider habitual lip licking or picking to be a form of nervous tic. This habit is sometimes termed perlèche (derived from the French word pourlècher meaning "to lick ones lips"). Factitious cheilitis is significantly more common in young females.Exfoliative cheilitis has also been linked to HIV/AIDS. Management consists mostly of keeping the lips moist and the application of topical corticosteroids ranging from hydrocortisone to clobetasol. There have also been reports of using topical tacrolimus ointment.

Cheilitis glandularis
Chelitis glandularis is a rare inflammatory condition of the minor salivary glands, usually in the lower lip, which appears swollen and everted. There may also be ulceration, crusting, abscesses, and sinus tracts. It is an acquired disorder, but the cause is uncertain </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 Ossification of the posterior longitudinal ligament 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 Hypertrophic scar and explain in detail? [/INST] A hypertrophic scar is a cutaneous condition characterized by deposits of excessive amounts of collagen which gives rise to a raised scar, but not to the degree observed with keloids. Like keloids, they form most often at the sites of pimples, body piercings, cuts and burns. They often contain nerves and blood vessels. They generally develop after thermal or traumatic injury that involves the deep layers of the dermis and express high levels of TGF-β.

Cause
Mechanical tension on a wound has been identified as a leading cause for hypertrophic scar formation.When a normal wound heals, the body produces new collagen fibers at a rate which balances the breakdown of old collagen. Hypertrophic scars are red and thick and may be itchy or painful </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 Familial dysalbuminemic hyperthyroxinemia 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 Neutrophilia 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 Facial eczema and explain in detail? [/INST] Facial eczema is a mycotoxic disease that affects the liver of several animals, mainly sheep and cattle, but can also infect other ungulates. It is caused by ingesting sporidesmins released by the fungus Pithomyces chartarum. Its visible symptoms are characterized by red skin that turns black and crusty before peeling off, as well as inflammation that can cause swelling of the udder, teats, ears and face. The disease is not always visible. Other symptoms include weight loss, weakness and death.

P. chartarum
It grows mostly in New Zealand but also occurs in Australia, France, South Africa, and South America. The fungus grows on dead plants, especially on perennial ryegrass near the ground (25mm height). It most commonly grows between January and May, as it requires warm, humid conditions, as well as moisture at ground level. Areas of spore growth can include urine patches and areas sheltered by hedges. The fungus grows in clusters and is normally invisible to human eye. It produces millions of spores with the toxic substance sporidesmin. Fresh spores are particularly toxic. Contaminated pasture loses its toxicity after 2 weeks.

Pathophysiology
The incubation period is 7-20 days after poison intake. Sporidesmin is hepatotoxic and leads to hepatogenous photosensitization and phylloerythrin accumulation in the bloodstream. It damages the bile ducts and then the liver. The worst case is liver necrosis. This causes – as a secondary effect – photosensitization, this means the inflammation of unpigmented areas and exposed skin (ears, teat, face) and photodynamic dermatitis. Only 5% of affected animals show the respective clinical signs.

Symptoms
Sheep
Infected sheep experience sunburn at face, ears, teats and vulva. It is the primary symptom of the poisoning caused by sporidesmin. The sunburn is caused by the fact that the lower tissue is swollen. The skin gets crusty, dark and then peels, </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 Cyclosporiasis and explain in detail? [/INST] Cyclosporiasis is a disease caused by infection with Cyclospora cayetanensis, a pathogenic protozoan transmitted by feces or feces-contaminated food and water. Outbreaks have been reported due to contaminated fruits and vegetables. It is not spread from person to person, but can be a hazard for travelers as a cause of diarrhea.

Cause
Cyclosporiasis primarily affects humans and other primates. When an oocyst of Cyclospora cayetanensis enters the small intestine, it invades the mucosa, where it incubates for about one week. After incubation, the infected person begins to experience severe watery diarrhea, bloating, fever, stomach cramps, and muscle aches.The parasite particularly affects the jejunum of the small intestine. Of nine patients in Nepal who were diagnosed with cyclosporiasis, all had inflammation of the lamina propria along with an increase of plasma in the lamina propria. Oocysts were also observed in duodenal aspirates.Oocysts are often present in the environment as a result of using contaminated water or human feces as fertilizer.

Diagnosis
Diagnosis can be difficult due to the lack of recognizable oocysts in the feces. PCR-based DNA tests and acid-fast staining can help with identification.

Prevention
There is no vaccine to prevent cyclosporiasis in humans at present, but one is available for reduction of fetal losses in sheep.

Treatment
The infection is often treated with trimethoprim/sulfamethoxazole, also known as Bactrim or co-trimoxazole, because traditional anti-protozoal drugs are not sufficient. To prevent transmission, food should be cooked thoroughly and drinking water from streams should be avoided.

Epidemiology
The first recorded cases of cyclosporiasis in humans were as recent as 1977, 1978, and 1979. They were reported by Ashford, a British parasitologist who discovered three cases while working in Papua New Guinea. Ashford found that the parasite had very late sporulation, from 8–11 days, making the illness difficult to diagnose. When examining feces, the unsporulated oocysts can easily be mistaken for fungal spores, and thus can be easily overlooked.In 2007, Indian researchers published a case report that found an association between Cyclospora infection and Bells palsy. This was the first reported case of Bell’s palsy following chronic Cyclospora infection. In addition to other extra-intestinal reports, cyclosporiasis might be involved in either reversible neuronal damage or other unknown mechanisms to lead to Guillain-Barré syndrome or Bells palsy.
In 2010, a report of Cyclospora transmission via swimming in the Kathmandu Valley was published in the Journal of Institute of Medicine. The researchers found that openly defecated human stool samples around the swimmers living quarters and near the swimming pool were positive for Cyclospora. However, they did not find the parasite in dog stool, bird stool, cattle dung, vegetable samples, or water samples. They concluded that pool water contaminated via environmental pollution might have caused the infection, as the parasite can resist chlorination in water.Cyclosporiasis infections have been well reported in Nepal. In one study, Tirth Raj Ghimire, Purna Nath Mishra, and Jeevan Bahadur Sherchan collected samples of vegetables, sewage, and water from ponds, rivers, wells, and municipal taps in the Kathmandu Valley from 2002 to 2004. They found Cyclospora in radish, cauliflower, cabbage, and mustard leaves, as well as sewage and river water. This first epidemiological study determined the seasonal character of cyclosporiasis outbreaks in Nepal  during the rainy season, from May to September.

Cyclosporiasis in AIDS patients
At the beginning of the AIDS epidemic in the early 1980s, cyclosporiasis was identified as one of the most important opportunistic infections among AIDS patients.In 2005, Ghimire and Mishra reported a case of cyclosporiasis in a patient with low hemoglobin and suggested that this coccidian might be involved in reducing hemoglobin due to lack of immune system </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Progressive outer retinal necrosis and explain in detail? [/INST] Progressive outer retinal necrosis (PORN) syndrome is a form of chorio-retinitis, an infection in the retina, the back of the eye. The disease is most commonly caused by the Varicella zoster virus and is found almost exclusively in patients with HIV/AIDS (acquired immunodeficiency syndrome). Progressive outer retinal necrosis is the second most common opportunistic retinal infection in North America among people with AIDS. The reason this disease process is considered opportunistic is precisely because it only presents in patients with AIDS, a disease that attacks and weakens the immune system, making space for other infections, like Varicella zoster virus (VZV) and Herpes simplex virus (HSV), to attack the body.

The syndrome, PORN, falls under the umbrella of Necrotizing Herpetic Retinopathy, along with Acute Retinal Necrosis (ARN). Although fairly similar processes, the two forms of retinopathy have different presenting symptoms. Acute Retinal Necrosis, or ARN, is damage more central in the retinal portion of the eye with dead or necrotic areas well defined. ARN also presents with inflammation within the eye and is often painful. Progressive outer retinal necrosis (PORN) is a chorioretinitis presenting with multiple lesions in the peripheral retina. Unlike ARN, this disease process has no signs of intraocular inflammation, the hallmark feature, or vascular involvement.

Presentation (Signs and Symptoms)
The presentation of the disease is dependent on the patients AIDS prognosis </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 Prune belly syndrome and explain in detail? [/INST] Prune belly syndrome is a rare, genetic birth defect affecting about 1 in 40,000 births. About 97% of those affected are male. Prune belly syndrome is a congenital disorder of the urinary system, characterized by a triad of symptoms. The syndrome is named for the mass of wrinkled skin that is often (but not always) present on the abdomen of those with the disorder.

Signs and symptoms
Prune-belly triad consists of signs such as: Cryptorchidism, abdominal wall defects and genitourinary defects:
A partial or complete lack of abdominal wall muscles. There may be wrinkly folds of skin covering the abdomen.
Cryptorchidism (undescended testicles) in males
Urinary tract abnormality such as unusually large ureters, distended bladder, accumulation and backflow of urine from the bladder to the ureters and the kidneys (vesicoureteral reflux)Other signs include:

Frequent urinary tract infections due to the inability to properly expel urine.
Ventricular septal defect
Malrotation of the gut
Club foot
Later in life, a common symptom is post-ejaculatory discomfort.  Most likely a bladder spasm, it lasts about two hours.
Musculoskeletal abnormalities include pectus excavatum, scoliosis, and congenital joint dislocations including the hip. Diagnosis of prune belly syndrome necessitates a thorough orthopaedic evaluation because of the high prevalence of associated musculoskeletal abnormalities.
Pulmonary hypoplasia, pneumonia, and atelectasis involving lung lobes

Complications
Prune belly syndrome can result in distention and enlargement of internal organs such as the bladder and intestines. Surgery is often required but will not return the organs to a normal size. Bladder reductions have shown that the bladder will again stretch to its previous size due to lack of muscle. Complications may also arise from enlarged/malformed kidneys, which may result in kidney failure and the childs going on dialysis or requiring a kidney transplant. Many individuals with prune belly syndrome have good physical and mental health, despite all the concerns </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 Eosinophilic gastroenteritis and explain in detail? [/INST] Eosinophilic gastroenteritis (EG or EGE) is a rare and heterogeneous condition characterized by patchy or diffuse eosinophilic infiltration of gastrointestinal (GI) tissue, first described by Kaijser in 1937. Presentation may vary depending on location as well as depth and extent of bowel wall involvement and usually runs a chronic relapsing course. It can be classified into mucosal, muscular and serosal types based on the depth of involvement. Any part of the GI tract can be affected, and isolated biliary tract involvement has also been reported.
The stomach is the organ most commonly affected, followed by the small intestine and the colon.

Signs and symptoms
EG typically presents with a combination of chronic nonspecific GI symptoms which include abdominal pain, diarrhea, occasional nausea and vomiting, weight loss and abdominal distension. Approximately 80% have symptoms for several years; a high degree of clinical suspicion is often required to establish the diagnosis, as the disease is extremely rare. It doesnt come all of a sudden but takes about 3–4 years to develop depending upon the age of the patient. Occasionally, the disease may manifest itself as an acute abdomen or bowel obstruction.
Mucosal EG (25–100%) is the most common variety, which presents with features of malabsorption and protein losing enteropathy. Failure to thrive and anaemia may also be present. Lower gastrointestinal bleeding may imply colonic involvement.
Muscular EG (13–70%) present with obstruction of gastric outlet or small intestine; sometimes as an obstructing caecal mass or intussusception.
Subserosal EG (4.5% to 9% in Japan and 13% in the US) presents with ascites which is usually exudative in nature, abundant peripheral eosinophilia, and has favourable responses to corticosteroids.
Other documented features are cholangitis, pancreatitis, eosinophilic splenitis, acute appendicitis and giant refractory duodenal ulcer.

Pathophysiology
Peripheral blood eosinophilia and elevated serum IgE are usual but not universal. The damage to the gastrointestinal tract wall is caused by eosinophilic infiltration and degranulation.As a part of host defense mechanism, eosinophils are normally present in gastrointestinal mucosa, though the finding in deeper tissue is almost always pathologic. What triggers such dense infiltration in EG is not clear. It is possible that different pathogenetic mechanisms of disease is involved in several subgroups of patients. Food allergy and variable IgE response to food substances has been observed in some patients which implies role of hypersensitive response in pathogenesis. Many patients indeed have history of other atopic conditions like eczema, asthma, etc.Eosinophil recruitment into inflammatory tissue is a complex process, regulated by a number of inflammatory cytokines. In EG cytokines IL-3, IL-5 and granulocyte macrophage colony stimulating factor (GM-CSF) may be behind the recruitment and activation. They have been observed immunohistochemically in diseased intestinal wall.
In addition eotaxin has been shown to have an integral role in regulating the homing of eosinophils into the lamina propria of stomach and small intestine.
In the allergic subtype of disease, it is thought that food allergens cross the intestinal mucosa and trigger an inflammatory response that includes mast cell degranulation and recruitment of eosinophils.

Diagnosis
Talley et al </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 Intestinal neuronal dysplasia 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 Metabolic myopathy and explain in detail? [/INST] Metabolic myopathies are myopathies that result from defects in biochemical metabolism that primarily affect muscle. They are generally genetic defects that interfere with muscles ability to create energy. At the cellular level, metabolic myopathies lack some kind of enzyme that prevent the chemical reactions necessary to create adenosine triphosphate (ATP). This prevents the muscle cells from being able to function properly and disrupts communication between joints and bones. Some people with a metabolic myopathy never develop symptoms due to the bodys ability to produce enough ATP through alternative pathways. In the event more ATP is needed from the affected pathway, the lack of it becomes an issue and symptoms develop. People with a metabolic myopathy often experience symptoms such as progressive muscle weakness, fatigue, pain and cramping after exercise, and considerable breakdown of muscle tissue. The degree of symptoms varies greatly from person to person and is dependent on the severity of enzymatic defect. In extreme cases it can lead to Rhabdomyolysis.

Types
Metabolic myopathies are generally caused by an inherited genetic mutation. This mutation has an autosomal recessive inheritance pattern making it fairly rare to inherit, but it can also be caused by a random genetic mutation. Metabolic myopathies are named after the pathway in which the defective enzyme or a lack of enzymes is present </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 Ornithine translocase deficiency and explain in detail? [/INST] Ornithine translocase deficiency, also called hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome, is a rare autosomal recessive urea cycle disorder affecting the enzyme ornithine translocase, which causes ammonia to accumulate in the blood, a condition called hyperammonemia.
Ammonia, which is formed when proteins are broken down in the body, is toxic if the levels become too high. The nervous system is especially sensitive to the effects of excess ammonia.

Pathophysiology
Mutations in SLC25A15 cause ornithine translocase deficiency. Ornithine translocase deficiency belongs to a class of metabolic disorders referred to as urea cycle disorders. The urea cycle is a sequence of reactions that occurs in liver cells. This cycle processes excess nitrogen, generated when protein is used by the body, to make a compound called urea that is excreted by the kidneys. The SLC25A15 gene provides instructions for making a protein called a mitochondrial ornithine transporter. This protein is needed to move a molecule called ornithine within the mitochondria (the energy-producing centers in cells). Specifically, this protein transports ornithine across the inner membrane of mitochondria to the region called the mitochondrial matrix, where it participates in the urea cycle. Mutations in the SLC25A15 gene result in a mitochondrial ornithine transporter that is unstable or the wrong shape, and which cannot bring ornithine to the mitochondrial matrix. This failure of ornithine transport causes an interruption of the urea cycle and the accumulation of ammonia, resulting in the signs and symptoms of ornithine translocase deficiency.This disorder is inherited in an autosomal recessive pattern, which means the defective gene is located on an autosome, and two copies of the gene - one from each parent - are required to be born with the disorder </s>