<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 Posterior ischemic optic neuropathy and explain in detail? [/INST] Posterior ischemic optic neuropathy (PION) is a medical condition characterized by damage to the retrobulbar portion of the optic nerve due to inadequate blood flow (ischemia) to the optic nerve. Despite the term posterior, this form of damage to the eyes optic nerve due to poor blood flow also includes cases where the cause of inadequate blood flow to the nerve is anterior, as the condition describes a particular mechanism of visual loss as much as the location of damage in the optic nerve. In contrast, anterior ischemic optic neuropathy (AION) is distinguished from PION by the fact that AION occurs spontaneously and on one side in affected individuals with predisposing anatomic or cardiovascular risk factors.

Signs and symptoms
PION is characterized by moderate to severe painless vision loss of abrupt onset. One or both eyes may be affected and color vision is typically impaired.

Ophthalmoscopic exam
Looking inside the persons eyes at the time of onset, ophthalmoscope exam reveals no visible changes to the optic nerve head. Weeks after ischemic insult, nerve atrophy originating from the damaged posterior optic nerve progresses to involve the anterior optic nerve head. Four to eight weeks after onset, atrophy of the optic nerve head is observable upon ophthalmoscope exam.

Pupils
If both eyes are affected by PION, the pupils may look symmetrical. However, if the eyes are asymmetrically affected, i.e. one eyes optic nerve is more damaged than the other, it will produce an important sign called an afferent pupillary defect.Defective light perception in one eye causes an asymmetrical pupillary constriction reflex called the afferent pupillary defect (APD).

Arteritic PION
A-PION most commonly affects Caucasian women, with an average age of 73. At onset vision loss is unilateral, but without treatment it rapidly progresses to involve both eyes. Vision loss is usually severe, ranging from counting fingers to no light perception. Associated symptoms are jaw pain exacerbated by chewing, scalp tenderness, shoulder and hip pain, headache and fatigue.

Perioperative PION
Vision loss is usually apparent upon waking from general anesthesia. Signs observable to a bystander include long surgery duration and facial swelling. Vision loss is usually bilateral and severe, ranging from counting fingers to no light perception.

Cause
PION is a watershed infarction of the optic nerve that may cause either unilateral or, more often, bilateral blindness. PION typically occurs in two categories of people:
People who have undergone non-ocular surgery that is particularly prolonged or is associated with a significant blood loss.
People who have experienced significant bleeding from an accident or ruptured blood vessels.  In these cases, the person may develop anemia (too few oxygen-delivering red blood cells in the bloodstream) and often have low blood pressure as well. This combination can produce circulatory shock, and PION has sometimes been called shock-induced optic neuropathy.The combination of anemia and low blood pressure means that the blood is carrying less oxygen to the tissues. The optic nerve can be at very high risk for damage from insufficient blood supply due to swelling (from lack of oxygen) in a confined bony space resulting in a compartment syndrome. Restricted blood flow can lead to permanent damage to the optic nerve and result in blindness (often in both eyes). For technical reasons this occurs more frequently with spinal surgeries.

Cardiovascular risk factors
Perioperative PION patients have a higher prevalence of cardiovascular risk factors than in the general population. Documented cardiovascular risks in people affected by perioperative PION include high blood pressure, diabetes mellitus, high levels of cholesterol in the blood, tobacco use, abnormal heart rhythms, stroke, and obesity. Men are also noted to be at higher risk, which is in accordance with the trend, as men are at higher risk of cardiovascular disease. These cardiovascular risks all interfere with adequate blood flow, and also may suggest a contributory role of defective vascular autoregulation.

Perioperative PION
As illustrated by the risk factors above, perioperative hypoxia is a multifactorial problem. Amidst these risk factors it may be difficult to pinpoint the optic nerves threshold for cell death, and the exact contribution of each factor.Low blood pressure and anemia are cited as perioperative complications in nearly all reports of PION, which suggests a causal relationship. However, while low blood pressure and anemia are relatively common in the perioperative setting, PION is exceedingly rare. Spine and cardiac bypass surgeries have the highest estimated incidences of PION, 0.028% and 0.018% respectively, and this is still extremely low. This evidence suggests that optic nerve injury in PION patients is caused by more than just anemia and low blood pressure.Evidence suggests that the multifactorial origin of perioperative PION involves the risks discussed above and perhaps other unknown factors. Current review articles of PION propose that vascular autoregulatory dysfunction and anatomic variation are under-investigated subjects that may contribute to patient-specific susceptibility.

Pathogenesis
PION
In both types of PION, decreased blood flow leads to the death of optic nerve cells. Ischemic injury to the optic nerve causes inflammation and swelling. Because the posterior optic nerve passes through the optic canal, a bony tunnel leading to the brain, swelling in this rigid space causes compression of the optic nerve. This compression worsens ischemia and perpetuates the cycle of injury, and swelling, and compression.

A-PION
A-PION is caused by an inflammatory disease called giant cell arteritis (GCA). GCA is an inflammatory disease of blood vessels. It is believed to be an autoimmune disease caused by inappropriate T-cell activity. When T-cells damage arteries supplying the optic nerve, a blood clot forms and stops blood flow. When blood flow stops, oxygen delivery stops and optic nerve fibers die.

Perioperative PION
The exact cause of perioperative PION is unknown. Many risk factors have been identified, all of which contribute to inadequate delivery of oxygen to optic nerve cells. Alone, none of these risk factors is enough to cause PION. However, in susceptible individuals, a combination of these risk factors produces devastating blindness. This evidence suggests that PION is a disease of multifactorial origin.Risks of perioperative PION can be divided into two categories, intraoperative ischemic pressures, and cardiovascular risk factors.

Intraoperative ischemic pressures
Many causes of decreased blood flow during surgery are systemic, i.e. they decrease blood flow throughout the body. Studies have shown that nearly all perioperative PION patients had prolonged periods of low blood pressure during the operation and postoperative anemia. The average perioperative PION patient loses 4 liters of blood during surgery, and the majority receive blood transfusions. Massive blood loss is just one cause of low blood pressure. Medications used for general anesthesia can also lower blood pressure. The average surgery duration in PION cases is 7 to 9 hours, which increases the risk of prolonged low blood pressure.Other intraoperative ischemic pressures are local, i.e. they decrease blood flow to the affected area, the optic nerve. Facial swelling, periorbital swelling, direct orbital compression, facedown position during surgery, and a tilted operating table in feet-above-head position, have all been reported to be associated with perioperative PION. All of these factors are believed to increase tissue pressure and venous pressure around the optic nerve, thereby decreasing local blood flow and oxygen delivery.Surgeries with the highest estimated incidence of PION are surgeries with a higher risk of the aforementioned conditions. In spine surgery, patients are susceptible to significant blood loss, and they are positioned face down for long periods of time, which increases venous pressure, decreases arterial perfusion pressure, and often causes facial swelling (increased tissue pressure). Spine surgery is estimated to have the highest incidence of PION, 0.028%. Long duration of feet-above-head position in prostate surgery has also been suggested to increase risk of PION.

Diagnosis
The diagnosis of PION is often difficult since the optic nerves initially appear normal.  The injury occurs posterior to that portion of the nerve visible during ophthalmoscopic examination.  There may be an abnormal relative pupillary response (APD) if the injury is confined to one optic nerve, but often it is bilateral and the symmetry of pupillary responses is maintained.  Furthermore, MRI scanning may not be helpful.  It is not uncommon for the erroneous diagnoses of malingering or cortical blindness to be made. If possible, an urgent neuro-ophthalmology consult is most likely to lead to the correct diagnosis.There is no confirmatory test for PION. PION is a diagnosis of exclusion. To prevent impending blindness, it is urgent to rule out giant cell arteritis when a patient over 50 presents with sudden vision loss.

Differential diagnosis
In the postoperative setting, without gross eye injury, visual loss requires an assessment of the whole visual system for ischemic damage. The optic nerve is not the only tissue of the visual pathway susceptible to decreased blood flow. Decreased oxygenation of the retina or brain could also impair vision.

Anterior ischemic optic neuropathy
PION is less common than Anterior Ischemic Optic Neuropathy (AION). Blood supply and surrounding anatomy make the anterior and posterior portions of the optic nerve susceptible to different ischemic pressures.The posterior optic nerve receives blood primarily from the pial branches of the ophthalmic artery. The optic canal, a boney tunnel leading to the brain, surrounds the most posterior part of this optic nerve segment.The anterior optic nerve receives blood primarily from the posterior ciliary arteries. The anterior optic nerve, a.k.a. the optic nerve head, is surrounded by the scleral canal, and is vulnerable to crowding of nerve fibers. The portion of the optic nerve head that is visible by looking into the eye with an ophthalmoscope is called the optic disc.

PION versus AION
At the onset of symptoms, ophthalmoscope examination can differentiate AION from PION. If optic nerve head involvement is observed, it is AION. PION does not produce optic atrophy that is observable via ophthalmoscope until four to eight weeks after onset. In addition, AION often shows a characteristic altitudinal defect on a Humphrey Visual Field test.

GCA
The American College of Rheumatology has defined a combination of physical symptoms and inflammatory changes to diagnose giant cell arteritis.

Prevention
Individuals with a history of high blood pressure, diabetes, and smoking are most susceptible to PION as they have a compromised system of blood vessel autoregulation.  Hence, extra efforts may need to be taken for them in the form of careful or staged surgery or the controlling the anemia from blood loss (by administration of blood transfusions), and the careful maintenance of their blood pressure.

Treatment
Once visual loss has occurred, it becomes more problematic, but there are reports of recovered vision if blood transfusions and agents that raise blood pressure are administered within hours.

A-PION
If a diagnosis of GCA is suspected, treatment with steroids should begin immediately. A sample (biopsy) of the temporal artery should be obtained to confirm the diagnosis and guide future management, but should not delay initiation of treatment. Treatment does not recover lost vision, but prevents further progression and second eye involvement. High dose corticosteroids may be tapered down to low doses over approximately one year.

Perioperative
Rapid blood transfusions, to correct anemia and raise blood pressure, may improve PION outcomes. In one report of a related disease, hypotension-induced AION, 3 out of 3 patients who received rapid transfusions reported partial recovery of vision. While rapid transfusions offer some hope, the prognosis for perioperative PION remains poor. Prevention remains the best way to reduce PION.
One retrospective report proposes that incidence of PION could be reduced in high-risk cases by altering surgical management. For example, for patients undergoing spine surgery, measures could be taken to minimize intraoperative hypotension, to accelerate the process of blood replacement, and to aggressively treat facial swelling.

Epidemiology
PION most commonly affects the elderly. The mean patient age was 62 years in one series (range 18 to 90 years).The mean age varies by etiology category; patients with giant cell arteritis (GCA) are older (mean 78 years, range 50 to 82 years), while those with PION in the setting of spine surgery are younger on average.There is a higher than expected prevalence of atherosclerotic risk factors and comorbid vascular disease, especially in patients with nonarteritic (idiopathic) PION, with 87 percent of patients having at least one risk factor for, or one other manifestation of, atherosclerotic vascular disease.
While anterior ischemic optic neuropathy (AION) appears to be more common than PION after cardiac surgery, PION is relatively more common in cases of spine surgery.

References
Further reading
Luneau K, Newman NJ, Biousse V (November 2008). "Ischemic optic neuropathies". The Neurologist. 14 (6): 341–54. doi:10.1097/NRL.0b013e318177394b. PMID 19008740. S2CID 8445417.
Remigio D, Wertenbaker C (2000) </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 Athletic heart syndrome and explain in detail? [/INST] Athletic heart syndrome (AHS) is a non-pathological condition commonly seen in sports medicine in which the human heart is enlarged, and the resting heart rate is lower than normal.
The athletes heart is associated with physiological cardiac remodeling as a consequence of repetitive cardiac loading. Athletes heart is common in athletes who routinely exercise more than an hour a day, and occurs primarily in endurance athletes, though it can occasionally arise in heavy weight trainers. The condition is generally considered benign, but may occasionally hide a serious medical condition, or may even be mistaken for one.

Signs and symptoms
Athletes heart most often does not have any physical symptoms, although an indicator would be a consistently low resting heart rate. Athletes with AHS often do not realize they have the condition unless they undergo specific medical tests, because athletes heart is a normal, physiological adaptation of the body to the stresses of physical conditioning and aerobic exercise. People diagnosed with athletes heart commonly display three signs that would usually indicate a heart condition when seen in a regular person: bradycardia, cardiomegaly, and cardiac hypertrophy. Bradycardia is a slower than normal heartbeat, at around 40–60 beats per minute. Cardiomegaly is the state of an enlarged heart, and cardiac hypertrophy the thickening of the muscular wall of the heart, specifically the left ventricle, which pumps oxygenated blood to the aorta. Especially during an intensive workout, more blood and oxygen are required to the peripheral tissues of the arms and legs in highly trained athletes bodies. A larger heart results in higher cardiac output, which also allows it to beat more slowly, as more blood is pumped out with each beat.Another sign of athletes heart syndrome is an S3 gallop, which can be heard through a stethoscope. This sound can be heard as the diastolic pressure of the irregularly shaped heart creates a disordered blood flow. However, if an S4 gallop is heard, the patient should be given immediate attention. An S4 gallop is a stronger and louder sound created by the heart, if diseased in any way, and is typically a sign of a serious medical condition.

Cause
Athletes heart is a result of dynamic physical activity, such as aerobic training more than 5 hours a week rather than static training such as weightlifting. During intensive prolonged endurance or strength training, the body signals the heart to pump more blood through the body to counteract the oxygen deficit building in the skeletal muscles. Enlargement of the heart is a natural physical adaptation of the body to deal with the high pressures and large amounts of blood that can affect the heart during these periods of time. Over time, the body will increase both the chamber size of the left ventricle, and the muscle mass and wall thickness of the heart.Cardiac output, the amount of blood that leaves the heart in a given time period (i.e. liters per minute), is proportional to both the chamber sizes of the heart and the rate at which the heart beats. With a larger left ventricle, the heart rate can decrease and still maintain a level of cardiac output necessary for the body. Therefore, athletes with AHS commonly have lower resting heart rates than nonathletes.The heart becomes enlarged, or hypertrophic, due to intense cardiovascular workouts, creating an increase in stroke volume, an enlarged left ventricle (and right ventricle), and a decrease in resting heart rate along with irregular rhythms. The wall of the left ventricle increases in size by about 15–20% of its normal capacity. No decrease of the diastolic function of the left ventricle occurs. The athlete may also experience an irregular heartbeat and a resting pulse rate between 40 and 60 beats per minute (bradycardia).The level of physical activity in a person determines what physiological changes the heart makes. The two types of exercise are static (strength-training) and dynamic (endurance-training). Static exercise consists of weight lifting and is mostly anaerobic, meaning the body does not rely on oxygen for performance. It also moderately increases heart rate and stroke volume (oxygen debt). Dynamic exercises include running, swimming, skiing, rowing, and cycling, which rely on oxygen from the body. This type of exercise also increases both heart rate and stroke volume of the heart. Both static and dynamic exercises involve the thickening of the left ventricular wall due to increased cardiac output, which leads to physiologic hypertrophy of the heart. Once athletes stop training, the heart returns to its normal size.

Diagnosis
Athletes heart is usually an incidental finding during a routine screening or during tests for other medical issues. An enlarged heart can be seen at echocardiography or sometimes on a chest X-ray. Similarities at presentation between athletes heart and clinically relevant cardiac problems may prompt electrocardiography (ECG) and exercise cardiac stress tests. The ECG can detect sinus bradycardia, a resting heart rate of fewer than 60 beats per minute. This is often accompanied by sinus arrhythmia. The pulse of a person with athletes heart can sometimes be irregular while at rest, but usually returns to normal after exercise begins.Regarding differential diagnosis, left ventricular hypertrophy is usually indistinguishable from athletes heart and at ECG, but can usually be discounted in the young and fit.It is important to distinguish between athletes heart and hypertrophic cardiomyopathy (HCM), a serious cardiovascular disease characterised by thickening of the hearts walls, which produces a similar ECG pattern at rest. This genetic disorder is found in one of 500 Americans and is a leading cause of sudden cardiac death in young athletes (although only about 8% of all cases of sudden death are actually exercise-related). The following table shows some key distinguishing characteristics of the two conditions.Athletes heart should not be confused with bradycardia that occurs secondary to Relative energy deficiency in sport or Anorexia nervosa, which involve slowing of metabolic rate and sometimes shrinkage of the heart muscle and reduced heart volume.
The medical history of the patient (endurance sports) and physical examination (bradycardia, and maybe a third or fourth heart sound), can give important hints.

ECG – typical findings in resting position are, for example, sinus bradycardia, atrioventricular block (primary and secondary) and incomplete (IRBBB) or complete right bundle branch block (RBBB) – all those findings normalize during exercise.
Echocardiography – differentiation between physiological and pathological increases of the hearts size is possible, especially by estimating the mass of the wall (not over 130 g/m2) and its end diastolic diameter (not much less 60 mm) of the left ventricle.
X-ray examination of the chest may show increased heart size (mimicking other possible causes of enlargement).
Cardiac MRI - In athletes heart, there is balanced atrioventricular remodeling, reduced thickening of the heart after detraining, no late gadolinium enhancement, low to normal T1 signal, and normal extracellular volume.

Screening related conditions
Because several well-known and high-profile cases of athletes experiencing sudden unexpected death due to cardiac arrest, such as Reggie White and Marc-Vivien Foé, a growing movement is making an effort to have both professional and school-based athletes screened for cardiac and other related conditions, usually through a careful medical and health history, a good family history, a comprehensive physical examination including auscultation of heart and lung sounds and recording of vital signs such as heart rate and blood pressure, and increasingly, for better efforts at detection, such as an electrocardiogram.An electrocardiogram (ECG) is a relatively straightforward procedure to administer and interpret, compared to more invasive or sophisticated tests; it can reveal or hint at many circulatory disorders and arrhythmias. Part of the cost of an ECG may be covered by some insurance companies, though routine use of ECGs or other similar procedures such as echocardiography (ECHO) are still not considered routine in these contexts. Widespread routine ECGs for all potential athletes during initial screening and then during the yearly physical assessment could well be too expensive to implement on a wide scale, especially in the face of the potentially very large demand. In some places, a shortage of funds, portable ECG machines, or qualified personnel to administer and interpret them (medical technicians, paramedics, nurses trained in cardiac monitoring, advanced practice nurses or nurse practitioners, physician assistants, and physicians in internal or family medicine or in some area of cardiopulmonary medicine) exist.If sudden cardiac death occurs, it is usually because of pathological hypertrophic enlargement of the heart that went undetected or was incorrectly attributed to the benign "athletic" cases. Among the many alternative causes are episodes of isolated arrhythmias which degenerated into lethal VF and asystole, and various unnoticed, possibly asymptomatic cardiac congenital defects of the vessels, chambers, or valves of the heart. Other causes include carditis, endocarditis, myocarditis, and pericarditis whose symptoms were slight or ignored, or were asymptomatic.The normal treatments for episodes due to the pathological look-alikes are the same mainstays for any other episode of cardiac arrest: cardiopulmonary resuscitation, defibrillation to restore normal sinus rhythm, and if initial defibrillation fails, administration of intravenous epinephrine or amiodarone. The goal is avoidance of infarction, heart failure, and/or lethal arrhythmias (ventricular tachycardia, ventricular fibrillation, asystole, or pulseless electrical activity), so ultimately to restore normal sinus rhythm.

Management
Athletes heart is not dangerous for athletes (though if a nonathlete has symptoms of bradycardia, cardiomegaly, and cardiac hypertrophy, another illness may be present). Athletes heart is not the cause of sudden cardiac death during or shortly after a workout, which mainly occurs due to hypertrophic cardiomyopathy and arrhythmogenic cardiomyopathy (ARVC), two genetic disorders. Although a link between intensive exercise and exercise-induced arythmogenic right ventricular cardiomyopathy exists.No treatment is required for people with athletic heart syndrome; it does not pose any physical threats to the athlete, and despite some theoretical concerns that the ventricular remodeling might conceivably predispose for serious arrhythmias, no evidence has been found of any increased risk of long-term events. Athletes should see a physician and receive a clearance to be sure their symptoms are due to athletes heart and not another heart disease, such as cardiomyopathy. If the athlete is uncomfortable with having athletes heart or if a differential diagnosis is difficult, deconditioning from exercise for a period of three months allows the heart to return to its regular size </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 Exertional rhabdomyolysis and explain in detail? [/INST] Exertional rhabdomyolysis (ER) is the breakdown of muscle from extreme physical exertion. It is one of many types of rhabdomyolysis that can occur, and because of this, the exact prevalence and incidence are unclear.

Cause
ER is more likely to occur when strenuous exercise is performed under high temperatures and humidity. Poor hydration levels before, during, and after strenuous bouts of exercise have also been reported to lead to ER. This condition and its signs and symptoms are not well known amongst the sport and fitness community and because of this it is believed that the incidence is greater but highly underreported.Risks that lead to ER include exercise in hot and humid conditions, improper hydration, inadequate recovery between bouts of exercise, intense physical training, and inadequate fitness levels for beginning high-intensity workouts. Eccentric contraction of muscles can result in ER more often than concentric contraction.  Dehydration is one of the biggest factors that can give almost immediate feedback from the body by producing very dark-colored urine.

Mechanism
Anatomy
Exertional rhabdomyolysis results from damage to the intercellular proteins inside the sarcolemma. Myosin and actin break down in the sarcomeres when ATP is no longer available due to injury to the sarcoplasmic reticulum. Damage to the sarcolemma and sarcoplasmic reticulum from direct trauma or high force production causes a high influx of calcium into the muscle fibers increasing calcium permeability. Calcium ions build up in the mitochondria, impairing cellular respiration. The mitochondria are unable to produce enough ATP to power the cell properly. Reduction in ATP production impairs the cells ability to extract calcium from the muscle cell.  The ion imbalance causes calcium-dependent enzymes to activate which break down muscle proteins even further. A high concentration of calcium activates muscle cells, causing the muscle to contract while inhibiting its ability to relax.  The increase of sustained muscle contraction leads to oxygen and ATP depletion with prolonged exposure to calcium. The muscle cell membrane pump may become damaged allowing free form myoglobin to leak into the bloodstream.

Physiology
Rhabdomyolysis causes the myosin and actin to degenerate into smaller proteins that travel into the circulatory system. The body reacts by increasing intracellular swelling to the injured tissue to send repair cells to the area. This allows creatine kinase and myoglobin to be flushed from the tissue where it travels in the blood until reaching the kidneys. In addition to the proteins released, large quantities of ions such as intracellular potassium, sodium, and chloride find their way into the circulatory system. Intracellular potassium ion has deleterious effects on the hearts ability to generate action potentials leading to cardiac arrhythmias.  Consequently, this can affect peripheral and central perfusion which in turn can affect all major organ systems in the body.When the protein reaches the kidneys it causes a strain on the anatomical structures reducing its effectiveness as a filter for the body. The protein acts as a dam as it forms into tight aggregates when it enters the renal tubules. In addition, the increased intracellular calcium has greater time to bind due to the blockage allowing for renal calculi to form. As a result this causes urine output to decrease allowing for the uric acid to build up inside the organ. The increased acid concentration allows the iron from the aggregate protein to be released into the surrounding renal tissue. Iron then strips away molecular bonds of the surrounding tissue which eventually will lead to kidney failure if the tissue damage is too great.

Mechanical consideration
Muscle degeneration from rhabdomyolysis destroys the myosin and actin filaments in the affected tissue. This initiates the bodys natural reaction to increasing perfusion to the area allowing for an influx of specialized cells to repair the injury. However, the swelling increases the intracellular pressure beyond normal limits. As the pressure builds in the muscle tissue, the surrounding tissue is crushed against the underlying tissue and bone. This is known as compartment syndrome which leads to greater death of the surrounding muscle tissue around the injury.  As the muscle dies this will cause pain to radiate from the affected area into the compartmentalized tissue. A loss of range of motion from swelling will also be seen in the affected limb. Along with muscle strength weakness associated with the muscles involved from loss of filament interaction.

Dehydration is a common risk factor for exertional rhabdomyolysis because it causes a reduction of plasma volume during exertion. This leads to a reduction of blood flow through the vascular system which inhibits blood vessel constriction.

Diagnosis
Exertional rhabdomyolysis, the exercise-induced muscle breakdown that results in muscle pain/soreness, is commonly diagnosed using the urine myoglobin test accompanied by high levels of creatine kinase (CK). Myoglobin is the protein released into the bloodstream when skeletal muscle is broken down. The urine test simply examines whether myoglobin is present or absent. When results are positive the urine normally obtains a dark, brown color followed by serum CK level evaluation to determine the severity of muscle damage. Elevated levels of serum CK greater than 5,000 U/L that are not caused by myocardial infarction, brain injury or disease, generally indicate serious muscle damage confirming the diagnosis of ER.
Urine is often a dark "cola" color as a result of the excretion of muscle cell components.

Prevention
Military data suggest that the risk of exertional rhabdomyolysis can be lowered by engaging in prolonged lower-intensity exercise, as opposed to high-intensity exercise over a shorter time period.  In all athletic programs, three features should be present: (1) emphasizing prolonged lower-intensity exercise, as opposed to repetitive max intensity exercises; (2) adequate rest periods and a high-carbohydrate diet, to replenish glycogen stores; and (3) proper hydration, to enhance renal clearance of myoglobin. Also, exercise in above-average temperature and humidity can increase risk for ER. ER can be avoided by gradually increasing intensity during new exercise regimens, properly hydrating, acclimatization, and avoidance of diuretics during times of strenuous activity.

Treatment
After ER is diagnosed, treatment is applied to 1) avoid renal dysfunction and 2) alleviate symptoms. This should be followed by recommended rehabilitation program, exercise prescription (ExRx). Treatment involves extensive hydration normally done through IV fluid replacement with administration of normal saline until CK levels reduce to a maximum of 1,000 U/L </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 Proteus syndrome and explain in detail? [/INST] Proteus syndrome is a rare disorder with a genetic background that can cause tissue overgrowth involving all three embryonic lineages. Patients with Proteus syndrome tend to have an increased risk of embryonic tumor development. The clinical and radiographic symptoms of Proteus syndrome are highly variable, as are its orthopedic manifestations.Only a few more than 200 cases have been confirmed worldwide, with estimates that about 120 people are currently alive with the condition. As attenuated forms of the disease may exist, there could be many people with Proteus syndrome who remain undiagnosed. Those most readily diagnosed are also the most severely disfigured.
The syndrome is named after the Greek sea-god Proteus, who could change his shape. The condition appears to have been first described in the American medical literature by Samia Temtamy and John Rogers in 1976. American pathologist Michael Cohen described it in 1979.

Signs and symptoms
Proteus syndrome causes an overgrowth of skin, bones, muscles, fatty tissues, and blood and lymphatic vessels. Proteus syndrome is a progressive condition wherein children are usually born without any obvious deformities. Tumors of skin and bone growths appear as they age typically in early childhood. The musculoskeletal manifestations are cardinal for the diagnosis of Proteus syndrome. The severity and locations of these various asymmetrical growths vary greatly but typically the skull, one or more limbs, and soles of the feet will be affected. There is a risk of premature death in affected individuals due to deep vein thrombosis and pulmonary embolism caused by the vessel malformations that are associated with this disorder. Because of carrying excess weight and enlarged limbs, arthritis and muscle pain may also be symptoms. Further risks may occur due to the mass of extra tissue.The disorder itself does not uniformly cause learning impairments: the distribution of intelligence deficits among those with Proteus syndrome appears higher than that of the general population, although this is difficult to determine with statistical significance. In addition, the presence of visible deformity may have a negative effect on the social experiences of the affected individual, causing cognitive and social deficits.Affected individuals are at increased risk for developing certain tumors including unilateral ovarian cystadenomas, testicular tumors, meningiomas, and monomorphic adenomas of the parotid gland.Hemimegalencephaly is often found to be associated.

Orthopaedic features
The musculoskeletal manifestations of Proteus syndrome are frequent and recognizable. Patients tend to demonstrate a unique pattern of skeletal abnormalities. The orthopaedic features are usually bilateral, asymmetrical, progressive and involving all four limbs and spine. Affected patients usually have localized periarticular limb distortions, limb length discrepancy, and spine deformity. Patients with Proteus syndrome can have regular bone configuration and contours despite the bone enlargement. Patients can also exhibit deformation of the skull in the form of dolichocephaly or elongated skull and facial abnormalities. Because of the rarity of the syndrome and the variability of signs, the orthopaedic management should be individualized.

Genetics
In 2011 researchers determined the cause of Proteus syndrome. In 26 of 29 patients who met strict clinical criteria for the disorder, Lindhurst et al. identified an activating mutation in AKT1 kinase in a mosaic state gene.Previous research had suggested the condition linked to PTEN on chromosome 10, while other research pointed to chromosome 16. Prior to the findings regarding AKT1 in 2011, other researchers expressed doubt regarding the involvement of PTEN or GPC3, which codes for glypican 3 and may play a role in regulating cell division and growth regulation.

Diagnosis
Differential diagnosis
Macrodystrophia lipomatosa
Fibrolipomatous hamartoma
Neurofibromatosis type 1
Klippel–Trénaunay syndrome
Parkes Weber syndrome
Sotos syndrome
Hemangiomas

Classification
Many sources classify Proteus syndrome to be a type of nevus syndrome </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Geotrichosis and explain in detail? [/INST] Geotrichosis is a mycosis caused by Geotrichum candidum.: 311

Human colonization and disease
Geotrichum candidum is also a frequent member of the human microbiome, notably associated with skin, sputum and feces where it occurs in 25-30% of specimens. The fungus can cause an infection known as geotrichosis, affecting the oral, bronchial, skin and bronchopulmonary epithelia. The inoculum may arise from endogenous or exogenous sources.In 1847 Bennett described Geotrichum candidum causing a superinfection in the tuberculous cavity. Bennett was able to differentiate infection by Geotrichum candidum from candidiasis, and diagnose the first case of geotrichosis. Other early medical case reports in 1916 and 1928 also described lung infections. Most cases affect the bronchopulmonary tree, although other sites can be involved, such as oral mucosa and vagina. Skin and gut infections are also known. Reported cases of geotrichosis have been characterized with symptoms of chronic or acute bronchitis. Exogenous geotrichosis may arise from contact with contaminated soil, fruits or dairy products.
Pulmonary geotrichosis is the most frequent form of geotrichosis. The symptoms appear to be secondary symptoms of tuberculosis. This includes symptoms such as light, thick, grey sputum, which in some cases may be blood-tinged. Patients often have a cough that produces clear or yellow sputum. Another symptom of pulmonary geotrichosis includes fine to medium rales. Patients may develop fever, rapid pulse and leukocytosis. The condition appears chronic with the presence of a little debilitation and fever. There is no chest pain and occasional wheezing can occur.
Bronchial geotrichosis does not involve the lung instead the disease persists within the bronchial. Geotrichum candidum grows in the lumen of the bronchi. The disease is characterized as an endobronchial infection. Bronchial geotrichosis is similar to the allergic reaction of aspergillosis. Symptoms include prominent chronic cough, gelatinous sputum, lack of fever and medium to coarse rales. Patients with the bronchial condition their pulse and respiration are rarely elevated. Fine mottling may be present in the middle or basilar pulmonary region. Colonization of the bronchi can be associated with Candida albicans and usually occur with patients with chronic obstructive lung disease.
Oral and vaginal geotrichosis is similar to thrush in its appearances and was often confused with this infection. The difference between oral and vaginal geotrichosis can be determined using microscope analysis. The infected area forms a white plaque and patients usually report burning sensation in the affected areas. The vaginal geotrichosis is more common in pregnant women and is often associated with vaginitis.
Gastrointestinal geotrichosis is enterocolitis associated with glutamic therapy. The symptoms usually stop once the glutamic therapy is discontinued. Establishment of the etiology of the fungi is difficult since G. candidum is found within the gut normal flora. The difference between normal gut flora form and the disease causing form is the production of toxins.
Cutaneous geotrichosis has two different types of variants which include superficial and deep infection. The superficial form the infection occurs on skin folds including submammary, inguinal, perianal and interdigital folds. The deep form develops nodules, tumours and ulcers on legs, face and hands. Geotrichosis can cause a cystic lesion appears as soft tissue on the skin.

Diagnosis
Laboratory culture
The diagnoses of geotrichosis cannot be determined without using culture or microscopic measurements. The laboratory diagnosis of geotrichosis involves collected fungi samples areas of infections without contamination. Scraping of the mouth lesions and the ulcers can provide a sample of G. candidum. Samples can also be collected from pus and mucus can be obtained from the feces. Sputum can be searched for the mucoid-like white flakes for further examination. Culturing the cylindrical barrel-shaped or elliptical fungi in considerable numbers in oral lesions is an indicator that a patient may have geotrichosis. Under the microscope the fungi appears yeast-like and septate branching hyphae that can be broken down into chains or individual arthrospores. Arthrospores appear rectangular with flat or rounded ends. Under the microscope the arthroconidia size range from 6-12μm x 3-6μm. Arthroconidia and coarse true hyphae can be observed can be observed under the microscope. Another identification method for G. candidum is selective isolation method. A selection isolation method based on the fungi tolerance to novobiocin and carbon dioxide can determine if G. candidum is the cause of illness.

Diagnostic imaging
X-rays can be used to examine the lung tissue, however it can not be used to positively diagnose geotrichosis. X-rays may show cavitation that is located the walls of the lungs tissues. The lung tissue resemble the early signs of tuberculosis. The results of an x-ray examination of pulmonary geotrichosis presents smooth, dense patchy infiltrations and some cavities. Bronchial geotrichosis shows peribronchial thickening with fine mottling may be present on middle or basilar pulmonary fields </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 Acrogeria 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 Giant axonal neuropathy and explain in detail? [/INST] Giant axonal neuropathy is a rare, autosomal recessive neurological disorder that causes disorganization of neurofilaments. Neurofilaments form a structural framework that helps to define the shape and size of neurons and are essential for normal nerve function </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 Sesamoiditis 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 Baboon 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 Larsen syndrome and explain in detail? [/INST] Larsen syndrome (LS) is a congenital disorder discovered in 1950 by Larsen and associates when they observed dislocation of the large joints and face anomalies in six of their patients.  Patients with Larsen syndrome normally present with a variety of symptoms, including congenital anterior dislocation of the knees, dislocation of the hips and elbows, flattened facial appearance, prominent foreheads, and depressed nasal bridges.  Larsen syndrome can also cause a variety of cardiovascular and orthopedic abnormalities.  This rare disorder is caused by a genetic defect in the gene encoding filamin B, a cytoplasmic protein that is important in regulating the structure and activity of the cytoskeleton.  The gene that influences the emergence of Larsen syndrome is found in chromosome region, 3p21.1-14.1, a region containing human type VII collagen gene.  Larsen syndrome has recently been described as a mesenchyme disorder that affects the connective tissue of an individual.  Autosomal dominant and recessive forms of the disorder have been reported, although most cases are autosomal dominant. Reports have found that in Western societies, Larsen syndrome can be found in one in every 100,000 births, but this is most likely an underestimate because the disorder is frequently unrecognized or misdiagnosed.

Signs and symptoms
Common symptoms
Symptoms are related to defects in connective tissue.

Congenital anterior dislocation of the knees
Dislocation of hips and shoulders
Flattened facial appearance
Prominent forehead
Depressed nasal bridge
Club foot
Cervical kyphosis

Cardiac anomalies
Cardiac defects are similar to those associated with Marfans syndrome, a disorder of the connective tissue.

Elongation of aorta
Bicuspid aortic valve
Subaortic stenosis
Mitral valve prolapse with mitral regurgitation
Atrial septal defect
Patent ductus arteriosus
Tricuspid valve prolapse
Aortic dissection and aneurysm
Aneurysm of ductus arteriosus

Other reported symptoms
These symptoms were found in rare cases of Larsen syndrome.
Cataracts
Cleft palate
Extra bones of wrist
Malocclusion
Microdontia and hypodontia
Complete agenesis of anus
Bifid uterus
Bifid tongue

Causes
Mutations in gene encoding filamin B
Filamins are cytoplasmic proteins that regulate the structure and activity of the cytoskeleton.  These proteins serve as scaffolds on which intracellular signaling and protein trafficking are organized. Filamin B has been found to be expressed in human growth plate chondrocytes, which are especially important in vertebrae segmentation and skeleton morphogenesis.  Genetic analysis of patients with Larsen syndrome has found the syndrome is caused by missense mutations in the gene that codes for filamin B.  These mutations cause an accelerated rate of apoptosis in the epiphyseal growth plates of individuals with the mutation.  The defects can cause short stature and other symptoms associated with Larsen syndrome.

Localization
Genetic analysis has found that a gene linked to Larsen syndrome, LAR1, is strongly linked to chromosome 3p markers.  The locus of this gene is found in a region defined distally by D3S1581 and proximally by D3S1600.  This location can be mapped to chromosome region 3p21.1-14.1.  Human type VII collagen gene is found within this region in chromosome region 3p21.1.  It is reasonable to believe that the joint abnormalities and cardiac anomalies associated with Larsen syndrome are related to the fact that the human type VII collagen gene is found within the same chromosome region as the LAR1 gene.

Genetics
Both autosomal dominant and recessive forms of Larsen syndrome have been reported.  The former is significantly more common than the latter </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 Liebenberg syndrome and explain in detail? [/INST] Liebenberg syndrome is a rare autosomal genetic disease that involves a deletion mutation upstream of the PITX1 gene, which is one thats responsible for the bodys organization, specifically in forming lower limbs. In animal studies, when this deletion was introduced to developing birds, their wing buds were noted to take on limb-like structures.The condition was first described by Dr. F. Liebenberg in 1973 while he followed multiple generations of a South African family, but it has since been noticed in other family lineages across the world.

Symptoms and signs
People who are affected by Liebenberg Syndrome suffer from three main symptoms:
Dysplasia (improper formation) of the bony components of the elbow
Abnormal shape of carpal bones
Brachydactyly, a symptom where the fingers and toes are shorter than normal.

Phenotype
People with Liebenberg Syndrome have normal overall body structure. Their morphological differences are in both of their distal humeri, elbows, hands and wrists. The elbows are enlarged with abnormally large olecranons and radial heads. Patients have relatively fixed elbow positions and are therefore unable to pronate or supinate their forearms. Their wrists are also limited in their active movements and have very prominent ulnar sides of the joints. The fingers adopt toe-like structures. Brachydactyly and camptodactyly occur; fingers are short and abnormally bent. These changes in finger shape result in small club shaped appendages. Motion is reduced in all digital joints of the hand.

Genetics
Liebenberg Syndrome follows an autosomal dominant mode of inheritance, whereby heterozygotes with this mutation express the disease phenotype.
It is caused by a heterozygous mutation to chromosome 5. It involves the inappropriate enhancement of the PITX1 gene due to genetic deletions and chromosome translocations.PITX1 is a homeobox gene which are genes that regulate proper body structure development. This PT1X gene encodes a transcription factor expressed in hind limbs </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 Tolosa–Hunt syndrome and explain in detail? [/INST] Tolosa–Hunt syndrome is a rare disorder characterized by severe and unilateral headaches with orbital pain, along with weakness and paralysis (ophthalmoplegia) of certain eye muscles (extraocular palsies).In 2004, the International Headache Society provided a definition of the diagnostic criteria which included granuloma.

Signs and symptoms
Symptoms are usually limited to one side of the head, and in most cases the individual affected will experience intense, sharp pain and paralysis of muscles around the eye. Symptoms may subside without medical intervention, yet recur without a noticeable pattern.In addition, affected individuals may experience paralysis of various facial nerves and drooping of the upper eyelid (ptosis) </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 thoracic aortic aneurysm and aortic dissection 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 Pagetoid reticulosis 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 Smokers melanosis and explain in detail? [/INST] Smokers melanosis is seen with the naked eye as a brown to black pigmentation of the oral tissue i.e. the gums, cheeks or palate  as well as in larynx. It is most often seen in the lower labial gingiva of tobacco users. Most easily it is found in Caucasians, due to their lack of a genetically caused melanin pigmentation.The brown to black colour is melanin. In skin, melanin prevents harmful UV-light from reaching deeper, sensible parts of the tissue. If UV-light penetrates deep, some of the toxic substances due to the UV-light damage to the cells, are bound to melanin in the epithelial cells and travel with the ageing cells to the skin surface, where they are expelled from the tissue surface. In this way the melanocytes and keratinocytes together protect the tissue, with melanin serving as a toxic defence and cleaning agent.
In the oral mucosa, where the ageing epithelial cells move faster to the surface compared to skin, a similar defence-mechanism seems to be present, cleaning the mucosa from different toxic chemicals penetrating the epithelium. Besides chemicals in tobacco  also antimalaria-drugs cause an oral pigmentation. Smokers melanosis is like the genetic melanin pigmentations, a defence-system in action.
The microscope shows smokers melanosis to be characterized by a melanin hyperpigmentation of the lower part of the oral epithelium, similar to sun-tanned skin. The hyperpigmentation consists of melanin granules which have the shape and colour of "coffea beans". They are produced by the dendritic, octopus-like melanocytes, seen between the epithelial cells situated closest to the epithelium/connective tissue border.In tobacco-users the melanocytes are stimulated to produce melanin granules and to distribute them out to the surrounding epithelial cells for further transport to the mucosal surface, like the mechanism in melanin-pigmented skin.
Small amounts of melanin-like granules together with other electron-dense particles can also be seen within large melanosome complexes in the underlying connective tissue. If the granules derive from the epithelium,  a phenomenon known as melanin incontinence, is not known. In Caucasians these granules are not expected to influence on the clinically observed degree of smokers melanosis.

Causes
Smoking or the use of nicotine-containing drugs is the cause to Smokers melanosis,. Also tar-components (benzopyrenes) are known to stimulate melanocytes to melanin production, and other unknown toxic agents in tobacco may also be the cause.  These chemical agents have a polycyclic, chain-like structure.  Environmental tobacco smoke from parents is causing smokers melanosis in their children    Swedish snuff causes a small elevation of oral melanin pigmented individuals from 3.0% to 4.7%. Nicotine tablets have shown to stimulate to melanin pigmentation of the oral mucosa.

Treatment and prognosis
Lesions usually disappear between 3 months to 3 years for those who stop smoking.  Smokers melanosis is a benign, normal physiological reaction, and does not develop into cancer </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 Atrichia with papular lesions 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 Childhood granulomatous periorificial dermatitis and explain in detail? [/INST] Childhood granulomatous periorificial dermatitis (CGPD), is a rare benign granulomatous skin disease of unknown cause. The disorder was first described in 1970 by Gianotti in a case series of five children. CGPD is more common in boys than girls.

Signs and symptoms
CGPD is characterized by the presence of small, raised, dome-shaped, flesh-colored or yellow-brown papules primarily distributed around the mouth, eyes, and nose. Affected children may also have papules on the ears, eyelids, cheeks, forehead, and nose. CGPD skin lesions rarely affect areas of the skin other than the face.

Cause
The cause of CGPD is unknown.

Diagnosis
The approach to diagnosing CGPD is controversial. Certain dermatologists suggest that ruling out infectious and allergic causes of similar skin eruptions and a skin biopsy demonstrating features consistent with CGPD is adequate for diagnosis. In contrast, other dermatologists advocate for performing a complete history and physical examination and obtaining laboratories and appropriate imaging to rule out cutaneous sarcoidosis. On microscopy, non-tuberculous granulomas with surrounding lymphocytes clustered around hair follicles may be seen; additionally, infiltrates of epithelioid macrophages, lymphocytes, and giant cells may also be seen.Several conditions exhibit skin findings similar to those of CGPD. These conditions include perioral dermatitis, acne vulgaris, granulomatous rosacea, contact dermatitis, folliculitis, atopic dermatitis, cheilitis, medication-induced acneiform eruptions, lupus miliaris disseminatus faciei, benign cephalic histiocytosis, granulosis rubra nasi, xanthomas, zinc deficiency, glucagonoma, cutaneous sarcoidosis, and scabies.

Treatment
Treatment recommendations for CGPD vary and may include observation without treatment, stopping the use of topical corticosteroids, and the use of topical or oral antibiotics as well as isotretinoin. Topical antibiotics such as metronidazole and erythromycin have been used for CGPD. Oral antibiotics of the tetracycline class such as minocycline, doxycycline, and tetracycline have been recommended for CGPD. Trimethoprim/sulfamethoxazole has also been used. The use of oral systemic antibiotics is limited by side effects such as nausea, vomiting, and sensitivity of the skin to sunlight. Tetracycline antibiotics are not recommended for children under the age of 8 since tetracyclines are known to deposit in teeth (thereby staining them) and impair bone growth in children.The use of calcineurin inhibitor creams such as tacrolimus or pimecrolimus on the skin is controversial and results have been mixed. Certain studies found the use of topical calcineurin inhibitors led to resolution of CGPD whereas others saw incomplete resolution or prolonged symptoms </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 Cylindroma 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 Renovascular hypertension and explain in detail? [/INST] Renovascular hypertension is a condition in which high blood pressure is caused by the kidneys hormonal response to narrowing of the arteries supplying the kidneys. When functioning properly this hormonal axis regulates blood pressure. Due to low local blood flow, the kidneys mistakenly increase blood pressure of the entire circulatory system. It is a form of secondary hypertension - a form of hypertension whose cause is identifiable.

Signs and symptoms
Symptoms of renovascular hypertension include the following:
High blood pressure (early age)
Kidney dysfunction
Narrowing of arteries elsewhere in the body
Pulmonary edema

Cause
The cause of renovascular hypertension is consistent with any narrowing/blockage of blood supply to the renal organ (renal artery stenosis). As a consequence of this action the renal organs release hormones that indicate to the body to maintain a higher amount of sodium and water, which in turn causes blood pressure to rise. Factors that may contribute are: diabetes, high cholesterol and advanced age, also of importance is that a unilateral
condition is sufficient to cause renovascular hypertension.

Pathogenesis
The pathogenesis of renovascular hypertension involves the narrowing of the arteries supplying the kidneys which causes a low perfusion pressure that is detected by the juxtaglomerular apparatus (via the macula densa cells, which act as baroreceptors; located on the afferent arteriole wall). This leads to renin secretion that causes the angiotensinogen conversion to angiotensin I. Angiotensin I then proceeds to the lung where it is converted to angiotensin II via angiotensin converting enzyme (ACE).In most people fibromuscular dysplasia or atherosclerosis is the reason for the occlusion of a renal artery which ultimately leads to this condition.

Diagnosis
The diagnosis for renovascular hypertension is done by:
Blood test (for renal function)
Urinary test (tests for microalbuminuria)
Serology (to exclude systemic lupus erythematosus )
Lipid profile
Urinalysis (to exclude presence of red blood cells)

Treatment
In terms of treatment for renovascular hypertension surgical revascularization versus medical therapy for atherosclerosis, it is not clear if one option is better than the other according to a 2014 Cochrane review; balloon angioplasty did show a small improvement in blood pressure .Surgery can include percutaneous surgical revascularization, and also nephrectomy or autotransplantation, and the individual may be given beta-adrenergic blockers. Early therapeutic intervention is important if ischemic nephropathy is to be prevented. Inpatient care is necessary for the management of hypertensive urgencies, quick intervention is required to prevent further damage to the kidneys.

Prognosis
The prognosis of individuals with renovascular hypertension is not easy to determine. Those with atherosclerotic renal artery disease have a high risk of mortality, furthermore, those who also have renal dysfunction have a higher mortality risk.
However, the majority of renovascular diseases can be improved with surgery.

See also
Fibromuscular dysplasia
Hypertensive nephropathy
Kidney failure
Renal artery stenosis

References
Further reading
Advances in Renal Hypertension Research and Treatment: 2012 Edition: ScholarlyPaper. ScholarlyEditions. 2012-12-26. ISBN 9781481636018.
Textor, Stephen C. (2009). "Current Approaches to Renovascular Hypertension". Medical Clinics of North America </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 Mantleoma 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 Boutonneuse fever 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 List of phobias and explain in detail? [/INST] The English suffixes -phobia, -phobic, -phobe (from Greek φόβος phobos, "fear") occur in technical usage in psychiatry to construct words that describe irrational, abnormal, unwarranted, persistent, or disabling fear as a mental disorder (e.g. agoraphobia), in chemistry to describe chemical aversions (e.g. hydrophobic), in biology to describe organisms that dislike certain conditions (e.g. acidophobia), and in medicine to describe hypersensitivity to a stimulus, usually sensory (e.g. photophobia). In common usage, they also form words that describe dislike or hatred of a particular thing or subject (e.g. homophobia). The suffix is antonymic to -phil-.
For more information on the psychiatric side, including how psychiatry groups phobias such as agoraphobia, social phobia, or simple phobia, see phobia. The following lists include words ending in -phobia, and include fears that have acquired names. In some cases, the naming of phobias has become a word game, of notable example being a 1998 humorous article published by BBC News. In some cases, a word ending in -phobia may have an antonym with the suffix -phil-, e.g. Germanophobe/Germanophile.
Many -phobia lists circulate on the Internet, with words collected from indiscriminate sources, often copying each other. Also, a number of psychiatric websites exist that at the first glance cover a huge number of phobias, but in fact use a standard text to fit any phobia and reuse it for all unusual phobias by merely changing the name. Sometimes it leads to bizarre results, such as suggestions to cure "prostitute phobia". Such practice is known as content spamming and is used to attract search engines.
An article published in 1897 in American Journal of Psychology noted "the absurd tendency to give Greek names to objects feared (which, as Arndt says, would give us such terms as klopsophobia – fear of thieves, triakaidekaphobia – fear of the number 13....)".

Psychological conditions
Specialists may prefer to avoid the suffix -phobia and use more descriptive terms such as personality disorders, anxiety disorders, and avoidant personality disorder. Terms should strictly have a Greek prefix although many are irregularly formed with Latin or even English prefixes. Many use inaccurate or imprecise prefixes, such as aerophobia (fear of air) for fear of flying.

A
B
C
D
E
F
G
H
I
K
L
M
N
O
P
R
S
T
V
W
X
Z
Cultural prejudices and discrimination
Ethnic prejudices and discrimination
The suffix -phobia is used to coin terms that denote a particular anti-ethnic or anti-demographic sentiment, such as Americanophobia, Europhobia, Francophobia, Hispanophobia, and Indophobia. Often a synonym with the prefix "anti-" already exists (e.g. Polonophobia vs. anti-Polonism). Anti-religious sentiments are expressed in terms such as Christianophobia and Islamophobia.

Medical conditions
Cultural phenomena
-phobia in the natural sciences
In the natural sciences, words with the suffix -phobia/-phobic generally describe a predisposition for avoidance and/or exclusion. For antonyms, see here

Jocular and fictional phobias
Aibohphobia – a humorous term for the fear of palindromes, which is a palindrome itself. The term is a piece of computer humor entered into the 1981 The Devils DP Dictionary.
Anatidaephobia – the fictional fear that one is being watched by a duck. The word comes from the name of the family Anatidae, and was used in Gary Larsons The Far Side.
Anoraknophobia – a portmanteau of "anorak" and "arachnophobia". It was used in the Wallace and Gromit comic book Anoraknophobia. Also the title of an album by Marillion.
Arachibutyrophobia – fear of peanut butter sticking to the roof of the mouth, from Latin arachis "peanut" and butyrum "butter". The word is used by Charles M. Schulz in a 1982 installment of his Peanuts comic strip, and by Peter ODonnell in his 1985 Modesty Blaise adventure novel Dead Mans Handle.
Charlophobia – the fictional fear of any person named Charlotte or Charlie, mentioned in the comedic book A Duck is Watching Me: Strange and Unusual Phobias (2014), by Bernie Hobbs. The phobia was created to mock name bias, a form of discrimination studied by researchers at the University of California, Berkeley and the University of Chicago.
Hippopotomonstrosesquipedaliophobia – fear of long words, from the root word sesquipedalophobia combined with monstrum and hippopotamus. This was mentioned on the first episode of Brainiac Series Five as a Tickles Teaser.
Keanuphobia – fear of Keanu Reeves, portrayed in the Dean Koontz book, False Memory, where a woman has an irrational fear of Reeves and has to see her psychiatrist, Mark Ahriman, each week, unaware that she only has the fear in the first place because Ahriman implanted it via hypnotic suggestion to amuse himself </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 Intracranial pressure and explain in detail? [/INST] Intracranial pressure (ICP) is the pressure exerted by fluids such as cerebrospinal fluid (CSF) inside the skull and on the brain tissue. ICP is measured in millimeters of mercury (mmHg) and at rest, is normally 7–15 mmHg for a supine adult. The body has various mechanisms by which it keeps the ICP stable, with CSF pressures varying by about 1 mmHg in normal adults through shifts in production and absorption of CSF.
Changes in ICP are attributed to volume changes in one or more of the constituents contained in the cranium. CSF pressure has been shown to be influenced by abrupt changes in intrathoracic pressure during coughing (which is induced by contraction of the diaphragm and abdominal wall muscles, the latter of which also increases intra-abdominal pressure), the valsalva maneuver, and communication with the vasculature (venous and arterial systems).
Intracranial hypertension (IH), also called increased ICP (IICP) or raised intracranial pressure (RICP), is elevation of the pressure in the cranium. ICP is normally 7–15 mm Hg; at 20–25 mm Hg, the upper limit of normal, treatment to reduce ICP may be needed.

Signs and symptoms of raised intracranial pressure
In general, symptoms and signs that suggest a rise in ICP include headache, vomiting without nausea, ocular palsies, altered level of consciousness, back pain, and papilledema. If papilledema is protracted, it may lead to visual disturbances, optic atrophy, and eventually blindness. The headache is classically a morning headache that may wake the person up. The brain is relatively poorly supplied by oxygen as a result of mild hypoventilation during the sleeping hours, and cerebral edema may worsen during the night due to the lying position. The headache is worse on coughing, sneezing, or bending and progressively worsens over time. There may also be personality or behavioral changes.In addition to the above, if mass effect is present with resulting displacement of brain tissue, additional signs may include pupillary dilatation, abducens palsies, and Cushings triad. Cushings triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern. In children, a low heart rate is especially suggestive of high ICP.Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive. Biots respiration, in which breathing is rapid for a period and then absent for a period, occurs because of injury to the cerebral hemispheres or diencephalon. Hyperventilation can occur when the brain stem or tegmentum is damaged.As a rule, patients with normal blood pressure retain normal alertness with ICP of 25–40 mmHg (unless tissue shifts at the same time). Only when ICP exceeds 40–50 mmHg does CPP and cerebral perfusion decrease to a level that results in loss of consciousness. Any further elevations will lead to brain infarction and brain death.In infants and small children, the effects of ICP differ because their cranial sutures have not closed. In infants, the fontanels, or soft spots on the head where the skull bones have not yet fused, bulge when ICP gets too high. ICP correlates with intraocular pressure (IOP) but seems to lack the accuracy necessary for close management of intracranial pressure in the acute posttraumatic period.Papilledema, or the swelling of the optic disc, can be a reliable sign that ICP is elevated. Unlike other conditions that may result in the swelling of the optic disc, it is in the case of papilledema that vision may go largely unaffected.

Causes of abnormal intracranial pressure
Increased ICP
Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased:

Mass effect such as brain tumor, infarction with edema, contusions, subdural or epidural hematoma, or abscesses all tend to deform the adjacent brain.
Generalized brain swelling can occur in ischemic-anoxia states, acute liver failure, hypertensive encephalopathy, hypercarbia (hypercapnia), and Reye hepatocerebral syndrome. These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts.
Increase in venous pressure can be due to venous sinus thrombosis, heart failure, or obstruction of superior mediastinal or jugular veins.
Obstruction to CSF flow and/or absorption can occur in hydrocephalus (blockage in ventricles or subarachnoid space at base of brain, e.g., by Arnold–Chiari malformation), extensive meningeal disease (e.g., infection, carcinoma, granuloma, or hemorrhage), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).
Increased CSF production can occur in meningitis, subarachnoid hemorrhage, or choroid plexus tumor.
Idiopathic or unknown cause (idiopathic intracranial hypertension, a common cause in otherwise well people especially younger women)
CraniosynostosisOne of the most damaging aspects of brain trauma and other conditions, directly correlated with poor outcome, is an elevated intracranial pressure. ICP is very likely to cause severe harm if it rises too high. Very high intracranial pressures are usually fatal if prolonged, but children can tolerate higher pressures for longer periods. An increase in pressure, most commonly due to head injury leading to intracranial hematoma or cerebral edema, can crush brain tissue, shift brain structures, contribute to hydrocephalus, cause brain herniation, and restrict blood supply to the brain. It is a cause of reflex bradycardia.

Low ICP
Spontaneous intracranial hypotension may occur as a result of an occult leak of CSF into another body cavity. More commonly, decreased ICP is the result of lumbar puncture or other medical procedures involving the brain or spinal cord. Various medical imaging technologies exist to assist in identifying the cause of decreased ICP. Often, the syndrome is self-limiting, especially if it is the result of a medical procedure.If persistent intracranial hypotension is the result of a lumbar puncture, a "blood patch" may be applied to seal the site of CSF leakage. Various medical treatments have been proposed; only the intravenous administration of caffeine and theophylline has shown to be particularly useful.

Pathophysiology
Cerebral perfusion pressure (CPP), the pressure of blood flowing to the brain, is normally fairly constant due to autoregulation, but for abnormal mean arterial pressure (MAP) or abnormal ICP the cerebral perfusion pressure is calculated by subtracting the intracranial pressure from the mean arterial pressure: CPP = MAP − ICP . One of the main dangers of increased ICP is that it can cause ischemia by decreasing CPP. Once the ICP approaches the level of the mean systemic pressure, cerebral perfusion falls. The bodys response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels. This results in increased cerebral blood volume, which increases ICP, lowering CPP further and causing a vicious cycle. This results in widespread reduction in cerebral flow and perfusion, eventually leading to ischemia and brain infarction. Increased blood pressure can also make intracranial hemorrhages bleed faster, also increasing ICP.Severely raised ICP, if caused by a unilateral space-occupying lesion (e.g. a hematoma) can result in midline shift, a dangerous sequela in which the brain moves toward one side as the result of massive swelling in a cerebral hemisphere. Midline shift can compress the ventricles and lead to hydrocephalus.

Monro–Kellie hypothesis
The pressure–volume relationship between ICP, volume of CSF, blood, and brain tissue, and cerebral perfusion pressure (CPP) is known as the Monro–Kellie doctrine or hypothesis.The Monro–Kellie hypothesis states that the cranial compartment is inelastic and that the volume inside the cranium is fixed. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another. *This concept only applies to adults, as the presence of fontanelles and open suture lines in infants that have not yet fused means there is potential for a change in size and intracranial volume.
The principal buffers for increased volumes include CSF and, to a lesser extent, blood volume. These buffers respond to increases in volume of the remaining intracranial constituents. For example, an increase in lesion volume (e.g., epidural hematoma) will be compensated by the downward displacement of CSF and venous blood.The Monro–Kellie hypothesis is named after Edinburgh doctors Alexander Monro and George Kellie.

Diagnosis
The most definitive way of measuring the intracranial pressure is with transducers placed within the brain. A catheter can be surgically inserted into one of the brains lateral ventricles and can be used to drain CSF (cerebrospinal fluid) in order to decrease ICPs. This type of drain is known as an external ventricular drain (EVD). This is rarely required outside brain injury and brain surgery settings.In situations when only small amounts of CSF are to be drained to reduce ICPs (e.g. in IIH), drainage of CSF via lumbar puncture can be used as a treatment. Non-invasive measurement of intracranial pressure is being studied.

Treatment
The treatment for ICP depends on the cause. In addition to management of the underlying causes, major considerations in acute treatment of increased ICP relates to the management of stroke and cerebral trauma.For long-term or chronic forms of raised ICP, especially idiopathic intracranial hypertension (IIH), a specific type of diuretic medication (acetazolamide) is used. In cases of confirmed brain neoplasm, dexamethasone is given to decrease ICP. Although the exact mechanism is unknown, current research shows that dexamethasone is capable of decreasing peritumoral water content and local tissue pressure to decrease ICP.

Ventilation
In people who have high ICP due to an acute injury, it is particularly important to ensure adequate airway, breathing, and oxygenation. Inadequate blood oxygen levels (hypoxia) or excessively high carbon dioxide levels (hypercapnia) cause cerebral blood vessels to dilate, increasing the flow of blood to the brain and causing the ICP to rise. Inadequate oxygenation also forces brain cells to produce energy using anaerobic metabolism, which produces lactic acid and lowers pH, also dilating blood vessels and exacerbating the problem. Conversely, blood vessels constrict when carbon dioxide levels are below normal, so hyperventilating a person with a ventilator or bag valve mask can temporarily reduce ICP. Hyperventilation was formerly a part of the standard treatment of traumatic brain injuries, but the induced constriction of blood vessels limits blood flow to the brain at a time when the brain may already be ischemic—hence it is no longer widely used. Furthermore, the brain adjusts to the new level of carbon dioxide after 48 to 72 hours of hyperventilation, which could cause the vessels to rapidly dilate if carbon-dioxide levels were returned to normal too quickly. Hyperventilation is still used if ICP is resistant to other methods of control, or there are signs of brain herniation, because the damage herniation can cause is so severe that it may be worthwhile to constrict blood vessels even if doing so reduces blood flow. ICP can also be lowered by raising the head of the bed, improving venous drainage. A side effect of this is that it could lower pressure of blood to the head, resulting in a reduced and possibly inadequate blood supply to the brain. Venous drainage may also be impeded by external factors such as hard collars to immobilize the neck in trauma patients, and this may also increase the ICP. Sandbags may be used to further limit neck movement.

Medication
In the hospital, the blood pressure can be increased in order to increase CPP, increase perfusion, oxygenate tissues, remove wastes, and thereby lessen swelling. Since hypertension is the bodys way of forcing blood into the brain, medical professionals do not normally interfere with it when it is found in a person with a head injury. When it is necessary to decrease cerebral blood flow, MAP can be lowered using common antihypertensive agents such as calcium channel blockers.If there is an intact blood–brain barrier, osmotherapy (mannitol or hypertonic saline) may be used to decrease ICP.It is unclear whether mannitol or hypertonic saline is superior, or if they improve outcomes.Struggling, restlessness, and seizures can increase metabolic demands and oxygen consumption, as well as increasing blood pressure. Analgesia and sedation are used to reduce agitation and metabolic needs of the brain, but these medications may cause low blood pressure and other side effects. Thus if full sedation alone is ineffective, people may be paralyzed with drugs such as atracurium. Paralysis allows the cerebral veins to drain more easily, but can mask signs of seizures, and the drugs can have other harmful effects. Paralysing drugs are only introduced if patients are fully sedated (this is essentially the same as a general anaesthetic)

Surgery
Craniotomies are holes drilled in the skull with the help of cranial drills to remove intracranial hematomas or relieve pressure from parts of the brain. As raised ICPs may be caused by the presence of a mass, removal of this via craniotomy will decrease raised ICPs.A drastic treatment for increased ICP is decompressive craniectomy, in which a part of the skull is removed and the dura mater is expanded to allow the brain to swell without crushing it or causing 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 Primordial cyst 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 Acne cosmetica 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 Anterior interosseous syndrome and explain in detail? [/INST] Anterior interosseous syndrome  is a medical condition in which damage to the anterior interosseous nerve (AIN), a distal motor and sensory branch of the median nerve, classically with severe weakness of the pincer movement of the thumb and index finger, and can cause transient pain in the wrist (the terminal, sensory branch of the AIN innervates the bones of the carpal tunnel).
Most cases of AIN syndrome are now thought to be due to a transient neuritis, although compression of the AIN in the forearm is a risk, such as pressure on the forearm from immobilization after shoulder surgery.  Trauma to the median nerve or around the proximal median nerve have also been reported as causes of AIN syndrome.
Although there is still controversy among upper extremity surgeons, AIN syndrome is now regarded as a neuritis (inflammation of the nerve) in most cases; this is similar to Parsonage–Turner syndrome.  Although the exact etiology is unknown, there is evidence that it is caused by an immune-mediated response that can follow other illnesses, such as pneumonia or severe viral illness.
Studies are limited, and no randomized controlled trials have been performed regarding the treatment of AIN syndrome.  While the natural history of AIN syndrome is not fully understood, studies following patients who have been treated without surgery show that symptoms can resolve starting as late as one year after onset.  Other retrospective studies have concluded that there is no difference in outcome in surgically versus nonsurgically treated patients.  The role of surgery in AIN syndrome remains controversial.  Indications for considering surgery include a known space-occupying lesion that is compressing the nerve (a mass) or fascial compression, and persistent symptoms beyond 1 year of conservative treatment.

Symptoms and signs
Patients may experience poorly localised, transient pain in the wrist, i.e. where the sensory branch of the AIN is mapped in the brain. The pain is sometimes referred into the cubital fossa and elbow pain has been reported as being a primary complaint.
The characteristic severe impairment of the pincer movement of the thumb and index finger is most striking.

Clinical signs
In a pure lesion of the anterior interosseous nerve there is weakness of the long flexor muscle of the thumb (Flexor pollicis longus), the deep flexor muscles of the index  and middle fingers (Flexor digitorum profundus I & II), and the pronator quadratus muscle.There is no sensory deficit since the anterior interosseous nerve has no cutaneous branch to skin, but there is a large sensory branch to the volar carpus, and transient wrist pain may be experienced.

Causes
Injuries of the forearm with compression of the nerve from swelling is the most common cause: examples include supracondylar fractures, often associated with haemorrhage into the deep musculature; injury secondary to open reduction of a forearm fracture; or dislocation of the elbow.Direct trauma from a penetrating injury such as a stab wound is a possible cause for the syndrome.Fibrous bands or Arcuate ligament~arcuate (curved) ligaments may entrap the median as well as the anterior interosseous nerve, in which case a patient may experience hand numbness as well as wrist pain.Very similar syndromes can be caused by more proximal lesions, such as brachial plexus neuritis.Anterior interosseous nerve entrapment or compression injury remains a difficult clinical diagnosis because it is mainly a motor nerve problem, and the syndrome is often mistaken for index finger and/or thumb tendon injury.

Anatomy
The anterior interosseous nerve is a branch of the median nerve, with a large sensory branch to the wrist bones, which arises just below the elbow. It passes distally, anteriorly along the interosseous membrane and innervates flexor pollicis longus, flexor digitorum profundus to index and middle finger as well as pronator quadratus, and supplies sensory feedback from the wrist bones, i.e </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 Pancoast tumor and explain in detail? [/INST] A Pancoast tumor is a tumor of the apex of the lung. It is a type of lung cancer defined primarily by its location situated at the top end of either the right or left lung. It typically spreads to nearby tissues such as the ribs and vertebrae. Most Pancoast tumors are non-small-cell lung cancers.
The growing tumor can cause compression of a brachiocephalic vein, subclavian artery, phrenic nerve, recurrent laryngeal nerve, vagus nerve, or, characteristically, compression of a sympathetic ganglion (the stellate ganglion), resulting in a range of symptoms known as Horners syndrome.
Pancoast tumors are named for Henry Pancoast, an American radiologist, who described them in 1924 and 1932.

Signs and symptoms
Aside from constitutional symptoms of cancer such as malaise, fever, weight loss and fatigue, Pancoast tumor can include a complete Horners syndrome in severe cases: miosis (constriction of the pupils), anhidrosis (lack of sweating), ptosis (drooping of the eyelid), and pseudoenophthalmos (as a result of the ptosis). In progressive cases, the brachial plexus is also affected, causing pain and weakness in the muscles of the arm and hand with a symptomatology typical of thoracic outlet syndrome. The tumor can also compress the recurrent laryngeal nerve and from this a hoarse voice and "bovine" (non-explosive) cough may occur.In superior vena cava syndrome, obstruction of the superior vena cava by a tumor (mass effect) causes facial swelling cyanosis and dilatation of the veins of the head and neck.A Pancoast tumor is an apical tumor that is typically found in conjunction with a history of smoking tobacco </s>