<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Syncope (medicine) and can you explain it in depth? [/INST] Syncope, commonly known as fainting, or passing out, is a loss of consciousness and muscle strength characterized by a fast onset, short duration, and spontaneous recovery. It is caused by a decrease in blood flow to the brain, typically from low blood pressure. There are sometimes symptoms before the loss of consciousness such as lightheadedness, sweating, pale skin, blurred vision, nausea, vomiting, or feeling warm. Syncope may also be associated with a short episode of muscle twitching. Psychiatric causes can also be determined when a patient experiences fear, anxiety, or panic; particularly before a stressful event usually medical in nature. When consciousness and muscle strength are not completely lost, it is called presyncope. It is recommended that presyncope be treated the same as syncope.Causes range from non-serious to potentially fatal. There are three broad categories of causes: heart or blood vessel related; reflex, also known as neurally mediated; and orthostatic hypotension. Issues with the heart and blood vessels are the cause in about 10% and typically the most serious while neurally mediated is the most common. Heart related causes may include an abnormal heart rhythm, problems with the heart valves or heart muscle and blockages of blood vessels from a pulmonary embolism or aortic dissection among others. Neurally mediated syncope occurs when blood vessels expand and heart rate decreases inappropriately. This may occur from either a triggering event such as exposure to blood, pain, strong feelings or a specific activity such as urination, vomiting, or coughing. Neurally mediated syncope may also occur when an area in the neck known as the carotid sinus is pressed. The third type of syncope is due to a drop in blood pressure when changing position such as when standing up. This is often due to medications that a person is taking but may also be related to dehydration, significant bleeding or infection. There also seems to be a genetic component to syncope.A medical history, physical examination, and electrocardiogram (ECG) are the most effective ways to determine the underlying cause. The ECG is useful to detect an abnormal heart rhythm, poor blood flow to the heart muscle and other electrical issues, such as long QT syndrome and Brugada syndrome. Heart related causes also often have little history of a prodrome. Low blood pressure and a fast heart rate after the event may indicate blood loss or dehydration, while low blood oxygen levels may be seen following the event in those with pulmonary embolism. More specific tests such as implantable loop recorders, tilt table testing or carotid sinus massage may be useful in uncertain cases. Computed tomography (CT) is generally not required unless specific concerns are present. Other causes of similar symptoms that should be considered include seizure, stroke, concussion, low blood oxygen, low blood sugar, drug intoxication and some psychiatric disorders among others. Treatment depends on the underlying cause. Those who are considered at high risk following investigation may be admitted to hospital for further monitoring of the heart.Syncope affects about three to six out of every thousand people each year. It is more common in older people and females. It is the reason for one to three percent of visits to emergency departments and admissions to hospital. Up to half of women over the age of 80 and a third of medical students describe at least one event at some point in their lives. Of those presenting with syncope to an emergency department, about 4% died in the next 30 days. The risk of a poor outcome, however, depends very much on the underlying cause.

Causes
Causes range from non-serious to potentially fatal. There are three broad categories of causes: heart or blood vessel related; reflex, also known as neurally mediated; and orthostatic hypotension. Issues with the heart and blood vessels are the cause in about 10% and typically the most serious while neurally mediated is the most common. There also seems to be a genetic component to syncope. A recent genetic study has identified first risk locus for syncope and collapse. The lead genetic variant, residing at chromosome 2q31.1, is an intergenic variant approximately 250 kb downstream of the ZNF804A gene. The variant effected the expression of ZNF804A, making this gene the strongest driver of the association.

Neurally mediated syncope
Reflex syncope or neurally mediated syncope occurs when blood vessels expand and heart rate decreases inappropriately leading to poor blood flow to the brain. This may occur from either a triggering event such as exposure to blood, pain, strong feelings, or a specific activity such as urination, vomiting, or coughing.

Vasovagal syncope
Vasovagal (situational) syncope is one of the most common types which may occur in response to any of a variety of triggers, such as scary, embarrassing or uneasy situations, during blood drawing, or moments of sudden unusually high stress. There are many different syncope syndromes which all fall under the umbrella of vasovagal syncope related by the same central mechanism. First, the person is usually predisposed to decreased blood pressure by various environmental factors. A lower than expected blood volume, for instance, from taking a low-salt diet in the absence of any salt-retaining tendency. Or heat causing vaso-dilation and worsening the effect of the relatively insufficient blood volume. The next stage is the adrenergic response. If there is underlying fear or anxiety (e.g., social circumstances), or acute fear (e.g., acute threat, needle phobia), the vaso-motor centre demands an increased pumping action by the heart (flight or fight response). This is set in motion via the adrenergic (sympathetic) outflow from the brain, but the heart is unable to meet requirements because of the low blood volume, or decreased return. A feedback response to the medulla is triggered via the afferent vagus nerve. The high (ineffective) sympathetic activity is thereby modulated by vagal (parasympathetic) outflow leading to excessive slowing of heart rate. The abnormality lies in this excessive vagal response causing loss of blood flow to the brain. The tilt-table test typically evokes the attack. Avoiding what brings on the syncope and possibly greater salt intake is often all that is needed.Associated symptoms may be felt in the minutes leading up to a vasovagal episode and are referred to as the prodrome. These consist of light-headedness, confusion, pallor, nausea, salivation, sweating, tachycardia, blurred vision, and sudden urge to defecate among other symptoms.Vasovagal syncope can be considered in two forms:

Isolated episodes of loss of consciousness, unheralded by any warning symptoms for more than a few moments. These tend to occur in the adolescent age group and may be associated with fasting, exercise, abdominal straining, or circumstances promoting vaso-dilation (e.g., heat, alcohol). The subject is invariably upright. The tilt-table test, if performed, is generally negative.
Recurrent syncope with complex associated symptoms. This is neurally mediated syncope (NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance ("spots before the eyes"), sweating, lightheadedness. The subject is usually but not always upright. The tilt-table test, if performed, is generally positive. It is relatively uncommon.Syncope has been linked with psychological triggers. This includes fainting in response to the sight or thought of blood, needles, pain, and other emotionally stressful situations. One theory in evolutionary psychology is that fainting at the sight of blood might have evolved as a form of playing dead which increased survival from attackers and might have slowed blood loss in a primitive environment. "Blood-injury phobia", as this is called, is experienced by about 15% of people. It is often possible to manage these symptoms with specific behavioral techniques.
Another evolutionary psychology view is that some forms of fainting are non-verbal signals that developed in response to increased inter-group aggression during the paleolithic. A non-combatant who has fainted signals that she or he is not a threat. This would explain the association between fainting and stimuli such as bloodletting and injuries seen in blood-injection-injury type phobias such as needle phobia as well as the gender differences.Much of this pathway was discovered in animal experiments by Bezold (Vienna) in the 1860s. In animals, it may represent a defence mechanism when confronted by danger ("playing possum").

Situational syncope
Syncope may be caused by specific behaviors including coughing, urination, defecation, vomiting, swallowing (deglutition), and following exercise.   Manisty et al. note: "Deglutition syncope is characterised by loss of consciousness on swallowing; it has been associated not only with ingestion of solid food, but also with carbonated and ice-cold beverages, and even belching." Fainting can occur in "cough syncope" following severe fits of coughing, such as that associated with pertussis or "whooping cough." Neurally mediated syncope may also occur when an area in the neck known as the carotid sinus is pressed. A normal response to carotid sinus massage is reduction in blood pressure and slowing of the heart rate. Especially in people with hypersensitive carotid sinus syndrome this response can cause syncope or presyncope.

Cardiac
Heart-related causes may include an abnormal heart rhythm, problems with the heart valves or heart muscle, or blockages of blood vessels from a pulmonary embolism or aortic dissection, among others.

Cardiac arrhythmias
The most common cause of cardiac syncope is cardiac arrhythmia (abnormal heart rhythm) wherein the heart beats too slowly, too rapidly, or too irregularly to pump enough blood to the brain. Some arrhythmias can be life-threatening.Two major groups of arrhythmias are bradycardia and tachycardia. Bradycardia can be caused by heart blocks. Tachycardias include SVT (supraventricular tachycardia) and VT (ventricular tachycardia). SVT does not cause syncope except in Wolff-Parkinson-White syndrome. Ventricular tachycardia originate in the ventricles. VT causes syncope and can result in sudden death. Ventricular tachycardia, which describes a heart rate of over 100 beats per minute with at least three irregular heartbeats as a sequence of consecutive premature beats, can degenerate into ventricular fibrillation, which is rapidly fatal without cardiopulmonary resuscitation (CPR) and defibrillation.Long QT syndrome can cause syncope when it sets off ventricular tachycardia or torsades de pointes. The degree of QT prolongation determines the risk of syncope. Brugada syndrome also commonly presents with syncope secondary to arrhythmia.Typically, tachycardic-generated syncope is caused by a cessation of beats following a tachycardic episode. This condition, called tachycardia-bradycardia syndrome, is usually caused by sinoatrial node dysfunction or block or atrioventricular block.

Obstructive cardiac lesion
Blockages in major vessels or within the heart can also impede blood flow to the brain. Aortic stenosis and mitral stenosis are the most common examples. Major valves of the heart become stiffened and reduce the efficiency of the hearts pumping action. This may not cause symptoms at rest but with exertion, the heart is unable to keep up with increased demands leading to syncope. Aortic stenosis presents with repeated episodes of syncope. Rarely, cardiac tumors such as atrial myxomas can also lead to syncope.

Structural cardiopulmonary disease
Diseases involving the shape and strength of the heart can be a cause of reduced blood flow to the brain, which increases risk for syncope. The most common cause in this category is fainting associated with an acute myocardial infarction or ischemic event. The faint in this case is primarily caused by an abnormal nervous system reaction similar to the reflex faints. Women are significantly more likely to experience syncope as a presenting symptom of a myocardial infarction. In general, faints caused by structural disease of the heart or blood vessels are particularly important to recognize, as they are warning of potentially life-threatening conditions.Among other conditions prone to trigger syncope (by either hemodynamic compromise or by a neural reflex mechanism, or both), some of the most important are hypertrophic cardiomyopathy, acute aortic dissection, pericardial tamponade, pulmonary embolism, aortic stenosis, and pulmonary hypertension.

Other cardiac causes
Sick sinus syndrome, a sinus node dysfunction, causing alternating bradycardia and tachycardia. Often there is a long pause (asystole) between heartbeats.Adams-Stokes syndrome is a cardiac syncope that occurs with seizures caused by complete or incomplete heart block. Symptoms include deep and fast respiration, weak and slow pulse, and respiratory pauses that may last for 60 seconds.
Subclavian steal syndrome arises from retrograde (reversed) flow of blood in the vertebral artery or the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian artery. Symptoms such as syncope, lightheadedness, and paresthesias occur while exercising the arm on the affected side (most commonly the left).
Aortic dissection (a tear in the aorta) and cardiomyopathy can also result in syncope.Various medications, such as beta blockers, may cause bradycardia induced syncope.A pulmonary embolism can cause obstructed blood vessels and is the cause of syncope in less than 1% of people who present to the emergency department.

Blood pressure
Orthostatic (postural) hypotensive syncope is caused primarily by an excessive drop in blood pressure when standing up from a previous position of lying or sitting down. When the head is elevated above the feet the pull of gravity causes blood pressure in the head to drop. This is sensed by stretch receptors in the walls of vessels in the carotid sinus and aortic arch. These receptors then trigger a sympathetic nervous response to compensate and redistribute blood back into the brain. The sympathetic response causes peripheral vasoconstriction and increased heart rate. These together act to raise blood pressure back to baseline. Apparently healthy individuals may experience minor symptoms ("lightheadedness", "greying-out") as they stand up if blood pressure is slow to respond to the stress of upright posture. If the blood pressure is not adequately maintained during standing, faints may develop. However, the resulting "transient orthostatic hypotension" does not necessarily signal any serious underlying disease. It is as common or perhaps even more common than vasovagal syncope.
This may be due to medications, dehydration, significant bleeding or infection. The most susceptible individuals are elderly frail individuals, or persons who are dehydrated from hot environments or inadequate fluid intake. For example, medical students would be at risk for orthostatic hypotensive syncope while observing long surgeries in the operating room. There is also evidence that exercise training can help reduce orthostatic intolerance. More serious orthostatic hypotension is often the result of certain commonly prescribed medications such as diuretics, β-adrenergic blockers, other anti-hypertensives (including vasodilators), and nitroglycerin. In a small percentage of cases, the cause of orthostatic hypotensive faints is structural damage to the autonomic nervous system due to systemic diseases (e.g., amyloidosis or diabetes) or in neurological diseases (e.g., Parkinsons disease).Hyperadrenergic orthostatic hypotension refers to an orthostatic drop in blood pressure despite high levels of sympathetic adrenergic response. This occurs when a person with normal physiology is unable to compensate for >20% loss in intravascular volume. This may be due to blood loss, dehydration or third-spacing. On standing the person will experience reflex tachycardia (at least 20% increased over supine) and a drop in blood pressure.Hypoadrenergic orthostatic hypotension occurs when the person is unable to sustain a normal sympathetic response to blood pressure changes during movement despite adequate intravascular volume. There is little to no compensatory increase in heart rate or blood pressure when standing for up to 10 minutes. This is often due to an underlying disorder or medication use and is accompanied by other hypoadrenergic signs.

Central nervous system ischemia
The central ischemic response is triggered by an inadequate supply of oxygenated blood in the brain. Common examples include strokes and transient ischemic attacks. While these conditions often impair consciousness they rarely meet the medical definition of syncope. Vertebrobasilar transient ischemic attacks may produce true syncope as a symptom.The respiratory system may compensate for dropping oxygen levels through hyperventilation, though a sudden ischemic episode may also proceed faster than the respiratory system can respond. These processes cause the typical symptoms of fainting: pale skin, rapid breathing, nausea, and weakness of the limbs, particularly of the legs. If the ischemia is intense or prolonged, limb weakness progresses to collapse. The weakness of the legs causes most people to sit or lie down if there is time to do so. This may avert a complete collapse, but whether the patient sits down or falls down, the result of an ischaemic episode is a posture in which less blood pressure is required to achieve adequate blood flow. An individual with very little skin pigmentation may appear to have all color drained from his or her face at the onset of an episode. This effect combined with the following collapse can make a strong and dramatic impression on bystanders.

Vertebro-basilar arterial disease
Arterial disease in the upper spinal cord, or lower brain that causes syncope if there is a reduction in blood supply. This may occur with extending the neck or with use of medications to lower blood pressure.

Other causes
There are other conditions which may cause or resemble syncope.
Seizures and syncope can be difficult to differentiate. Both often present as sudden loss of consciousness and convulsive movements may be present or absent in either. Movements in syncope are typically brief and more irregular than seizures. Akinetic seizures can present with sudden loss of postural tone without associated tonic-clonic movements. Absence of a long post-ictal state is indicative of syncope rather than an akinetic seizure.
Subarachnoid hemorrhage may result in syncope. Often this is in combination with sudden, severe headache. It may occur as a result of a ruptured aneurysm or head trauma.Heat syncope occurs when heat exposure causes decreased blood volume and peripheral vasodilatation. Position changes, especially during vigorous exercise in the heat, may lead to decreased blood flow to the brain. Closely related to other causes of syncope related to hypotension (low blood pressure) such as orthostatic syncope. Lactose intolerance can cause "a release of histamine, resulting in an extreme dilatation of the bloodvessels, resulting in a drop of blood pressure so that not enough blood reaches the brains, leading to dizziness, fainting, syncope, itching, hives, tingling or swelling of the lips, tongue, or throat; chest tightness, shortness of breath, or difficulty breathing, wheezing." (More in the article on
 Lactose intolerance).
Some psychological conditions (anxiety disorder, somatic symptom disorder, conversion disorder) may cause symptoms resembling syncope. A number of psychological interventions are available.Low blood sugar can be a rare cause of syncope.Narcolepsy may present with sudden loss of consciousness similar to syncope.

Diagnostic approach
A medical history, physical examination, and electrocardiogram (ECG) are the most effective ways to determine the underlying cause of syncope. Guidelines from the American College of Emergency Physicians and American Heart Association recommend a syncope workup include a thorough medical history, physical exam with orthostatic vitals, and a 12-lead ECG. The ECG is useful to detect an abnormal heart rhythm, poor blood flow to the heart muscle and other electrical issues, such as long QT syndrome and Brugada syndrome. Heart related causes also often have little history of a prodrome. Low blood pressure and a fast heart rate after the event may indicate blood loss or dehydration, while low blood oxygen levels may be seen following the event in those with pulmonary embolism. Routine broad panel laboratory testing detects abnormalities in <2–3% of results and is therefore not recommended.Based on this initial workup many physicians will tailor testing and determine whether a person qualifies as high-risk, intermediate risk or low-risk based on risk stratification tools. More specific tests such as implantable loop recorders, tilt table testing or carotid sinus massage may be useful in uncertain cases. Computed tomography (CT) is generally not required unless specific concerns are present. Other causes of similar symptoms that should be considered include seizure, stroke, concussion, low blood oxygen, low blood sugar, drug intoxication and some psychiatric disorders among others. Treatment depends on the underlying cause. Those who are considered at high risk following investigation may be admitted to hospital for further monitoring of the heart.A hemoglobin count may indicate anemia or blood loss. However, this has been useful in only about 5% of people evaluated for fainting. The tilt table test is performed to elicit orthostatic syncope secondary to autonomic dysfunction (neurogenic). A number of factors make a heart related cause more likely including age over 35, prior atrial fibrillation, and turning blue during the event.

Electrocardiogram
Electrocardiogram (ECG) finds that should be looked for include signs of heart ischemia, arrhythmias, atrioventricular blocks, a long QT, a short PR, Brugada syndrome, signs of hypertrophic obstructive cardiomyopathy (HOCM), and signs of arrhythmogenic right ventricular dysplasia (ARVD/C). Signs of HCM include large voltages in the precordial leads, repolarization abnormalities, and a wide QRS with a slurred upstroke. Signs of ARVD/C include T wave inversion and epsilon waves in lead V1 to V3.It is estimated that from 20 to 50% of people have an abnormal ECG. However, while an ECG may identify conditions such as atrial fibrillation, heart block, or a new or old heart attack, it typically does not provide a definite diagnosis for the underlying cause for fainting. Sometimes, a Holter monitor may be used. This is a portable ECG device that can record the wearers heart rhythms during daily activities over an extended period of time. Since fainting usually does not occur upon command, a Holter monitor can provide a better understanding of the hearts activity during fainting episodes. For people with more than two episodes of syncope and no diagnosis on "routine testing", an insertable cardiac monitor might be used. It lasts 28–36 months and is inserted just beneath the skin in the upper chest area.

Imaging
Echocardiography and ischemia testing may be recommended for cases where initial evaluation and ECG testing is nondiagnostic. For people with uncomplicated syncope (without seizures and a normal neurological exam) computed tomography or MRI is not generally needed. Likewise, using carotid ultrasonography on the premise of identifying carotid artery disease as a cause of syncope also is not indicated. Although sometimes investigated as a cause of syncope, carotid artery problems are unlikely to cause that condition. Additionally an electroencephalogram (EEG) is generally not recommended. A bedside ultrasound may be performed to rule out abdominal aortic aneurysm in people with concerning history or presentation.

Differential diagnosis
Other diseases which mimic syncope include seizure, low blood sugar, and certain types of stroke. While these may appear as "fainting", they do not fit the strict definition of syncope being a sudden reversible loss of consciousness due to decreased blood flow to the brain.

Management
Management of syncope focuses on treating the underlying cause. This can be challenging as the underlying cause is unclear in half of all cases. Several risk stratification tools (explained below) have been developed to combat the vague nature of this diagnosis. People with an abnormal ECG reading, history of congestive heart failure, family history of sudden cardiac death, shortness of breath, HCT<30, hypotension or evidence of bleeding should be admitted to the hospital for further evaluation and monitoring. Low-risk cases of vasovagal or orthostatic syncope in younger people with no significant cardiac history, no family history of sudden unexplained death, and a normal EKG and initial evaluation may be candidates for discharge to follow-up with their primary care provider.Recommended acute treatment of vasovagal and orthostatic (hypotension) syncope involves returning blood to the brain by positioning the person on the ground, with legs slightly elevated or sitting leaning forward and the head between the knees for at least 10–15 minutes, preferably in a cool and quiet place. For individuals who have problems with chronic fainting spells, therapy should focus on recognizing the triggers and learning techniques to keep from fainting. At the appearance of warning signs such as lightheadedness, nausea, or cold and clammy skin, counter-pressure maneuvers that involve gripping fingers into a fist, tensing the arms, and crossing the legs or squeezing the thighs together can be used to ward off a fainting spell. After the symptoms have passed, sleep is recommended. Lifestyle modifications are important for treating people experiencing repeated syncopal episodes. Avoiding triggers and situations where loss of consciousness would be seriously hazardous (operating heavy machinery, commercial pilot, etc.) has been shown to be effective.
If fainting spells occur often without a triggering event, syncope may be a sign of an underlying heart disease. In the case where syncope is caused by cardiac disease, the treatment is much more sophisticated than that of vasovagal syncope and may involve pacemakers and implantable cardioverter-defibrillators depending on the precise cardiac cause.

Risk tools
The San Francisco syncope rule was developed to isolate people who have higher risk for a serious cause of syncope. High risk is anyone who has: congestive heart failure, hematocrit <30%, electrocardiograph abnormality, shortness of breath, or systolic blood pressure <90 mmHg. The San Francisco syncope rule however was not validated by subsequent studies.The Canadian syncope risk score was developed to help select low-risk people that may be viable for discharge home. A score of <0 on the Canadian syncope risk score is associated with <2% risk of serious adverse event within 30 days. It has been shown to be more effective than older syncope risk scores even combined with cardiac biomarkers at predicting adverse events.

Epidemiology
There are 18.1–39.7 syncope episodes per 1000 people in the general population. Rates are highest between the ages of 10–30 years old. This is likely because of the high rates of vasovagal syncope in the young adult population. Older adults are more likely to have orthostatic or cardiac syncope.
Syncope affects about three to six out of every thousand people each year. It is more common in older people and females. It is the reason for 2–5% of visits to emergency departments and admissions to hospital. Up to half of women over the age of 80 and a third of medical students describe at least one event at some point in their lives.

Prognosis
Of those presenting with syncope to an emergency department, about 4% died in the next 30 days. The risk of a poor outcome, however, depends very much on the underlying cause </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Granulosis rubra nasi and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Pyromania and can you explain it in depth? [/INST] Pyromania is an impulse control disorder in which individuals repeatedly fail to resist impulses to deliberately start fires, to relieve some tension or for instant gratification. The term pyromania comes from the Greek word πῦρ (pyr, fire). Pyromania is distinct from arson, the deliberate setting of fires for personal, monetary or political gain. Pyromaniacs start fires to release anxiety and tension, or for arousal. Other impulse disorders include kleptomania and intermittent explosive disorder.
There are specific symptoms that separate pyromaniacs from those who start fires for criminal purposes or due to emotional motivations not specifically related to fire. Someone with this disorder deliberately and purposely sets fires on more than one occasion, and before the act of lighting the fire the person usually experiences tension and an emotional buildup. When around fires, a person with pyromania gains intense interest or fascination and may also experience pleasure, gratification or relief. Another long term contributor often linked with pyromania is the buildup of stress. When studying the lifestyle of someone with pyromania, a buildup of stress and emotion is often evident and this is seen in teens attitudes towards friends and family. At times it is difficult to distinguish the difference between pyromania and experimentation in childhood because both involve pleasure from the fire.

Classification
ICD
The World Health Organizations International Classification of Diseases (11th Revision) ICD-11, regarded as the global standard, was released in June 2018 and came into full effect from January 2022. It states the following about pyromania:
Pyromania is characterised by a recurrent failure to control strong impulses to set fires, resulting in multiple acts of, or attempts at, setting fire to property or other objects, in the absence of an apparent motive (e.g., monetary gain, revenge, sabotage, political statement, attracting attention or recognition). There is an increasing sense of tension or affective arousal prior to instances of fire setting, persistent fascination or preoccupation with fire and related stimuli (e.g., watching fires, building fires, fascination with firefighting equipment), and a sense of pleasure, excitement, relief or gratification during, and immediately after the act of setting the fire, witnessing its effects, or participating in its aftermath.
It also notes that pyromania has no relation to intellectual impairment, substance abuse, or other mental and behavioral disorder. ICD-11 was produced by professionals from 55 countries out of the 90 countries involved and is one of the most widely used reference worldwide by clinicians, with the other being the Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR from 2022, DSM-5 from 2013, or their predecessors)

DSM
The American Psychiatric Associations Diagnostic and Statistical Manual of Mental Disorders, First Edition, released in 1952, categorized pyromania as a subset of Obsessive–compulsive disorder. In the Second Edition, the disorder was dropped. In the Third Edition, it returned under the category of impulse-control disorders.The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR), released in 2022, states that the essential feature of pyromania is "the presence of multiple episodes of deliberate and purposeful fire setting." Pyromania moved from the DSM-4 chapter "Impulse-Control Disorders Not Otherwise Specified," to the chapter "Disruptive, impulse-control, and conduct disorders" in DSM-5.

Signs and symptoms
According to DSM-5, there are six signs of pyromania. Pyromania is mainly categorized by the purposeful setting of fire, tension or arousal before a fire is set, interest in or attraction to fire, and pleasure or relief after setting a fire. These fires not set for personal gain, are not meant to express anger or conceal illegal activity, are not in support of sociopolitical ideologies, are not in response to delusions, and are not signs of intellectual disability. For diagnosis, the setting of fire should not be better explained by a conduct disorder, manic episode, or a personality disorder (antisocial personality disorder). ICD-11 also adds substance abuse to this list. According to ICD-11, signs of fire setting may occur "in response to feelings of depressed mood, anxiety, boredom, loneliness, or other negative affective states." Those with pyromania exhibit problems in social environments and learning disabilities. Women pyromaniacs "often report histories of exposure to trauma, including sexual abuse, and self-harm." Episodic fire setting may become more intense and violent over time, becoming potentially chronic if untreated.

Causes
Most studied cases of pyromania occur in children and teenagers. There is a range of causes, but an understanding of the different motives and actions of fire setters can provide a platform for prevention. Common causes of pyromania can be broken down into two main groups: individual and environmental. This includes the complex understanding of factors such as individual temperament, parental psychopathology, and possible neurochemical predispositions. Many studies have shown that patients with pyromania were in households without a father figure present.Pyromania can be common in those with substance use disorders, problem gambling, mood disorders, disruptive behaviour, anti-social disorders, another impulse-control disorder.

Environmental
Environmental factors that may lead to pyromania include an event that the patient has experienced in the environment they live in. Environmental factors include neglect from parents and physical or emotional abuse in earlier life. Other causes include early experiences of watching adults or teenagers using fire inappropriately and lighting fires as a stress reliever.

Treatment and prognosis
The appropriate treatment for pyromania varies with the age of the patient and the seriousness of the condition. For children and adolescents treatment usually is cognitive behavioral therapy sessions in which the patients situation is diagnosed to find out what may have caused this impulsive behavior. Once the situation is diagnosed, repeated therapy sessions usually help continue to a recovery. Other important steps must be taken as well with the interventions and the cause of the impulse behavior. Some other treatments include parenting training, over-correction/satiation/negative practice with corrective consequences, behavior contracting/token reinforcement, special problem-solving skills training, relaxation training, covert sensitization, fire safety and prevention education, individual and family therapy, and medication. The prognosis for recovery in adolescents and children with pyromania depends on the environmental or individual factors in play, but is generally positive. Pyromania is generally harder to treat in adults, often due to lack of cooperation by the patient. Treatment usually consists of more medication to prevent stress or emotional outbursts, in addition to long-term psychotherapy. In adults, however, the recovery rate is generally poor, and if an adult does recover, it usually takes a longer period of time.

History
Pyromania was thought in the 1800s to be a concept involved with moral insanity and moral treatment, but had not been categorized under impulse control disorders </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Hydranencephaly and can you explain it in depth? [/INST] Hydranencephaly is a condition in which the brains cerebral hemispheres are absent to a great degree and the remaining cranial cavity is filled with cerebrospinal fluid. "Cephalic" is the scientific term for "head" or "head end of body".
Hydranencephaly is a type of cephalic disorder. These disorders are congenital conditions that derive from damage to, or abnormal development of, the fetal nervous system in the earliest stages of development in utero. These conditions do not have any definitive identifiable cause factor. Instead, they are generally attributed to a variety of hereditary or genetic conditions, but also by environmental factors such as maternal infection, pharmaceutical intake, or even exposure to high levels of radiation.Hydranencephaly should not be confused with hydrocephalus, which is an accumulation of excess cerebrospinal fluid in the ventricles of the brain.
In hemihydranencephaly, only half of the cranial cavity is affected.

Signs and symptoms
An infant with hydranencephaly may appear normal at birth or may have some distortion of the skull and upper facial features due to fluid pressure inside the skull. The infants head size and spontaneous reflexes such as sucking, swallowing, crying, and moving the arms and legs may all seem normal, depending on the severity of the condition. However, after a few weeks the infant sometimes becomes irritable and has increased muscle tone (hypertonia). After several months of life, seizures and hydrocephalus may develop, if they did not exist at birth. Other symptoms may include visual impairment, lack of growth, deafness, blindness, spastic quadriparesis (paralysis), and intellectual deficits.Some infants may have additional abnormalities at birth including seizures, myoclonus (involuntary sudden, rapid jerks), limited thermoregulation abilities, and respiratory problems. Still other infants display no obvious symptoms at birth, going many months without a confirmed diagnosis of hydranencephaly. In some cases severe hydrocephalus, or another cephalic condition, is misdiagnosed.

Causes
Hydranencephaly is an extreme form of porencephaly, which is characterized by a cyst or cavity in the cerebral hemispheres.Although the exact cause of hydranencephaly remains undetermined in most cases, the most likely general cause is by vascular insult, such as stroke, injury, intrauterine infections, or traumatic disorders after the first trimester of pregnancy. In a number of cases where intrauterine infection was determined to be the causing factor, most involved toxoplasmosis and viral infections such as enterovirus, adenovirus, parvovirus, cytomegalovirus, herpes simplex, Epstein-Barr, and syncytial viruses. Another cause factor is monochorionic twin pregnancies, involving the death of one twin in the second trimester, which in turn causes vascular exchange to the living twin through placental circulation through twin-to-twin transfusion, causing hydranencephaly in the surviving fetus. One medical journal reports hydranencephaly as an autosomal inherited disorder with an unknown mode of transmission, causing a blockage of the carotid artery where it enters the cranium; this causes obstruction and damage to the cerebral cortex.

Genetic
Hydranencephaly is a recessive genetic condition, so both parents must carry the asymptomatic gene and pass it along to their child. There is a 25% chance that both parents will pass the gene to their child, resulting in hydranencephaly. Genetic hydranencephaly afflicts both males and females in equal numbers.

Post-natal brain injury
Though hydranencephaly is typically a congenital disorder, it can occur as a postnatal diagnosis in the aftermath of meningitis, intracerebral infarction, ischemia, or a traumatic brain injury.

Diagnosis
An accurate, confirmed diagnosis is generally impossible until after birth, though prenatal diagnosis using fetal ultrasonography (ultrasound) can identify characteristic physical abnormalities </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Vertebral column and can you explain it in depth? [/INST] The vertebral column, also known as the backbone or spine, is part of the axial skeleton. The vertebral column is the defining characteristic of a vertebrate in which the notochord (a flexible rod of uniform composition) found in all chordates has been replaced by a segmented series of bone: vertebrae separated by intervertebral discs. Individual vertebrae are named according to their region and position, and can be used as anatomical landmarks in order to guide procedures such as lumbar punctures. The vertebral column houses the spinal canal, a cavity that encloses and protects the spinal cord.
There are about 50,000 species of animals that have a vertebral column. The human vertebral column is one of the most-studied examples. Many different diseases in humans can affect the spine, with spina bifida and scoliosis being recognisable examples.
The general structure of human vertebrae is fairly typical of that found in mammals, reptiles, and birds. The shape of the vertebral body does, however, vary somewhat between different groups.

Structure
The number of vertebrae in a region can vary but overall the number remains the same. In a human vertebral column, there are normally 33 vertebrae. The upper 24 pre-sacral vertebrae are articulating and separated from each other by intervertebral discs, and the lower nine are fused in adults, five in the sacrum and four in the coccyx, or tailbone. The articulating vertebrae are named according to their region of the spine. There are 7 cervical vertebrae, 12 thoracic vertebrae and 5 lumbar vertebrae. The number of those in the cervical region, however, is only rarely changed, while that in the coccygeal region varies most. One study of 908 human adults found 43 individuals with 23 pre-sacral vertebrae (4.7%), 826 individuals with 24 pre-sacral vertebrae (91%), and 39 with 25 pre-sacral vertebrae (4.3%).There are ligaments extending the length of the column at the front and the back, and in between the vertebrae joining the spinous processes, the transverse processes and the vertebral laminae.

Vertebrae
The vertebrae in the human vertebral column is divided into different regions, which correspond to the curves of the vertebral column. The articulating vertebrae are named according to their region of the spine.  Vertebrae in these regions are essentially alike, with minor variation. These regions are called the cervical spine, thoracic spine, lumbar spine, sacrum, and coccyx. There are seven cervical vertebrae, twelve thoracic vertebrae, and five lumbar vertebrae.
The number of vertebrae in a region can vary but overall the number remains the same. The number of those in the cervical region, however, is only rarely changed. The vertebrae of the cervical, thoracic, and lumbar spines are independent bones and generally quite similar. The vertebrae of the sacrum and coccyx are usually fused and unable to move independently. Two special vertebrae are the atlas and axis, on which the head rests.

A typical vertebra consists of two parts: the vertebral body and the vertebral arch. The vertebral arch is posterior, meaning it faces the back of a person. Together, these enclose the vertebral foramen, which contains the spinal cord. Because the spinal cord ends in the lumbar spine, and the sacrum and coccyx are fused, they do not contain a central foramen. The vertebral arch is formed by a pair of pedicles and a pair of laminae, and supports seven processes, four articular, two transverse, and one spinous, the latter also being known as the neural spine. Two transverse processes and one spinous process are posterior to (behind) the vertebral body. The spinous process comes out the back, one transverse process comes out the left, and one on the right. The spinous processes of the cervical and lumbar regions can be felt through the skin.
Above and below each vertebra are joints called facet joints. These restrict the range of movement possible, and are joined by a thin portion of the neural arch called the pars interarticularis. In between each pair of vertebrae are two small holes called intervertebral foramina. The spinal nerves leave the spinal cord through these holes.
Individual vertebrae are named according to their region and position. From top to bottom, the vertebrae are:

Cervical spine: 7 vertebrae (C1–C7)
Thoracic spine: 12 vertebrae (T1–T12)
Lumbar spine: 5 vertebrae (L1–L5)
Sacrum: 5 (fused) vertebrae (S1–S5)
Coccyx: 4 (3–5) (fused) vertebrae (Tailbone)The combined region of the thoracic and lumbar vertebrae is known as the thoracolumbar division, or region.

Shape
The vertebral column is curved in several places, a result of human bipedal evolution. The curves allow the human spine to better stabilize the body in the upright position.The upper cervical spine has a curve, convex forward, that begins at the axis (second cervical vertebra) at the apex of the odontoid process or dens and ends at the middle of the second thoracic vertebra; it is the least marked of all the curves. This inward curve is known as a lordotic curve.

The thoracic curve, concave forward, begins at the middle of the second and ends at the middle of the twelfth thoracic vertebra. Its most prominent point behind corresponds to the spinous process of the seventh thoracic vertebra. This curve is known as a kyphotic curve.

The lumbar curve is more marked in the female than in the male; it begins at the middle of the last thoracic vertebra, and ends at the sacrovertebral angle. It is convex anteriorly, the convexity of the lower three vertebrae being much greater than that of the upper two. This curve is described as a lordotic curve.
The sacral curve begins at the sacrovertebral articulation, and ends at the point of the coccyx; its concavity is directed downward and forward as a kyphotic curve.
The thoracic and sacral kyphotic curves are termed primary curves, because they are present in the fetus. The cervical and lumbar curves are compensatory, or secondary, and are developed after birth. The cervical curve forms when the infant is able to hold up its head (at three or four months) and sit upright (at nine months). The lumbar curve forms later from twelve to eighteen months, when the child begins to walk.

Surfaces
Anterior surfaceWhen viewed from in front, the width of the bodies of the vertebrae is seen to increase from the second cervical to the first thoracic; there is then a slight diminution in the next three vertebrae. Below this, there is again a gradual and progressive increase in width as low as the sacrovertebral angle. From this point there is a rapid diminution, to the apex of the coccyx.
Posterior surfaceFrom behind, the vertebral column presents in the median line the spinous processes. In the cervical region (with the exception of the second and seventh vertebrae), these are short, horizontal, and bifid. In the upper part of the thoracic region they are directed obliquely downward; in the middle they are almost vertical, and in the lower part they are nearly horizontal. In the lumbar region they are nearly horizontal. The spinous processes are separated by considerable intervals in the lumbar region, by narrower intervals in the neck, and are closely approximated in the middle of the thoracic region. Occasionally one of these processes deviates a little from the median line — which can sometimes be indicative of a fracture or a displacement of the spine. On either side of the spinous processes is the vertebral groove formed by the laminae in the cervical and lumbar regions, where it is shallow, and by the laminae and transverse processes in the thoracic region, where it is deep and broad; these grooves lodge the deep muscles of the back. Lateral to the spinous processes are the articular processes, and still more laterally the transverse processes. In the thoracic region, the transverse processes stand backward, on a plane considerably behind that of the same processes in the cervical and lumbar regions. In the cervical region, the transverse processes are placed in front of the articular processes, lateral to the pedicles and between the intervertebral foramina. In the thoracic region they are posterior to the pedicles, intervertebral foramina, and articular processes. In the lumbar region they are in front of the articular processes, but behind the intervertebral foramina.
Lateral surfacesThe sides of the vertebral column are separated from the posterior surface by the articular processes in the cervical and thoracic regions and by the transverse processes in the lumbar region. In the thoracic region, the sides of the bodies of the vertebrae are marked in the back by the facets for articulation with the heads of the ribs. More posteriorly are the intervertebral foramina, formed by the juxtaposition of the vertebral notches, oval in shape, smallest in the cervical and upper part of the thoracic regions and gradually increasing in size to the last lumbar. They transmit the special spinal nerves and are situated between the transverse processes in the cervical region and in front of them, in the thoracic and lumbar regions.

Ligaments
There are different ligaments involved in the holding together of the vertebrae in the column, and in the columns movement. The anterior and posterior longitudinal ligaments extend the length of the vertebral column along the front and back of the vertebral bodies. The interspinous ligaments connect the adjoining spinous processes of the vertebrae. The supraspinous ligament extends the length of the spine running along the back of the spinous processes, from the sacrum to the seventh cervical vertebra. From there it is continuous with the nuchal ligament.

Development
The striking segmented pattern of the spine is established during embryogenesis when somites are rhythmically added to the posterior of the embryo. Somite formation begins around the third week when the embryo begins gastrulation and continues until all somites are formed. Their number varies between species: there are 42 to 44 somites in the human embryo and around 52 in the chick embryo. The somites are spheres, formed from the paraxial mesoderm that lies at the sides of the neural tube and they contain the precursors of spinal bone, the vertebrae ribs and some of the skull, as well as muscle, ligaments and skin. Somitogenesis and the subsequent distribution of somites is controlled by a clock and wavefront model acting in cells of the paraxial mesoderm. Soon after their formation, sclerotomes, which give rise to some of the bone of the skull, the vertebrae and ribs, migrate, leaving the remainder of the somite now termed a dermamyotome behind. This then splits to give the myotomes which will form the muscles and dermatomes which will form the skin of the back.  Sclerotomes become subdivided into an anterior and a posterior compartment. This subdivision plays a key role in the definitive patterning of vertebrae that form when the posterior part of one somite fuses to the anterior part of the consecutive somite during a process termed resegmentation. Disruption of the somitogenesis process in humans results in diseases such as congenital scoliosis. So  far, the human homologues of three genes associated to the mouse segmentation clock, (MESP2, DLL3 and LFNG), have been shown to be mutated in cases of congenital scoliosis, suggesting that the mechanisms involved in vertebral segmentation are conserved across vertebrates. In humans the first four somites are incorporated in the base of the occipital bone of the skull and the next 33 somites will form the vertebrae, ribs, muscles, ligaments and skin. The remaining posterior somites degenerate. During the fourth week of embryogenesis, the sclerotomes shift their position to surround the spinal cord and the notochord. This column of tissue has a segmented appearance, with alternating areas of dense and less dense areas.
As the sclerotome develops, it condenses further eventually developing into the vertebral body. Development of the appropriate shapes of the vertebral bodies is regulated by HOX genes.
The less dense tissue that separates the sclerotome segments develop into the intervertebral discs.
The notochord disappears in the sclerotome (vertebral body) segments but persists in the region of the intervertebral discs as the nucleus pulposus. The nucleus pulposus and the fibers of the anulus fibrosus make up the intervertebral disc.
The primary curves (thoracic and sacral curvatures) form during fetal development. The secondary curves develop after birth. The cervical curvature forms as a result of lifting the head and the lumbar curvature forms as a result of walking.

Function
Spinal cord
The vertebral column surrounds the spinal cord which travels within the spinal canal, formed from a central hole within each vertebra. The spinal cord is part of the central nervous system that supplies nerves and receives information from the peripheral nervous system within the body. The spinal cord consists of grey and white matter and a central cavity, the central canal. Adjacent to each vertebra emerge spinal nerves. The spinal nerves provide sympathetic nervous supply to the body, with nerves emerging forming the sympathetic trunk and the splanchnic nerves.
The spinal canal follows the different curves of the column; it is large and triangular in those parts of the column that enjoy the greatest freedom of movement, such as the cervical and lumbar regions, and is small and rounded in the thoracic region, where motion is more limited. The spinal cord terminates in the conus medullaris and cauda equina.

Clinical significance
Disease
Spina bifida is a congenital disorder in which there is a defective closure of the vertebral arch. Sometimes the spinal meninges and also the spinal cord can protrude through this, and this is called spina bifida cystica. Where the condition does not involve this protrusion it is known as spina bifida occulta. Sometimes all of the vertebral arches may remain incomplete.Another, though rare, congenital disease is Klippel–Feil syndrome, which is the fusion of any two of the cervical vertebrae.
Spondylolisthesis is the forward displacement of a vertebra and retrolisthesis is a posterior displacement of one vertebral body with respect to the adjacent vertebra to a degree less than a dislocation.
Spondylolysis, also known as a pars defect, is a defect or fracture at the pars interarticularis of the vertebral arch.
Spinal disc herniation, more commonly called a "slipped disc", is the result of a tear in the outer ring (anulus fibrosus) of the intervertebral disc, which lets some of the soft gel-like material, the nucleus pulposus, bulge out in a hernia.
Spinal stenosis is  a narrowing of the spinal canal which can occur in any region of the spine though less commonly in the thoracic region. The stenosis can constrict the spinal canal giving rise to a neurological deficit.
Pain at the coccyx (tailbone) is known as coccydynia.Spinal cord injury is damage to the spinal cord that causes changes in its function, either temporary or permanent. Spinal cord injuries can be divided into categories: complete transection, hemisection, central spinal cord lesions, posterior spinal cord lesions, and anterior spinal cord lesions.
Scalloping vertebrae is the increase in the concavity of the posterior vertebral body. It can be seen on lateral X-ray and sagittal views of CT and MRI scans. Its concavity is due to the increased pressure exerting on the vertebrae due to a mass. Internal spinal mass such as spinal astrocytoma, ependymoma, schwannoma, neurofibroma, and achondroplasia causes vertebrae scalloping.

Curvature
Excessive or abnormal spinal curvature is classed as a spinal disease or dorsopathy and includes the following abnormal curvatures:

Kyphosis is an exaggerated kyphotic (convex) curvature of the thoracic region in the sagittal plane, also called hyperkyphosis. This produces the so-called "humpback" or "dowagers hump", a condition commonly resulting from osteoporosis.
Lordosis is an exaggerated lordotic (concave) curvature of the lumbar region in the sagittal plane, is known as lumbar hyperlordosis and also as "swayback". Temporary lordosis is common during pregnancy.
Scoliosis, lateral curvature, is the most common abnormal curvature, occurring in 0.5% of the population. It is more common among females and may result from unequal growth of the two sides of one or more vertebrae, so that they do not fuse properly.  It can also be caused by pulmonary atelectasis (partial or complete deflation of one or more lobes of the lungs) as observed in asthma or pneumothorax.
Kyphoscoliosis, a combination of kyphosis and scoliosis.

Anatomical landmarks
Individual vertebrae of the human vertebral column can be felt and used as surface anatomy, with reference points are taken from the middle of the vertebral body. This provides anatomical landmarks that can be used to guide procedures such as a lumbar puncture and also as vertical reference points to describe the locations of other parts of human anatomy, such as the positions of organs.

Other animals
Variations in vertebrae
The general structure of vertebrae in other animals is largely the same as in humans. Individual vertebrae are composed of a centrum (body), arches protruding from the top and bottom of the centrum, and various processes projecting from the centrum and/or arches. An arch extending from the top of the centrum is called a neural arch, while the haemal arch or chevron is found underneath the centrum in the caudal (tail) vertebrae of fish, most reptiles, some birds, some dinosaurs and some mammals with long tails. The vertebral processes can either give the structure rigidity, help them articulate with ribs, or serve as muscle attachment points. Common types are transverse process, diapophyses, parapophyses, and zygapophyses (both the cranial zygapophyses and the caudal zygapophyses). The centrum of the vertebra can be classified based on the fusion of its elements. In temnospondyls, bones such as the spinous process, the pleurocentrum and the intercentrum are separate ossifications. Fused elements, however, classify a vertebra as having holospondyly.
A vertebra can also be described in terms of the shape of the ends of the centrum. Centra with flat ends are acoelous, like those in mammals. These flat ends of the centra are especially good at supporting and distributing compressive forces. Amphicoelous vertebra have centra with both ends concave. This shape is common in fish, where most motion is limited. Amphicoelous centra often are integrated with a full notochord. Procoelous vertebrae are anteriorly concave and posteriorly convex. They are found in frogs and modern reptiles. Opisthocoelous vertebrae are the opposite, possessing anterior convexity and posterior concavity. They are found in salamanders, and in some non-avian dinosaurs. Heterocoelous vertebrae have saddle-shaped articular surfaces. This type of configuration is seen in turtles that retract their necks, and birds, because it permits extensive lateral and vertical flexion motion without stretching the nerve cord too extensively or wringing it about its long axis.
In horses, the Arabian (breed) can have one less vertebrae and pair of ribs.  This anomaly disappears in foals that are the product of an Arabian and another breed of horse.

Regional vertebrae
Vertebrae are defined by the regions of the vertebral column that they occur in, as in humans. Cervical vertebrae are those in the neck area. With the exception of the two sloth genera (Choloepus and Bradypus) and the manatee genus, (Trichechus), all mammals have seven cervical vertebrae. In other vertebrates, the number of cervical vertebrae can range from a single vertebra in amphibians to as many as 25 in swans or 76 in the extinct plesiosaur Elasmosaurus. The dorsal vertebrae range from the bottom of the neck to the top of the pelvis. Dorsal vertebrae attached to the ribs are called thoracic vertebrae, while those without ribs are called lumbar vertebrae. The sacral vertebrae are those in the pelvic region, and range from one in amphibians, to two in most birds and modern reptiles, or up to three to five in mammals. When multiple sacral vertebrae are fused into a single structure, it is called the sacrum. The synsacrum is a similar fused structure found in birds that is composed of the sacral, lumbar, and some of the thoracic and caudal vertebra, as well as the pelvic girdle. Caudal vertebrae compose the tail, and the final few can be fused into the pygostyle in birds, or into the coccygeal or tail bone in chimpanzees (and humans).

Fish and amphibians
The vertebrae of lobe-finned fishes consist of three discrete bony elements. The vertebral arch surrounds the spinal cord, and is of broadly similar form to that found in most other vertebrates. Just beneath the arch lies a small plate-like pleurocentrum, which protects the upper surface of the notochord, and below that, a larger arch-shaped intercentrum to protect the lower border. Both of these structures are embedded within a single cylindrical mass of cartilage. A similar arrangement was found in the primitive Labyrinthodonts, but in the evolutionary line that led to reptiles (and hence, also to mammals and birds), the intercentrum became partially or wholly replaced by an enlarged pleurocentrum, which in turn became the bony vertebral body.
In most ray-finned fishes, including all teleosts, these two structures are fused with, and embedded within, a solid piece of bone superficially resembling the vertebral body of mammals. In living amphibians, there is simply a cylindrical piece of bone below the vertebral arch, with no trace of the separate elements present in the early tetrapods.In cartilaginous fish, such as sharks, the vertebrae consist of two cartilaginous tubes. The upper tube is formed from the vertebral arches, but also includes additional cartilaginous structures filling in the gaps between the vertebrae, and so enclosing the spinal cord in an essentially continuous sheath. The lower tube surrounds the notochord, and has a complex structure, often including multiple layers of calcification.Lampreys have vertebral arches, but nothing resembling the vertebral bodies found in all higher vertebrates. Even the arches are discontinuous, consisting of separate pieces of arch-shaped cartilage around the spinal cord in most parts of the body, changing to long strips of cartilage above and below in the tail region. Hagfishes lack a true vertebral column, and are therefore not properly considered vertebrates, but a few tiny neural arches are present in the tail.

Other vertebrates
The general structure of human vertebrae is fairly typical of that found in mammals, reptiles, and birds. The shape of the vertebral body does, however, vary somewhat between different groups. In mammals, such as humans, it typically has flat upper and lower surfaces, while in reptiles the anterior surface commonly has a concave socket into which the expanded convex face of the next vertebral body fits. Even these patterns are only generalisations, however, and there may be variation in form of the vertebrae along the length of the spine even within a single species. Some unusual variations include the saddle-shaped sockets between the cervical vertebrae of birds and the presence of a narrow hollow canal running down the centre of the vertebral bodies of geckos and tuataras, containing a remnant of the notochord.Reptiles often retain the primitive intercentra, which are present as small crescent-shaped bony elements lying between the bodies of adjacent vertebrae; similar structures are often found in the caudal vertebrae of mammals. In the tail, these are attached to chevron-shaped bones called haemal arches, which attach below the base of the spine, and help to support the musculature. These latter bones are probably homologous with the ventral ribs of fish. The number of vertebrae in the spines of reptiles is highly variable, and may be several hundred in some species of snake.In birds, there is a variable number of cervical vertebrae, which often form the only truly flexible part of the spine. The thoracic vertebrae are partially fused, providing a solid brace for the wings during flight </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Café au lait spot and can you explain it in depth? [/INST] Café au lait spots, or café au lait macules, are flat, hyperpigmented birthmarks. The name café au lait is French for "coffee with milk" and refers to their light-brown color. Café au lait lesions with rough borders ("coast of Maine") may be seen in McCune-Albright syndrome </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Triangular alopecia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Stenosis of pulmonary artery and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Myospherulosis and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Infantile esotropia and can you explain it in depth? [/INST] Infantile esotropia is an ocular condition of early onset in which one or either eye turns inward. It is a specific sub-type of esotropia and has been a subject of much debate amongst ophthalmologists with regard to its naming, diagnostic features, and treatment.

Presentation
Historically the term congenital strabismus was used to describe constant esotropias with onset between birth and six months of age. However, this term was felt to be an inadequate classification as it covered a variety of esotropias with different causes, features and prognoses.

In 1988, American ophthalmologist Gunter K. Von Noorden discussed what he described as Essential Infantile Esotropia. He described the condition as:
"early acquired, not... congenital ..., although congenital factors may favor its development between the ages of 3 and 6 months"

 and identified this squint sub-type as having the following features:
Onset between birth and six months of age.
Large size (greater than 30 dioptres)
Stable size
Not associated with abnormalities of the central nervous system.
Often associated with defective abduction (outward movement) and excessive adduction (inward movement) of the eyes.
Also associated with oblique muscle dysfunction and Dissociated Vertical Deviation.
Initial alternation of the squint present with crossed fixation, i.e. the affected individual uses the left eye to look right and the right eye to look left.
Limited potential for binocular vision.The same condition had also previously been described by other ophthalmologists, notably Cianca (1962) who named it Ciancas Syndrome and noted the presence of manifest latent nystagmus, and Lang (1968) who called it Congenital Esotropia Syndrome and noted the presence of abnormal head postures. In both cases, however, the essential characteristics were the same, but with emphasis placed on different elements of the condition.
Helveston  (1993) further clarified and expanded upon von Noordens work, and incorporated the work of both Lang and Cianca into his summary of the characteristics of the condition:

Esotropia between 10 and 90 dioptres in size
Either alternation or fixation preference may be present (if the latter then amblyopia may result).
Neurologically normal.
Hyperopic correction does not eliminate or significantly reduce the squint size.
Frequent nystagmus (latent or manifest latent).
The patient may or may not have any or all of the following associated conditions: Oblique muscle dysfunction, vertical incomitance, dissociated vertical deviation, asymmetric optokinetic nystagmus, torticollis.
Presence will be confirmed by six months.
Best treatment results in subnormal binocular vision.The expressions congenital esotropia, infantile esoptropia, idiopathic infantile esotropia and essential infantile esotropia are often used interchangeably.

Cross-fixation
Cross-fixation congenital esotropia, also called Ciancis syndrome is a particular type of large-angle infantile esotropia associated with tight medius rectus muscles. With the tight muscles, which hinder adduction, there is a constant inward eye turn. The patient cross-fixates, that is, to fixate objects on the left, the patient looks across the nose with the right eye, and vice versa. The patient tends to adopt a head turn, turning the head to the right to better see objects in the left visual field and turning the head to the left to see those in the right visual field. Binasal occlusion can be used to discourage cross-fixation. However, the management of cross-fixation congenital esotropia usually involves surgery.

Cause
This remains undetermined at the present time. A recent study by Major et al. reports that:

Prematurity, family history or secondary ocular history, perinatal or gestational complications, systemic disorders, use of supplemental oxygen as a neonate, use of systemic medications, and male sex were found to be significant risk factors for infantile esotropia.

Further recent evidence indicates that a cause for infantile strabismus may lie with the input that is provided to the visual cortex. In particular, neonates who suffer injuries that, directly or indirectly, perturb binocular inputs into the primary visual cortex (V1) have a far higher risk of developing strabismus than other infants.

Diagnosis
Differential Diagnosis
Clinically Infantile esotropia must be distinguished from:

VIth Cranial nerve or abducens palsy
Nystagmus Blockage Syndrome
Esotropia arising secondary to central nervous system abnormalities (in cerebral palsy for example)
Primary Constant esotropia
Duanes Syndrome

Treatment
According to a Cochrane review of 2012, controversies remain regarding type of surgery, non-surgical intervention and age of intervention.The aims of treatment are as follows:

The elimination of any amblyopia
A cosmetically acceptable ocular alignment
Long-term stability of eye position
Binocular cooperation

Initially
It is essential that a child with strabismus is presented to the ophthalmologist as early as possible for diagnosis and treatment in order to allow best possible monocular and binocular vision to develop. Initially, the patient will have a full eye examination to identify any associated pathology, and any glasses required to optimise acuity will be prescribed – although infantile esotropia is not typically associated with refractive error. Studies have found that approximately 15% of infantile esotropia patients have accommodative esotropia. For these patients, antiaccommodative therapy (with spectacles) is indicated before any surgery as antiaccommodative therapy fully corrects their esotropia in many cases and significantly decreases their deviation angle in others.Amblyopia will be treated via occlusion treatment (using patching or atropine drops) of the non-squinting eye with the aim of achieving full alternation of fixation. Management thereafter will be surgical. As alternative to surgery, also botulinum toxin therapy has been used in children with infantile esotropia. Furthermore, as accompaniment to ophthalmologic treatment, craniosacral therapy may be performed in order to relieve tension (see also: Management of strabismus).

Surgery
Controversy has arisen regarding the selection and planning of surgical procedures, the timing of surgery and about what constitutes a favourable outcome.
1. Selection and planning
Some ophthalmologists, notably Ing  and Helveston, favour a prescribed approach often involving multiple surgical episodes whereas others prefer to aim for full alignment of the eyes in one procedure and let the number of muscles operated upon during this procedure be determined by the size of the squint.
2 </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Boutonniere deformity and can you explain it in depth? [/INST] Boutonniere deformity is a deformed position of the fingers or toes, in which the joint nearest the knuckle (the proximal interphalangeal joint, or PIP) is permanently bent toward the palm while the farthest joint (the distal interphalangeal joint, or DIP) is bent back away (PIP flexion with DIP hyperextension). Causes include injury, inflammatory conditions like rheumatoid arthritis, and genetic conditions like Ehlers-Danlos syndrome.

Pathophysiology
This flexion deformity of the proximal interphalangeal joint is due to interruption of the central slip of the extensor tendon such that the lateral slips separate and the head of the proximal phalanx pops through the gap like a finger through a button hole (thus the name, from French boutonnière "button hole"). The distal joint is subsequently drawn into hyperextension because the two peripheral slips of the extensor tendon are stretched by the head of the proximal phalanx (note that the two peripheral slips are inserted into the distal phalanx, while the proximal slip is inserted into the middle phalanx). This deformity makes it difficult or impossible to extend the proximal interphalangeal joint.

Diagnosis
Stages
Mild extension lag, passively correctable
Moderate extension lag, passively correctable
Mild flexion contracture
Advanced flexion contractureHigher numbers indicate a more severe problem and greater likelihood of a poor outcome.

Treatment
Usually treated with a splint placing the proximal interphalangeal joint in extension for 4–6 weeks. Occasionally surgery is needed when splinting is unsuccessful.

See also
Swan neck deformity
Z-deformity

References
Further reading
Coons, Matthew S.; Green, Steven M. (August 1995). "Boutonniere deformity". Hand Clinics. 11 (3): 387–402. doi:10.1016/S0749-0712(21)00060-3. PMID 7559817.
Souter, William A. (October 1974). "The Problem of Boutonniere Deformity". Clinical Orthopaedics and Related Research. 104 (104): 116–133. doi:10.1097/00003086-197410000-00012. PMID 4607222.
Nalebuff, Edward A.; Millender, Lewis H. (July 1975). "Surgical Treatment of the Boutonniere Deformity in Rheumatoid Arthritis". Orthopedic Clinics of North America. 6 (3): 753–763. doi:10.1016/S0030-5898(20)30987-1. PMID 1099508.
Littler, J. William; Eaton, Richard G. (October 1967). "Redistribution of Forces in the Correction of the Boutonnière Deformity". JBJS. 49 (7): 1267–1274. doi:10.2106/00004623-196749070-00002. PMID 5622971.
To, Philip; Watson, Jeffry T. (January 2011). "Boutonniere Deformity". The Journal of Hand Surgery. 36 (1): 139–142. doi:10.1016/j.jhsa.2010.10.032. PMID 21193133.
Massengill, James B. (November 1992). "The boutonniere deformity". Hand Clinics. 8 (4): 787–801. doi:10.1016/S0749-0712(21)00744-7. PMID 1460075.
Aiache, Adrien; Barsky, Arthur J.; Weiner, Daniel L. (August 1970). "Prevention of the boutonniere deformity". Plastic and Reconstructive Surgery. 46 (2): 164–167. doi:10.1097/00006534-197008000-00010. PMID 5423482. S2CID 39268503.
Curtis, Raymond M.; Reid, Robert L.; Provost, John M. (March 1983). "A staged technique for the repair of the traumatic boutonniere deformity". The Journal of Hand Surgery. 8 (2): 167–171. doi:10.1016/s0363-5023(83)80009-4. PMID 6833725.
Urbaniak, James R.; Hayes, Michael G. (July 1981). "Chronic boutonniere deformity—An anatomic reconstruction" </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Incidental imaging finding and can you explain it in depth? [/INST] In medical or research imaging, an incidental imaging finding (also called an incidentaloma) is an unanticipated finding which is not related to the original diagnostic inquiry. As with other types of incidental medical findings, they may represent a diagnostic, ethical, and philosophical dilemma because their significance is unclear. While some coincidental findings may lead to beneficial diagnoses, others may lead to overdiagnosis that results in unnecessary testing and treatment, sometimes called the "cascade effect".Incidental findings are common in imaging. For instance, around 1 in every 3 cardiac MRIs result in an incidental finding. Incidence is similar for chest CT scans (~30%).As the use of medical imaging increases, the number of incidental findings also increases.

Adrenal
Incidental adrenal masses on imaging are common (0.6 to 1.3% of all abdominal CT). Differential diagnosis include adenoma, myelolipoma, cyst, lipoma, pheochromocytoma, adrenal cancer, metastatic cancer, hyperplasia, and tuberculosis.  Some of these lesions are easily identified by radiographic appearance; however, it is often adenoma vs. cancer/metastasis that is most difficult to distinguish.  Thus, clinical guidelines have been developed to aid in diagnosis and decision-making. Although adrenal incidentalomas are common, they are not commonly cancerous - less than 1% of all adrenal incidentalomas are malignant.The first considerations are size and radiographic appearance of the mass.  Suspicious adrenal masses or those ≥4 cm are recommended for complete removal by adrenalectomy.  Masses <4 cm may also be recommended for removal if they are found to be hormonally active, but are otherwise recommended for observation.  All adrenal masses should receive hormonal evaluation. Hormonal evaluation includes:
1-mg overnight dexamethasone suppression test
24-hour urinary specimen for measurement of fractionated metanephrines and catecholamines
Blood plasma aldosterone concentration and plasma renin activity, if hypertension is presentOn CT scan, benign adenomas typically are of low radiodensity (due to fat content). A radiodensity equal to or below 10 Hounsfield units (HU) is considered diagnostic of an adenoma. An adenoma also shows rapid radiocontrast washout (50% or more of the contrast medium washes out at 10 minutes). If the hormonal evaluation is negative and imaging suggests benign lesion, follow up may be considered. Imaging at 6, 12, and 24 months and repeat hormonal evaluation yearly for 4 years is often recommended, but there exists controversy about harm/benefit of such screening as there is a high subsequent false-positive rate (about 50:1) and overall low incidence of adrenal carcinoma.

Brain
Autopsy series have suggested that pituitary incidentalomas may be quite common. It has been estimated that perhaps 10% of the adult population may harbor such endocrinologically inert lesions. Most of these lesions, especially those which are small, will not grow. However, some form of long-term surveillance has been recommended based on the size and presentation of the lesion. With pituitary adenomas larger than 1cm, a baseline pituitary hormonal function test should be done, including measurements of serum levels of TSH, prolactin, IGF-1 (as a test of growth hormone activity), adrenal function (i.e. 24 hour urine cortisol, dexamethasone suppression test), testosterone in men, and estradiol in amenorrheic women.

Thyroid and parathyroid
Incidental thyroid masses may be found in 9% of patients undergoing bilateral carotid duplex ultrasonography.Some experts recommend that nodules > 1 cm (unless the TSH is suppressed) or those with ultrasonographic features of malignancy should be biopsied by fine needle aspiration </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Periorbital hyperpigmentation and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Verrucous carcinoma and can you explain it in depth? [/INST] Verrucous carcinoma (VC) is an uncommon variant of squamous cell carcinoma </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Choreoathetosis and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Warm antibody autoimmune hemolytic anemia and can you explain it in depth? [/INST] Warm antibody autoimmune hemolytic anemia (WAIHA) is the most common form of autoimmune haemolytic anemia. About half of the cases are of unknown cause, with the other half attributable to a predisposing condition or medications being taken. Contrary to cold autoimmune hemolytic anemia (e.g., cold agglutinin disease and paroxysmal cold hemoglobinuria) which happens in cold temperature (28–31 °C), WAIHA happens at body temperature.

Causes
AIHA may be:

Idiopathic, that is, without any known cause
Secondary to another disease, such as an antecedent upper respiratory tract infection, systemic lupus erythematosus or a malignancy, such as chronic lymphocytic leukemia (CLL)

Medications
Several medications have been associated with the development of warm AIHA. These medications include quinidine, nonsteroidal anti-inflammatory drugs (NSAIDs),  alpha methyldopa, and antibiotics such as penicillins, cephalosporins (such as ceftriaxone and cefotetan), and ciprofloxacin.

Pathophysiology
The most common antibody isotype involved in warm antibody AIHA is IgG, though sometimes IgA is found.  The IgG antibodies attach to a red blood cell, leaving their FC portion exposed with maximal reactivity at 37 °C (versus cold antibody induced hemolytic anemia whose antibodies only bind red blood cells at low body temperatures, typically 28-31 °C).  The FC region is recognized and grabbed onto by FC receptors found on monocytes and macrophages in the spleen.  These cells will pick off portions of the red cell membrane, almost as if they are taking a bite.  The loss of membrane causes the red blood cells to become spherocytes.  Spherocytes are not as flexible as normal RBCs and will be singled-out for destruction in the red pulp of the spleen as well as other portions of the reticuloendothelial system </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Systemic vasculitis and can you explain it in depth? [/INST] Necrotizing vasculitis, also called systemic necrotizing vasculitus, is a category of vasculitis, comprising vasculitides that present with necrosis.Examples include giant cell arteritis, microscopic polyangiitis, and granulomatosis with polyangiitis.
ICD-10 uses the variant "necrotizing vasculopathy". ICD-9, while classifying these conditions together, does not use a dedicated phrase, instead calling them "polyarteritis nodosa and allied conditions".
When using the influential classification known as the "Chapel Hill Consensus Conference", the terms "systemic vasculitis" or "primary systemic vasculitides" are commonly used. Although the word necrotizing is omitted, the conditions described are largely the same.

Classification
Large vessel vasculitis
Giant-cell arteritis and Takayasus arteritis have much in common, but usually affect patients of different ages, with Takayasus arteritis affecting younger people, and giant-cell arteritis having a later age of onset.
Aortitis can also be considered a large-vessel disease.Takayasu arteritis. Primarily affects the aorta and its main branches. At least three out of six criteria yields sensitivity and specificity of 90.5 and 97.8%:

Onset < 40 years affects young and middle -aged women (ages 15–45)
Claudication of extremities
Decreased pulsation of one or both brachial arteries
At least 10 mmHg systolic difference in both arms
Bruit over one or both carotid arteries or abdominal aorta
Arteriographic narrowing of aorta, its primary branches, or large arteries in upper or lower extremities
Ocular manifestation
Visual loss or field defects
Retinal hemorrhages
Neurological abnormalities
Treatment: steroidsGiant cell (temporal) arteritis. Chronic vasculitis of both large and medium vessels, primarily affecting cranial branches of the arteries arising from the aortic arch. At least three out of five criteria yields sensitivity and specificity of 95 and 91%:

Age at onset ≥ 50 years
New onset headache with localized tenderness
Temporal artery tenderness or decreased pulsation
Elevated ESR ≥ 50 mm/hour Westergren
Temporal artery biopsy showing vasculitis with mononuclear cell infiltrate or granulomatous inflammation, usually with multinucleated giant cells

Medium vessel vasculitis
These conditions are sometimes considered together with the small vessel vasculitides.Polyarteritis nodosa (PAN). Systemic necrotizing vasculitis and aneurysm formation affecting both medium and small arteries. If only small vessels are affected, it is called microscopic polyangiitis, although it is more associated with granulomatosis with polyangiitis than to classic PAN. At least 3 out of 10 criteria yields sensitivity and specificity of 82 and 87%:

Unexplained weight loss > 4 kg
Livedo reticularis
Testicular pain
Myalgias, weakness
Abdominal pain, diarrhea, and GI bleeding
Mononeuropathy or polyneuropathy
New onset diastolic blood pressure > 90 mmHg
Elevated serum blood urea nitrogen (> 40 mg/dL) or serum creatinine (> 1.5 mg/dL)
Hepatitis B infection
Arteriographic abnormalities
Arterial biopsy showing polymorphonuclear cellsKawasaki disease. Usually in children (age<4), it affects large, medium, and small vessels, prominently the coronary arteries. Associated with a mucocutaneous lymph node syndrome. Diagnosis requires fever lasting five days or more with at least four out of five criteria:

Bilateral conjunctival injection
Injected or fissured lips, injected pharynx, or strawberry tongue
Erythema of palms/soles, edema of hands/feet, periungual desquamation
Polymorphous rash
Cervical lymphadenopathy (at least one node > 1.5 cm)Isolated cerebral vasculitis. Affects medium and small arteries over a diffuse CNS area, without symptomatic extracranial vessel involvement. Patients have CNS symptoms as well as cerebral vasculitis by angiography and leptomeningeal biopsy.

Small vessel vasculitis
There are several vasculitides that affect small vessels.

Pauci-immune
Granulomatosis with polyangiitis. Systemic vasculitis of medium and small arteries, including venules and arterioles. Produces granulomatous inflammation of the respiratory tracts and necrotizing, pauci-immune glomerulonephritis. Most common cause of saddle nose deformity in USA (nose flattened due to destruction of nasal septum by granulomatous inflammation). Almost all patients with granulomatosis with polyangiitis have c-antineutrophil cytoplasmic antibody, but not vice versa. Current treatment of choice is cyclophosphamide. At least two out of four criteria yields sensitivity and specificity of 88 and 92%.

Nasal or oral inflammation (oral ulcers or purulent/bloody nasal discharge, may be painful)
Abnormal chest X-ray with showing nodules, infiltrates, or cavities
Microscopic hematuria or red blood cell casts
Vessel biopsy shows granulomatous inflammation
Peak incidence: ages 40–60, males > femalesEosinophilic granulomatosis with polyangiitis (formerly known as Churg–Strauss syndrome). Affects medium and small vessels with vascular and extravascular granulomatosis. Classically involves arteries of lungs and skin, but may be generalized.  At least four criteria yields sensitivity and specificity of 85 and 99.7%.

Asthma (history of wheezing or presently wheezing)
Eosinophilia > 10% on complete blood count
Mononeuropathy or polyneuropathy
Migratory or transient pulmonary opacities on chest x-ray
Paranasal sinus abnormalities
Vessel biopsy showing eosinophils in extravascular areasMicroscopic polyarteritis/polyangiitis. Affects capillaries, venules, or arterioles. Thought to be part of a group that includes granulomatosis with polyangiitis since both are associated with antineutrophil cytoplasmic antibody and similar extrapulmonary manifestations. Patients do not usually have symptomatic or histologic respiratory involvement.

Immune complex
Hypersensitivity vasculitis (allergic vasculitis). Usually due to a hypersensitivity reaction to a known drug. Drugs most commonly implicated are penicillin, sulphonamides and thiazide diuretics. Methamphetamine and other sympathomimetics can cause a cerebral vasculitis alongside polyarteritis nodosa like systemic features. With other drugs,there is presence of skin vasculitis with palpable petechiae or purpura. Biopsy of these lesions reveal inflammation of the small vessels, termed leukocytoclastic vasculitis, which is most prominent in postcapillary venules. At least three out of five criteria yields sensitivity and specificity of 71 and 84%:

Age > 16
Use of possible triggering drug in relation to symptoms
Palpable purpura
Maculopapular rash
Skin biopsy showing neutrophils around vesselIgA vasculitis (formerly known as Henoch–Schonlein purpura). Systemic vasculitis due to tissue deposition of IgA-containing immune complexes. Biopsy of lesions shows inflammation of small vessels. It is considered a form of hypersensitivity vasculitis but is distinguished by prominent deposits of IgA. This is the most common vasculitis in children. Presence of three or more criteria yielded sensitivity of 87% while less than two criteria yielded hypersensitivity vasculitis in 74%:

Palpable purpura (usually of buttocks and legs)
Bowel angina
GI bleed
Hematuria
Onset < 20 years
No new medicationsEssential cryoglobulinemic vasculitis. Most often due to hepatitis C infection, immune complexes of cryoglobulins – proteins that consists of immunoglobulins and complement and precipitate in the cold while dissolving upon rewarming – are deposited in walls of capillaries, venules, or arterioles. Therefore, complement will be low with histology showing vessel inflammation with immune deposits.

Other/ungrouped
Vasculitis secondary to connective tissue disorders. Usually secondary to systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), relapsing polychondritis, Behçets disease, and other connective tissue disorders.
Vasculitis secondary to viral infection. Usually due to hepatitis B and C, human immunodeficiency virus, cytomegalovirus, Epstein–Barr virus, and parvovirus B19.

Signs and symptoms
Patients usually present with systemic symptoms with single or multiorgan dysfunction. Common (and nonspecific) complaints include fatigue, weakness, fever, joint pains, abdominal pain, hypertension, chronic kidney disease, and neurologic dysfunction. The following symptoms should raise a strong suspicion of a vasculitis:

Mononeuritis multiplex. Also known as asymmetric polyneuropathy, in a non-diabetic this is suggestive of vasculitis.
Palpable purpura. If patients have this in isolation, it is most likely due to cutaneous leukocytoclastic vasculitis. If the purpura is in combination with systemic organ involvement, it is most likely to be Henoch–Schönlein purpura or microscopic polyangiitis.
Pulmonary-renal syndrome. Individuals who are coughing up blood and have kidney involvement are likely to have granulomatosis with polyangiitis, microscopic polyangiitis, or anti-GBM disease (Goodpasture syndrome).

Diagnosis
A detailed history is important to elicit any recent medications, any risk of hepatitis infection, or any recent diagnosis with a connective tissue disorder such as systemic lupus erythematosus (SLE). A thorough physical exam is needed as usual.

Lab tests </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Atypical chronic myeloid leukemia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Abdominal migraine and can you explain it in depth? [/INST] Abdominal migraine is a variant type of migraine. It primarily affects children, and is rare in adults. It mainly causes episodes of abdominal pain without an accompanying headache. It is poorly understood. It is difficult to confirm the diagnosis, as periumbilical abdominal pain has an extensive differential diagnosis. It may be treated with analgesia in some patients, and other medications. Avoiding triggers can prevent an episode of abdominal migraine.

Signs and Symptoms
Symptoms of abdominal migraine may include:

Abdominal pain
Nausea
Vomiting
Headache
Photosensitivity
Loss of appetite
PallorThese occur in distinct episodes. This can have a significant effect on day-to-day life. It usually does not occur with a headache. Body mass index is usually unaffected, and physical development is normal.

Causes
Common migraine triggers may trigger abdominal migraines. Psychological stress (such as from school), a change in location (such as travel), changes to sleep, and exercise when this is not wanted, may all cause abdominal migraine.

Pathophysiology
Abdominal migraine is poorly understood.

Diagnosis
As with other types of migraines, there is no diagnostic test to identify abdominal migraines. Diagnosis is based on symptoms, a family history of migraines, and eliminations of other possible causes. It can take time before a diagnosis is made, as symptoms are not specific to abdominal migraine.Diagnostic criteria from the International Classification of Headache Disorders are:

A. At least 5 attacks fulfilling criteria B-D.
B. Attacks of abdominal pain lasting 1–72 hours (untreated or unsuccessfully treated)
C. Abdominal pain has all of the following characteristics:
1. midline location, periumbilical or poorly localized
2. dull or "just sore" quality
3. moderate or severe intensity
D. During abdominal pain at least 2 of the following:
1. loss of appetite
2. nausea
3. vomiting
4. pallor
E. Not attributed to another disorder

Differential diagnosis
Abdominal migraine must be distinguished from other causes of chronic or recurrent abdominal pain. These include irritable bowel syndrome, peptic ulcer disease, gastroesophageal reflux disease, mast cell activation syndrome, and celiac artery compression syndrome. It must also be distinguished from causes of acute abdominal pain, such as appendicitis, as wrong diagnosis may lead to unnecessary appendectomy.

Treatment
Short term
Analgesia may be effective against abdominal migraine in some patients. Avoidance of intense light tends to have a short-term beneficial effect.

Long term
Avoidance of triggers can be very helpful. Medications such as pizotifen, propanolol, and cyproheptadine may be used in rare circumstances.

Prognosis
Abdominal migraine can have a significant impact on day-to-day life </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Lathosterolosis and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Miller syndrome and can you explain it in depth? [/INST] Miller syndrome, also known as Genée–Wiedemann syndrome, Wildervanck–Smith syndrome or postaxial acrofacial dystosis, is an extremely rare genetic condition that manifests as craniofacial, limb and eye deformities. It is caused by a mutation in the DHODH gene. The incidence of the condition is not known, and nothing is known of its pathogenesis.

Presentation
The syndrome consists of severe micrognathia, cleft lip and/or palate, hypoplasia or aplasia of the postaxial elements of the limbs, coloboma of the eyelids and supernumerary nipples </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tricho–rhino–phalangeal syndrome type 2 and can you explain it in depth? [/INST]  </s>