<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 Hypertensive disease of pregnancy and can you explain it in depth? [/INST] Hypertensive disease of pregnancy, also known as maternal hypertensive disorder, is a group of high blood pressure disorders that include preeclampsia, preeclampsia superimposed on chronic hypertension, gestational hypertension, and chronic hypertension.Maternal hypertensive disorders occurred in about 20.7 million women in 2013. About 10% of pregnancies globally are complicated by hypertensive diseases. In the United States, hypertensive disease of pregnancy affects about 8% to 13% of pregnancies. Rates have increased in the developing world. They resulted in 29,000 deaths in 2013 down from 37,000 deaths in 1990. They are one of the three major causes of death in pregnancy (16%) along with post partum bleeding (13%) and puerperal infections (2%).

Signs and symptoms
Although many pregnant women with high blood pressure have healthy babies without serious problems, high blood pressure can be dangerous for both the mother and baby. Women with pre-existing, or chronic, high blood pressure are more likely to have certain complications during pregnancy than those with normal blood pressure. However, some women develop high blood pressure while they are pregnant (often called gestational hypertension).Chronic poorly-controlled high blood pressure before and during pregnancy puts a pregnant woman and her baby at risk for problems. It is associated with an increased risk for maternal complications such as preeclampsia, placental abruption (when the placenta separates from the wall of the uterus), and gestational diabetes. These women also face a higher risk for poor birth outcomes such as preterm delivery, having an infant small for his/her gestational age, and infant death.

Risk factors
Some women have a greater risk of developing hypertension during pregnancy. These are:

Women with chronic hypertension (high blood pressure before becoming pregnant).
Women who developed high blood pressure or preeclampsia during a previous pregnancy, especially if these conditions occurred early in the pregnancy.
Women who are obese prior to pregnancy.
Pregnant women under the age of 20 or over the age of 40.
Women who are pregnant with more than one baby.
Women with diabetes, kidney disease, rheumatoid arthritis, lupus, or scleroderma.

Diagnosis
There is no single test to predict or diagnose preeclampsia. Key signs are increased blood pressure and protein in the urine (proteinuria). Other symptoms that seem to occur with preeclampsia include persistent headaches, blurred vision or sensitivity to light, and abdominal pain.All of these sensations can be caused by other disorders; they can also occur in healthy pregnancies. Regular visits are scheduled to track blood pressure and level of protein in urine, to order and analyze blood tests that detect signs of preeclampsia, and to monitor fetal development more closely.

Classification
A classification of hypertensive disorders of pregnancy uses 4 categories as recommended by the U.S. National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy:
Chronic hypertension;
Preeclampsia-eclampsia;
Preeclampsia superimposed on chronic hypertension;
Gestational hypertension (transient hypertension of pregnancy or chronic hypertension identified in the latter half of pregnancy).This terminology is preferred over the older but widely used term pregnancy-induced hypertension (PIH) because it is more precise. The newer terminology reflects simply relation of pregnancy with either the onset or first detection of hypertension; the question of causation, while pathogenetically interesting, is not the important point for most health care purposes. This classification treats HELLP syndrome as a type of preeclampsia rather than a parallel entity.

Chronic hypertension
Chronic hypertension is a type of high blood pressure in a pregnant woman that is pre-existing before conception, diagnosed early in pregnancy, or persists significantly after the end of pregnancy. It affects about 5% of all pregnancies and can be a primary disorder of essential hypertension or secondary to another condition; it is not caused by pregnancy itself.The diagnostic criteria for chronic hypertension are typically considered to be at least two separate blood pressure readings taken at least four hours apart with systolic blood pressure ≥ 140mmHg, diastolic blood pressure ≥90 mmHg, or both, identified before pregnancy, before 20 weeks gestation, or persisting at least 12 weeks after giving birth. However, there is some controversy over the utility of adopting lower thresholds for diagnosis of chronic hypertension, which is more consistent with recent recommendations from the American College of Cardiology and the American Heart Association for the diagnosis of hypertension in adults. Chronic hypertension in pregnancy is now considered mild if blood pressures do not exceed 159 mmHg systolic and 109 mmHg diastolic and severe if pressures are ≥ 160 mmHg systolic or 110 mmHg diastolic, although controversy also exists as to the most appropriate cutoffs for this definition.Because chronic hypertension can progress to more severe forms of disease, it is important to accurately diagnose the condition early, ideally prior to pregnancy, and initiate management to control parental blood pressure. This is often difficult, as many reproductive individuals may not regularly visit the doctor and, when pregnant, may initially present for prenatal care in the second trimester.

Pre-eclampsia and eclampsia
Preeclampsia is a medical condition which usually develops after 20 weeks of gestation and traditionally involves both newly increased blood pressure (blood pressure > 140/90 mmHg) and proteinuria.
Preeclampsia is a leading cause of fetal complications, which include low birth weight, preterm birth, and stillbirth. Women with preeclampsia are encouraged to deliver the child after 37 weeks of gestation to minimize the risks of the severe complications.Preeclampsia can also be diagnosed if a woman has both increased blood pressure and 1 or more signs of significant organ damage. Signs of significant organ damage include:
Severely elevated blood pressure (blood pressure > 160/110)
Thrombocytopenia
Increased or rapidly elevating levels of creatinine in the blood
Increased liver enzymes
Pulmonary edema
New or persistent headaches that do not respond to pain medication
Blurred or altered visionIf a woman with preeclampsia has any of these signs of significant organ damage, then her condition is classified as preeclampsia with severe features. This diagnosis can be made even if the patient does not have proteinuria. Women with preeclampsia with severe features are encouraged to deliver the child after 34 weeks of gestation to minimize the risks of the severe complications.Preeclampsia can also present with seizures in the pregnant mother. In this case, the patient would be diagnosed with eclampsia.There is no proven way to prevent preeclampsia/eclampsia. Most women who develop signs of preeclampsia, however, are closely monitored to lessen or avoid related problems. The only way to "cure" preeclampsia/eclampsia is to deliver or abort the baby.

Eclampsia
Eclampsia is one particularly concerning form of preeclampsia in which a pregnant woman who previously presented with signs of newly increased blood pressure begins to experience new generalized seizures or coma. Up to 70% of patients with eclampsia experience complications associated with pregnancy. These complications can include HELLP syndrome, acute kidney injury, and disseminated intravascular coagulation among others.

HELLP Syndrome
HELLP Syndrome is a type of preeclampsia with severe features that involves increased hemolysis, increased liver enzymes, and low platelet levels. While most women with HELLP syndrome have high blood pressure and proteinuria, up to 20% of HELLP syndrome cases do not present with these classical signs of preeclampsia. However, like pre-eclampsia, HELLP syndrome can also lead to low birth weight and premature birth of the fetus/neonate. HELLP syndrome has a fetal/neonatal mortality rate of 7-20%.

Preeclampsia superimposed on chronic hypertension
Preeclampsia superimposed on chronic hypertension occurs when a pregnant woman with chronic hypertension develops signs of pre-eclampsia, typically defined as new onset of proteinuria ≥30 mg/dL (1+ in the dipstick) in at least 2 random urine specimens that were collected ≥4 h apart (but within a 7-day interval) or 0.3 g in a 24-h period. Like ordinary pre-eclampsia, superimposed pre-eclampsia can also occur with severe features, which are defined as: systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg despite escalation of antihypertensive therapy; thrombocytopenia (platelet count <100,000/microL); impaired liver function; new-onset or worsening renal insufficiency; pulmonary edema; or persistent cerebral or visual disturbances. As a result, superimposed pre-eclampsia can be diagnosed without proteinuria when a sudden increase in previously well-controlled blood pressure is accompanied by severe features of pre-eclampsia.

Gestational hypertension
Gestational hypertension is a provisional diagnosis that involves newly increased blood pressure in a pregnant woman that usually develops after 20 weeks of gestation, but does not currently show any signs of proteinuria or other features associated with preeclampsia. Up to 50% of gestational hypertension patients go on to develop some form of preeclampsia.Gestational hypertension will normally resolve by 12 weeks postpartum. In this case, the diagnosis of gestational hypertension will be updated to be transient hypertension of pregnancy. If the increased blood pressure does not resolve by 12 weeks postpartum, then the diagnosis of gestational hypertension will be updated to be chronic hypertension.

Prevention
Blood pressure control can be accomplished before pregnancy. Medications can control blood pressure. Certain medications may not be ideal for blood pressure control during pregnancy such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (AII) receptor antagonists. Controlling weight gain during pregnancy can help reduce the risk of hypertension during pregnancy.There is limited evidence to suggest that calcium supplementation may reduce the risk of pre-eclampsia or stillbirth but it is unclear if it has other benefits.

Management
The only way to definitively treat a hypertensive disease of pregnancy (i.e. preeclampsia/eclampsia, gestational hypertension, etc. ) is to deliver the fetus. This prevents further development of complications related to the disorder in both the mother and the fetus. Therefore, the first line approach to management of these conditions is to consider induction of preterm labor. The exact timing of when to induce labor is dependent on the severity of symptoms related to the hypertensive disease, as well as the medical condition of both the mother and the fetus. Generally, in mothers with preeclampsia, labor is induced once the gestational age is >37 weeks. In patients with preeclampsia with severe features or eclampsia, labor is induced once the gestational age is >34 weeks. In patients with gestational hypertension and no other signs of severe disease, labor is generally induced at term.In cases where the fetus has not yet reached a safe gestational age to be delivered, management is focused on managing symptoms to give the fetus more time to mature. In women with gestational hypertension, some studies have found that usage of baby aspirin can prevent the progression of the condition to preeclampsia/eclampsia and reduce the risk of complications associated with hypertensive disorders of pregnancy.Pregnant women with chronic hypertension diagnosed before or early in pregnancy should be evaluated to identify the underlying cause of hypertension as well as possible existing end-organ damage caused by hypertension, such as cardiac and kidney injury. Although most cases of chronic hypertension are primary, and thus classified as essential hypertension, secondary causes such as renal, vascular, and endocrine disorders must also be considered, especially in patients with chronic hypertension presenting abnormally, for instance at a young age or refractory to first-line treatment. If end-organ damage or an underlying cause of hypertension is identified, these conditions must also be treated. Women with chronic hypertension in pregnancy must be closely monitored because they are five times as likely as those with normal blood pressure to develop pre-eclampsia, which is a much more severe condition with serious risks for the mother and fetus.For all hypertensive disorders of pregnancy, a major component of care is management of the associated hypertension. This involves use of antihypertensive medication as well as restricting activity to lower blood pressure to reduce the risk of stroke. In women with preeclampsia or eclampsia, magnesium sulfate is often prescribed to prevent the occurrence of seizures in the gestational parent </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 Gastroschisis and can you explain it in depth? [/INST] Gastroschisis is a birth defect in which the babys intestines extend outside of the abdomen through a hole next to the belly button. The size of the hole is variable, and other organs including the stomach and liver may also occur outside the babys body. Complications may include feeding problems, prematurity, intestinal atresia, and intrauterine growth restriction.The cause is typically unknown. Rates are higher in babies born to mothers who smoke, drink alcohol, or are younger than 20 years old. Ultrasounds during pregnancy may make the diagnosis. Otherwise diagnosis occurs at birth. It differs from omphalocele in that there is no covering membrane over the intestines.Treatment involves surgery. This typically occurs shortly after birth. In those with large defects the exposed organs may be covered with a special material and slowly moved back into the abdomen. The condition affects about 4 per 10,000 newborns. Rates of the condition appear to be increasing.

Signs and symptoms
There are no signs during pregnancy.  About sixty percent of infants with gastroschisis are born prematurely. At birth, the baby will have a relatively small (<4 cm) hole in the abdominal wall, usually just to the right of the belly button. Some of the intestines are usually outside the body, passing through this opening.  In rare circumstances, the liver and stomach may also come through the abdominal wall. After birth these organs are directly exposed to air.

Causes
The cause of gastroschisis is not known.  There may be genetic causes in some cases, and there may be environmental factors to which the mother is exposed during pregnancy.Risk factors include the mother being young, and use of alcohol or tobacco.

Pathophysiology
During the fourth week of human embryonic development, the lateral body wall folds of the embryo meet at the midline and fuse together to form the anterior body wall. However, in gastroschisis and other anterior body wall defects, this fails to occur by either one or both of the lateral body wall folds not moving properly to meet with the other and fusing together. This incomplete fusion results in a defect that allows abdominal organs to protrude through the abdominal wall, and the intestines typically herniate through the rectus abdominis muscle, lying to the right of the umbilicus. The forces responsible for the movement of the lateral body wall folds are poorly understood, and a better understanding of these forces would help to explain why gastroschisis occurs mostly to the right of the umbilicus, while other ventral body wall defects occur in the midline.At least six hypotheses have been proposed for the pathophysiology:

Failure of mesoderm to form in the body wall
Rupture of the amnion around the umbilical ring with subsequent herniation of bowel
Abnormal involution of the right umbilical vein leading to weakening of the body wall and gut herniation
Disruption of the right vitelline (yolk sac) artery with subsequent body wall damage and gut herniation
Abnormal folding of the body wall results in a ventral body wall defect through which the gut herniates
Failure to incorporate the yolk sac and related vitelline structures into the umbilical stalkThe first hypothesis does not explain why the mesoderm defect would occur in such a specific small area. The second hypothesis does not explain the low percentage of associated abnormality compared with omphalocele. The third hypothesis was criticized due to no vascular supplement of anterior abdominal wall by umbilical vein </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 Hyperemesis gravidarum and can you explain it in depth? [/INST] Hyperemesis gravidarum (HG) is a pregnancy complication that is characterized by severe nausea, vomiting, weight loss, and possibly dehydration. Feeling faint may also occur. It is considered more severe than morning sickness. Symptoms often get better after the 20th week of pregnancy but may last the entire pregnancy duration.The exact causes of hyperemesis gravidarum are unknown. Risk factors include the first pregnancy, multiple pregnancy, obesity, prior or family history of HG, trophoblastic disorder, and a history of eating disorders. Diagnosis is usually made based on the observed signs and symptoms. HG has been technically defined as more than three episodes of vomiting per day such that weight loss of 5% or three kilograms has occurred and ketones are present in the urine. Other potential causes of the symptoms should be excluded, including urinary tract infection and an overactive thyroid.Treatment includes drinking fluids and a bland diet. Recommendations may include electrolyte-replacement drinks, thiamine, and a higher protein diet. Some people require intravenous fluids. With respect to medications, pyridoxine or metoclopramide are preferred. Prochlorperazine, dimenhydrinate, ondansetron (sold under the brand-name Zofran) or corticosteroids may be used if these are not effective. Hospitalization may be required due to the severe symptoms associated. Psychotherapy may improve outcomes. Evidence for acupressure is poor.While vomiting in pregnancy has been described as early as 2,000 BC, the first clear medical description of HG was in 1852 by Paul Antoine Dubois. HG is estimated to affect 0.3–2.0% of pregnant women, although some sources say the figure can be as high as 3%. While previously known as a common cause of death in pregnancy, with proper treatment this is now very rare. Those affected have a lower risk of miscarriage but a higher risk of premature birth. Some pregnant women choose to have an abortion due to HG symptoms.

Signs and symptoms
When vomiting is severe, it may result in the following:
Loss of 5% or more of pre-pregnancy body weight
Dehydration, causing ketosis, and constipation
Nutritional disorders, such as vitamin B1 (thiamine) deficiency, vitamin B6 (pyridoxine) deficiency or vitamin B12 (cobalamin) deficiency
Metabolic imbalances such as metabolic ketoacidosis or thyrotoxicosis
Physical and emotional stress
Difficulty with activities of daily livingSymptoms can be aggravated by hunger, fatigue, prenatal vitamins (especially those containing iron), and diet. Many women with HG are extremely sensitive to odors in their environment; certain smells may exacerbate symptoms. Excessive salivation, also known as sialorrhea gravidarum, is another symptom experienced by some women.
Hyperemesis gravidarum tends to occur in the first trimester of pregnancy and lasts significantly longer than morning sickness. While most women will experience near-complete relief of morning sickness symptoms near the beginning of their second trimester, some people with HG will experience severe symptoms until they give birth to their baby, and sometimes even after giving birth.A small percentage rarely vomit, but the nausea still causes most (if not all) of the same issues that hyperemesis with vomiting does.

Causes
There are numerous theories regarding the cause of HG, but the cause remains controversial. It is thought that HG is due to a combination of factors which may vary between women and include genetics. Women with family members who had HG are more likely to develop the disease.One factor is an adverse reaction to the hormonal changes of pregnancy, in particular, elevated levels of beta human chorionic gonadotropin (β-hCG). This theory would also explain why hyperemesis gravidarum is most frequently encountered in the first trimester (often around 8–12 weeks of gestation), as β-hCG levels are highest at that time and decline afterward. Another postulated cause of HG is an increase in maternal levels of estrogens (decreasing intestinal motility and gastric emptying leading to nausea/vomiting).More recently, another cause of HG was discovered: "Evidence suggests abnormal levels of the hormone GDF15 are associated with HG. The validation of a second risk variant, rs1054221, provides further support for GDF15s role in the etiology of HG. Additionally, maternal genes appear to play a more significant role than paternal DNA in contributing to the severity of NVP."

Pathophysiology
Although the pathophysiology of HG is poorly understood, the most commonly accepted theory suggests that levels of β-hCG are associated with it. Leptin, a hormone that inhibits hunger, may also play a role.Possible pathophysiological processes involved are summarized in the following table:

Diagnosis
Hyperemesis gravidarum is considered a diagnosis of exclusion. HG can be associated with serious problems in the mother or baby, such as Wernickes encephalopathy, coagulopathy and peripheral neuropathy.Women experiencing hyperemesis gravidarum often are dehydrated and lose weight despite efforts to eat. The onset of the nausea and vomiting in hyperemesis gravidarum is typically before the 20th week of pregnancy.

Differential diagnosis
Diagnoses to be ruled out include the following:

Investigations
Common investigations include blood urea nitrogen (BUN) and electrolytes, liver function tests, urinalysis, and thyroid function tests. Hematological investigations include hematocrit levels, which are usually raised in HG. An ultrasound scan may be needed to know gestational status and to exclude molar or partial molar pregnancy.

Management
Dry bland food and oral rehydration are first-line treatments. Due to the potential for severe dehydration and other complications, HG is treated as an emergency. If conservative dietary measures fail, more extensive treatment such as the use of antiemetic medications and intravenous rehydration may be required. If oral nutrition is insufficient, intravenous nutritional support may be needed. For women who require hospital admission, thromboembolic stockings or low-molecular-weight heparin may be used as measures to prevent the formation of a blood clot.

Intravenous fluids
Intravenous (IV) hydration often includes supplementation of electrolytes as persistent vomiting frequently leads to a deficiency. Likewise, supplementation for lost thiamine (Vitamin B1) must be considered to reduce the risk of Wernickes encephalopathy. A and B vitamins are depleted within two weeks, so extended malnutrition indicates a need for evaluation and supplementation. In addition, electrolyte levels should be monitored and supplemented; of particular concern are sodium and potassium.
After IV rehydration is completed, patients typically begin to tolerate frequent small liquid or bland meals. After rehydration, treatment focuses on managing symptoms to allow normal intake of food. However, cycles of hydration and dehydration can occur, making continuing care necessary. Home care is available in the form of a peripherally inserted central catheter (PICC) line for hydration and nutrition.  Home treatment is often less expensive and reduces the risk for a hospital-acquired infection compared with long-term or repeated hospitalizations.

Medications
A number of antiemetics are effective and safe in pregnancy including: pyridoxine/doxylamine, antihistamines (such as diphenhydramine), and phenothiazines (such as promethazine). With respect to effectiveness, it is unknown if one is superior to another for relieving nausea or vomiting. Limited evidence from published clinical trials suggests the use of medications to treat hyperemesis gravidarum.While pyridoxine/doxylamine, a combination of vitamin B6 and doxylamine, is effective in nausea and vomiting of pregnancy, some have questioned its effectiveness in HG.Ondansetron may be beneficial, however, there are some concerns regarding an association with cleft palate, and there is little high-quality data. Metoclopramide is also used and relatively well tolerated. Evidence for the use of corticosteroids is weak; there is some evidence that corticosteroid use in pregnant women may slightly increase the risk of cleft lip and cleft palate in the infant and may suppress fetal adrenal activity. However, hydrocortisone and prednisolone are inactivated in the placenta and may be used in the treatment of hyperemesis gravidarum after 12 weeks.Medicinal cannabis has been used to treat pregnancy-associated hyperemesis.

Nutritional support
Women not responding to IV rehydration and medication may require nutritional support. Patients might receive parenteral nutrition (intravenous feeding via a PICC line) or enteral nutrition (via a nasogastric tube or a nasojejunal tube). There is only limited evidence from trials to support the use of vitamin B6 to improve outcome. An oversupply of nutrition (hyperalimentation) may be necessary in certain cases to help maintain volume requirements and allow weight gain. A physician might also prescribe Vitamin B1 (to prevent Wernickes encephalopathy) and folic acid.

Alternative medicine
Acupuncture (both with P6 and traditional method) has been found to be ineffective. The use of ginger products may be helpful, but evidence of effectiveness is limited and inconsistent, though three recent studies support ginger over placebo.

Complications
Pregnant woman
If HG is inadequately treated, anemia, hyponatremia, Wernickes encephalopathy, kidney failure, central pontine myelinolysis, coagulopathy, atrophy, Mallory-Weiss tears, hypoglycemia, jaundice, malnutrition, pneumomediastinum, rhabdomyolysis, deconditioning, deep vein thrombosis, pulmonary embolism, splenic avulsion, or vasospasms of cerebral arteries are possible consequences </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 Superficial pustular folliculitis 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 Attenuated patella alta and can you explain it in depth? [/INST] Attenuated patella alta is an extremely rare condition affecting mobility and leg strength.   It is characterized by an unusually small knee cap (patella) that develops out of and above the joint.  Typically, as the knee cap sits in the joint, it is stimulated to growth by abrasion from the opposing bones.  When not situated properly in the joint, the knee cap does not experience such stimulation and remains small and undeveloped. Note that the cartilage under and around the kneecap is eight times smoother than ice, so "abrasion" may not be the best term.A similar condition, patella alta, can occur as the result of a sports injury, though the large majority of the time it is a congenital/developmental condition that is unrelated to trauma </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 Leukemoid reaction and can you explain it in depth? [/INST] The term leukemoid reaction describes an increased
white blood cell count (> 50,000 cells/μL), which is a physiological response to stress or infection (as opposed to a primary blood malignancy, such as leukemia). It often describes the presence of immature cells such as myeloblasts or red blood cells with nuclei in the peripheral blood.
It may be lymphoid or myeloid.

Causes
As noted above, a leukemoid reaction is typically a response to an underlying medical issue. Causes of leukemoid reactions include:
Severe hemorrhage (retroperitoneal hemorrhage)
Drugs
Use of sulfa drugs
Use of dapsone
Use of glucocorticoids
Use of G-CSF or related growth factors
All-trans retinoic acid (ATRA)
Ethylene glycol intoxication
Infections
Clostridium difficile
Tuberculosis
Pertussis
Infectious mononucleosis (lymphocyte predominant)
Visceral larva migrans (eosinophil predominant)
Asplenia
Diabetic ketoacidosis
Organ necrosis
Hepatic necrosis
Ischemic colitis
As a feature of trisomy 21 in infancy (incidence of ~10%)
As a paraneoplastic phenomenon (rare)

Diagnosis
Conventionally, a leukocytosis exceeding 50,000 WBC/mm3 with a significant increase in early neutrophil precursors is referred to as a leukemoid reaction </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 Giant solitary trichoepithelioma 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 Autosomal dominant multiple pterygium syndrome 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 Corpus luteum cyst and can you explain it in depth? [/INST] A corpus luteum cyst is a type of ovarian cyst which may rupture about the time of menstruation, and take up to three months to disappear entirely. A corpus luteum cyst rarely occurs in women over the age of 50, because eggs are no longer being released after menopause. Corpus luteum cysts may contain blood and other fluids. The physical shape of a corpus luteum cyst may appear as an enlargement of the ovary itself,  rather than a distinct mass -like growth on the surface of the ovary.

Signs and symptoms
Corpus luteum cysts are a normal part of the menstrual cycle. They can, however, grow to almost 10 cm (4 inches) in diameter and have the potential to bleed into themselves or twist the ovary, causing pelvic or abdominal pain.  It is possible the cyst may rupture, causing internal bleeding and pain. This pain typically disappears within a few days of the rupture. If the corpus luteum becomes large it may cause ovarian torsion, where the ovary twists and blood flow is cut off. Ovarian torsion is rare and is accompanied by severe pain.

Pathophysiology
This type of functional cyst occurs after an egg has been released from a follicle.  The follicle then becomes a secretory gland that is known as the corpus luteum </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 Voyeurism and can you explain it in depth? [/INST] Voyeurism is the sexual interest in or practice of watching other people engaged in intimate behaviors, such as undressing, sexual activity, or other actions usually considered to be of a private nature.The term comes from the French voir which means "to see". A male voyeur is commonly labelled as "Peeping Tom" or a "Jags", a term which originates from the Lady Godiva legend. However, that term is usually applied to a male who observes somebody secretly and, generally, not in a public space.
The American Psychiatric Association has classified certain voyeuristic fantasies, urges and behaviour patterns as a paraphilia in the Diagnostic and Statistical Manual (DSM-IV) if the person has acted on these urges, or the sexual urges or fantasies cause marked distress or interpersonal difficulty. It is described as a disorder of sexual preference in the ICD-10. The DSM-IV defines voyeurism as the act of looking at "unsuspecting individuals, usually strangers, who are naked, in the process of disrobing, or engaging in sexual activity". The diagnosis would not be given to people who experience typical sexual arousal simply by seeing nudity or sexual activity. In order to be diagnosed with voyeuristic disorder the symptoms must persist for over six months and the person in question must be over the age of 18.

Historical perspectives
There is relatively little academic research regarding voyeurism. When a review was published in 1976 there were only 15 available resources. Voyeurs were well-paying hole-lookers in especially Parisian brothels, a commercial innovation described as far back as 1857 but not gaining much notoriety until the 1880s, and not attracting formal medical-forensic recognition until the early 1890s. Society has accepted the use of the term voyeur as a description of anyone who views the intimate lives of others, even outside of a sexual context. This term is specifically used regarding reality television and other media which allow people to view the personal lives of others. This is a reversal from the historical perspective, moving from a term which describes a specific population in detail, to one which describes the general population vaguely.
One of the few historical theories on the causes of voyeurism comes from psychoanalytic theory. Psychoanalytic theory proposes that voyeurism results from a failure to accept castration anxiety and as a result of failure to identify with the father.

Prevalence
Voyeurism has high prevalence rates in most studied populations. Voyeurism was initially believed to only be present in a small portion of the population. This perception changed when Alfred Kinsey discovered that 30% of men prefer coitus with the lights on. This behaviour is not considered voyeurism by todays diagnostic standards, but there was little differentiation between normal and pathological behaviour at the time. Subsequent research showed that 65% of men had engaged in peeping, which suggests that this behaviour is widely spread throughout the population. Congruent with this, research found voyeurism to be the most common sexual law-breaking behaviour in both clinical and general populations.

An earlier study, based on 60 college men from a rural area, indicates that 54% had voyeuristic fantasies, and that 42% had tried voyeurism, concluding that young men are more easily aroused by the idea.In a national study of Sweden it was found that 7.7% of the population (16% of men and 4% of women) had engaged in voyeurism at some point. It is also believed that voyeurism occurs up to 150 times more frequently than police reports indicate. This same study also indicates that there are high levels of co-occurrence between voyeurism and exhibitionism, finding that 63% of voyeurs also report exhibitionist behaviour.

Characteristics
People engage in voyeuristic behaviours for diverse reasons, but statistics can indicate which groups are likelier to engage in the act.
Early research indicated that voyeurs were more mentally healthy than other groups with paraphilias. Compared to the other groups studied, it was found that voyeurs were unlikely to be alcoholics or drug users. More recent research shows that, compared to the general population, voyeurs were moderately more likely to have psychological problems, use alcohol and drugs, and have higher sexual interest generally. This study also shows that voyeurs have a greater number of sexual partners per year, and are more likely to have had a same-sex partner than most of the populations. Both older and newer research found that voyeurs typically have a later age of first sexual intercourse. However, other research found no difference in sexual history between voyeurs and non-voyeurs. Voyeurs who are not also exhibitionists tend to be from a higher socioeconomic status than those who do show exhibitionist behaviour.

Gender differences
Research shows that, like almost all paraphilias, voyeurism is more common in men than in women. However, research has found that men and women both report roughly the same likelihood that they would hypothetically engage in voyeurism. There appears to be a greater gender difference when actually presented with the opportunity to perform voyeurism. There is very little research done on voyeurism in women, so very little is known on the subject. One of the few studies deals with a case study of a woman who also had schizoid personality disorder, which limits the degree to which it can generalize to normal populations.A 2021 study found that 36.4% of men and 63.8% of women were strongly repulsed by the idea of voyeurism. Men were more likely to be mildly or moderately aroused than women, but there was little gender difference among those who reported strong arousal. Men reported slightly higher willingness to commit voyeurism but, when risk is introduced, willingness diminishes in both sexes proportionally to the risk involved. Individual differences in sociosexuality and sexual compulsivity were found to contribute to the sex differences in voyeurism.

Current perspectives
Lovemap theory suggests that voyeurism exists because looking at naked others shifts from an ancillary sexual behaviour, to a primary sexual act. This results in a displacement of sexual desire making the act of watching someone the primary means of sexual satisfaction.
Voyeurism has also been linked with obsessive–compulsive disorder (OCD). When treated by the same approach as OCD, voyeuristic behaviours significantly decrease.

Treatment
Professional treatment
Historically voyeurism has been treated in a variety of ways. Psychoanalytic, group psychotherapy and shock aversion approaches have all been attempted with limited success. There is some evidence which shows that pornography can be used as a form of treatment for voyeurism. This is based on the idea that countries with pornography censorship have high amounts of voyeurism. Additionally shifting voyeurs from voyeuristic behaviour, to looking at graphic pornography, to looking at the nudes in Playboy has been successfully used as a treatment. These studies show that pornography can be used as a means of satisfying voyeuristic desires without breaking the law.
Voyeurism has also been successfully treated with a mix of anti-psychotics and antidepressants. However the patient in this case study had a multitude of other mental health problems. Intense pharmaceutical treatment may not be required for most voyeurs.There has also been success in treating voyeurism through using treatment methods for obsessive compulsive disorder. There have been multiple instances of successful treatment of voyeurism through putting patients on fluoxetine and treating their voyeuristic behaviour as a compulsion.

Techniques
The increased miniaturisation of hidden cameras and recording devices since the 1950s has enabled those so minded to surreptitiously photograph or record others without their knowledge and consent. The vast majority of mobile phones, for example, are readily available to be used for their camera and recording ability.

Criminology
Non-consensual voyeurism is considered to be a form of sexual abuse.
When the interest in a particular subject is obsessive, the behaviour may be described as stalking.
The United States FBI assert that some individuals who engage in "nuisance" offences (such as voyeurism) may also have a propensity for violence based on behaviours of serious sex offenders.  An FBI researcher has suggested that voyeurs are likely to demonstrate some characteristics that are common, but not universal, among serious sexual offenders who invest considerable time and effort in the capturing of a victim (or image of a victim); careful, methodical planning devoted to the selection and preparation of equipment; and often meticulous attention to detail.Little to no research has been done into the demographics of voyeurs.

Legal status
Voyeurism is not a crime at common law. In common law countries it is only a crime if made so by legislation.
In Canada, for example, voyeurism was not a crime when the case Frey v. Fedoruk et al. arose in 1947.  In that case, in 1950, the Supreme Court of Canada held that courts could not criminalise voyeurism by classifying it as a breach of the peace and that Parliament would have to specifically outlaw it.  On November 1, 2005, this was done when section 162 was added to the Canadian Criminal Code, declaring voyeurism to be a sexual offence when it violates a reasonable expectation of privacy. In the case of R v Jarvis, the Supreme Court of Canada held that for the purposes of that law, the expectation of privacy is not all-or-nothing; rather there are degrees of privacy, and although secondary-school pupils in the school building cannot reasonably expect as much privacy as in the bedroom, nonetheless they can expect enough privacy so that photographing them without their consent for the purpose of sexual gratification is forbidden.In some countries voyeurism is considered to be a sex crime. In the United Kingdom, for example, non-consensual voyeurism became a criminal offence on May 1, 2004. In the English case of R v Turner (2006), the manager of a sports centre filmed four women taking showers. There was no indication that the footage had been shown to anyone else or distributed in any way. The defendant pleaded guilty. The Court of Appeal confirmed a sentence of nine months imprisonment to reflect the seriousness of the abuse of trust and the traumatic effect on the victims.
In another English case in 2009, R v Wilkins (2010), a man who filmed his intercourse with five of his lovers for his own private viewing was sentenced to eight months in prison and ordered to sign onto the Sex Offender Register for ten years. In 2013, 40-year-old Mark Lancaster was found guilty of voyeurism and jailed for 16 months, after he tricked an 18-year-old student into traveling to a rented flat in Milton Keynes, where he filmed her with four secret cameras dressing up as a schoolgirl and posing for photographs before he had sex with her.In a more recent English case in 2020, the Court of Appeal upheld the conviction of Tony Richards after Richards sought "to have two voyeurism charges under section 67 of the Sexual Offences Act dismissed on the grounds that he had committed no crime". Richards "secretly videoed himself having sex with two women who had consented to sex in return for money but had not agreed to being captured on camera". In an unusual step, the court allowed Emily Hunt, a person not involved in the case, to intervene on behalf of the Crown Prosecution Service (CPS). Hunt had an ongoing judicial review against the CPS since the CPS had argued that Hunts alleged attacker had not violated the law when he "took a video lasting over one minute of her naked and unconscious" in a hotel room on the basis that there should be no expectation of privacy in the bedroom. However, in terms of what is considered a private act for the purposes of voyeurism, the CPS was arguing the opposite in the Richards appeal </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 Elbow fracture 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 Meningioma and can you explain it in depth? [/INST] Meningioma, also known as meningeal tumor, is typically a slow-growing tumor that forms from the meninges, the membranous layers surrounding the brain and spinal cord. Symptoms depend on the location and occur as a result of the tumor pressing on nearby tissue. Many cases never produce symptoms. Occasionally seizures, dementia, trouble talking, vision problems, one sided weakness, or loss of bladder control may occur.Risk factors include exposure to ionizing radiation such as during radiation therapy, a family history of the condition, and neurofibromatosis type 2. As of 2014 they do not appear to be related to cell phone use. They appear to be able to form from a number of different types of cells including arachnoid cells. Diagnosis is typically by medical imaging.If there are no symptoms, periodic observation may be all that is required. Most cases that result in symptoms can be cured by surgery. Following complete removal fewer than 20% recur. If surgery is not possible or all the tumor cannot be removed radiosurgery may be helpful. Chemotherapy has not been found to be useful. A small percentage grow rapidly and are associated with worse outcomes.About one per thousand people in the United States are currently affected. Onset is usually in adults. In this group they represent about 30% of brain tumors. Women are affected about twice as often as men. Meningiomata were reported as early as 1614 by Felix Plater.

Signs and symptoms
Small tumors (e.g., < 2.0 cm) usually are incidental findings at autopsy without having caused symptoms. Larger tumors may cause symptoms, depending on the size and location.
Focal seizures may be caused by meningiomata that overlie the cerebrum.
Progressive spastic weakness in legs and incontinence may be caused by tumors that overlie the parasagittal frontoparietal region.
Tumors of the Sylvian aqueduct may cause myriad motor, sensory, aphasic, and seizure symptoms, depending on the location.
Increased intracranial pressure eventually occurs, but is less frequent than in gliomas.
Diplopia (Double vision) or uneven pupil size may be symptoms if related pressure causes a third and/or sixth nerve palsy.

Causes
The causes of meningiomata are not well understood. Most cases are sporadic, appearing randomly, while some are familial. Persons who have undergone radiation, especially to the scalp, are more at risk for developing meningiomata, as are those who have had a brain injury. Atomic bomb survivors from Hiroshima had a higher than typical frequency of developing meningiomata, with the incidence increasing the closer that they were to the site of the explosion. Dental X-rays are correlated with an increased risk of meningioma, in particular for people who had frequent dental X-rays in the past, when the X-ray dose of a dental X-ray was higher than in the present.Having excess body fat increases the risk.A 2012 review found that mobile telephone use was unrelated to meningioma.People with neurofibromatosis type 2 (NF-2) have a 50% chance of developing one or more meningiomata.Ninety-two percent of meningiomata are benign. Eight percent are either atypical or malignant.

Genetics
The most frequent genetic mutations (~50%) involved in meningiomata are inactivation mutations in the neurofibromatosis 2 gene (merlin) on chromosome 22q.TRAF7 mutations are present in about one-fourth of meningiomata. Mutations in the TRAF7, KLF4, AKT1, and SMO genes are commonly expressed in benign skull-base meningiomata. Mutations in NF2 are commonly expressed in meningiomata located in the cerebral and cerebellar hemispheres.

Pathophysiology
Meningiomata arise from arachnoidal cap cells, most of which are near the vicinity of the venous sinuses, and this is the site of greatest prevalence for meningioma formation. Some subtypes may arise from the pial cap cells that migrate during the development together with blood vessels into the brain parenchyma. They most frequently are attached to the dura over the superior parasagittal surface of frontal and parietal lobes, along the sphenoid ridge, in the olfactory grooves, the sylvian region, superior cerebellum along the falx cerebri, cerebellopontine angle, and the spinal cord. The tumor is usually gray, well-circumscribed, and takes on the form of the space it occupies. They usually are dome-shaped, with the base lying on the dura.

Locations
Parasagittal/falcine (25%)
Convexity (surface of the brain) (19%)
Sphenoid ridge (17%)
Suprasellar (9%)
Posterior fossa (8%)
Olfactory groove (8%)
Middle fossa/Meckels cave (4%)
Tentorial (3%)
Peri-torcular (3%)
Intraparenchymal (rare)Other uncommon locations are the lateral ventricle, foramen magnum, and the orbit/optic nerve sheath. Meningiomata also may occur as a spinal tumor, more often in women than in men. This occurs more often in Western countries than Asian.Histologically, meningioma cells are relatively uniform, with a tendency to encircle one another, forming whorls and psammoma bodies (laminated calcific concretions). As such, they also have a tendency to calcify and are highly vascularized.Meningiomata often are considered benign tumors that can be removed by surgery, but most recurrent meningiomata correspond to histologic benign tumors. The metabolic phenotype of these benign recurrent meningiomata indicated an aggressive metabolism resembling that observed for atypical meningioma.

Diagnosis
Meningiomata are visualized readily with contrast CT, MRI with gadolinium, and arteriography, all attributed to the fact that meningiomata are extra-axial and vascularized. CSF protein levels are usually found to be elevated when lumbar puncture is used to obtain spinal fluid. On T1-weighted contrast-enhanced MRI, they may show a typical dural tail sign absent in some rare forms of meningiomas.Although the majority of meningiomata are benign, they may have malignant presentations.  Classification of meningiomata are based upon the WHO classification system.
Benign (Grade I) – (90%) – meningothelial, fibrous, transitional, psammomatous, angioblastic
Atypical (Grade II) – (7%) – chordoid, clear cell, atypical (includes brain invasion)
Anaplastic/malignant (Grade III) – (2%) – papillary, rhabdoid, anaplastic (most aggressive)In a 2008 review of the latter two categories, atypical and anaplastic-meningioma cases, the mean overall survival for atypical meningiomata was found to be 11.9 years vs. 3.3 years for anaplastic meningiomata. Mean relapse-free survival for atypical meningiomata was 11.5 years vs. 2.7 years for anaplastic meningiomata.Malignant anaplastic meningioma is aggressive. Although anaplastic meningioma has higher chances of distant metastasis than the other two types, the overall incidence of meningioma metastasis is only 0.18%; which is considered rare. Even if, by general rule, neoplasms of the nervous system (brain tumors) cannot metastasize into the body because of the blood–brain barrier, anaplastic meningioma can. Although they are inside the cerebral cavity, they are located on the bloodside of the BBB, because meningiomata tend to be connected to blood vessels. Thus, cancerized cells can escape into the bloodstream, which is why meningiomata, when they metastasize, often turn up around the lungs.Anaplastic meningioma and hemangiopericytoma are difficult to distinguish, even by pathological means, as they look similar, especially, if the first occurrence is a meningeal tumor, and both tumors occur in the same types of tissue.Although usually benign a "petro-clival" menigioma is typically fatal without treatment due to its location. Until the 1970s no treatment was available for this type of meningioma; however, since that time a range of surgical and radiological treatments have evolved. Nevertheless, the treatment of this type of meningioma remains a challenge with relatively frequent poor outcomes.

Prevention
The risk of meningioma can be reduced by maintaining a normal body weight, and by avoiding unnecessary dental x-rays.

Treatment
Observation
Observation with close imaging follow-up may be used in select cases if a meningioma is small and asymptomatic. In a retrospective study on 43 patients, 63% of patients were found to have no growth on follow-up, and the 37% found to have growth at an average of 4 mm / year. In this study, younger patients were found to have tumors that were more likely to have grown on repeat imaging; thus are poorer candidates for observation. In another study, clinical outcomes were compared for 213 patients undergoing surgery vs. 351 patients under watchful observation. Only 6% of the conservatively treated patients developed symptoms later, while among the surgically treated patients, 5.6% developed persistent morbid condition, and 9.4% developed surgery-related morbid condition.Observation is not recommended in tumors already causing symptoms. Furthermore, close follow-up with imaging is required with an observation strategy to rule out an enlarging tumor.

Surgery
Meningiomata usually can be surgically resected (removed) and result in a permanent cure if the tumor is superficial on the dural surface and easily accessible. Transarterial embolization has become a standard preoperative procedure in the preoperative management. If invasion of the adjacent bone occurs, total removal is nearly impossible. It is rare for benign meningiomata to become malignant.The probability of a tumor recurring or growing after surgery may be estimated by comparing the tumors WHO (World Health Organization) grade and by the extent of surgery by the Simpson Criteria.

Radiation therapy
Radiation therapy may include photon-beam or proton-beam treatment, or fractionated external beam radiation.  Radiosurgery may be used in lieu of surgery in small tumors located away from critical structures. Fractionated external-beam radiation also can be used as primary treatment for tumors that are surgically unresectable or, for patients who are inoperable for medical reasons.Radiation therapy often is considered for WHO grade I meningiomata after subtotal (incomplete) tumor resections. The clinical decision to irradiate after a subtotal resection is somewhat controversial, as no class I randomized, controlled trials exist on the subject. Numerous retrospective studies, however, have suggested strongly that the addition of postoperative radiation to incomplete resections improves both progression-free survival (i.e. prevents tumor recurrence) and improves overall survival.In the case of a  grade III meningioma, the current standard of care involves postoperative radiation treatment regardless of the degree of surgical resection.  This is due to the proportionally higher rate of local recurrence for these higher-grade tumors.  Grade II tumors may behave variably and there is no standard of whether to give radiotherapy following a gross total resection. Subtotally resected grade II tumors should be radiated.

Chemotherapy
Likely, current chemotherapies are not effective. Antiprogestin agents have been used, but with variable results. A 2007 study of whether hydroxyurea has the capacity to shrink unresectable or recurrent meningiomata is being further evaluated.

Epidemiology
Many individuals have meningiomata, but remain asymptomatic, so the meningiomata are discovered during an autopsy. One to two percent of all autopsies reveal meningiomata that were unknown to the individuals during their lifetime, since there were never any symptoms. In the 1970s, tumors causing symptoms were discovered in 2 out of 100,000 people, while tumors discovered without causing symptoms occurred in 5.7 out of 100,000, for a total incidence of 7.7/100,000. With the advent of modern sophisticated imaging systems such as CT scans, the discovery of asymptomatic meningiomata has tripled.Meningiomata are more likely to appear in women than men, though when they appear in men, they are more likely to be malignant. Meningiomata may appear at any age, but most commonly are noticed in men and women age 50 or older, with meningiomata becoming more likely with age. They have been observed in all cultures, Western and Eastern, in roughly the same statistical frequency as other possible brain tumors.

History
The neoplasms currently referred to as meningiomata were referred to with a wide range of names in older medical literature, depending on the source. Various descriptors included "fungoid tumors", "fungus of the dura mater", "epithelioma", "psammoma", "dural sarcoma", "dural endothelioma", "fibrosarcoma", "angioendothelioma", "arachnoidal fibroboastoma", "endotheliosis of the meninges", "meningeal fibroblastoma", "meningoblastoma", "mestothelioma of the meninges", "sarcoma of the dura", and others.The modern term of "meningioma" was used first by Harvey Cushing (1869–1939) in 1922, to describe a set of tumors that occur throughout the neuraxis (brain and spinal cord), but have various commonalities. Charles Oberling then separated these into subtypes based on cell structure and, over the years, several other researchers have defined dozens of different subtypes as well </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 Irukandji syndrome and can you explain it in depth? [/INST] Irukandji syndrome is a condition that results from envenomation by certain box jellyfish. In rare instances the sting may result in cardiac arrest and death. The most common jellyfish involved is the Carukia barnesi, a species of Irukandji jellyfish. Those stung may experience severe or even excruciating pain.
The syndrome was given its name in 1952 by Hugo Flecker, after the Aboriginal Irukandji people who live in Palm Cove, north of Cairns, Queensland, Australia, where stings are common.

Signs and symptoms
Most stings occur during the summer wet season in October–May in North Queensland, with different seasonal patterns elsewhere. Because the jellyfish are very small, the venom is only injected through the tips of the nematocysts (the cnidocysts) rather than the entire lengths; as a result the sting may barely be noticed at first. It has been described as feeling like little more than a mosquito bite. The symptoms, however, gradually become apparent and then more and more intense in the subsequent 5 to 120 minutes (30 minutes on average). Irukandji syndrome includes an array of systemic symptoms, including severe headache, backache, muscle pains, chest and abdominal pain, nausea and vomiting, sweating, anxiety, hypertension, tachycardia, and pulmonary edema. Symptoms generally improve in four to 30 hours, but may take up to two weeks to resolve completely.

Toxicity
When properly treated, a single sting is almost never fatal; however, two people in Australia are believed to have died from Irukandji stings, which has greatly increased public awareness of Irukandji syndrome. It is unknown how many other deaths from Irukandji syndrome have been wrongly attributed to other causes.

Pathophysiology
The exact mechanism of action of the venom is unknown, but catecholamine excess may be an underlying mechanism in severe cases. Animal studies appear to confirm a relationship between envenoming and an increase in circulating noradrenaline and adrenaline.

Treatment
Similar to other box jellyfish stings, first aid consists of flushing the area with vinegar to neutralize the tentacle stinging apparatus. As no antivenom is available, treatment is largely supportive, with analgesia being the mainstay of management. Nitroglycerin, a common drug used for cardiac conditions, is utilised by medical personnel to minimise the risk of pulmonary edema and to reduce hypertension </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 TEMPI syndrome 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 Eosinophilic bronchitis and can you explain it in depth? [/INST] Eosinophilic bronchitis (EB) is a type of airway inflammation due to excessive mast cell recruitment and activation in the superficial airways as opposed to the smooth muscles of the airways as seen in asthma. It often results in a chronic cough. Lung function tests are usually normal. Inhaled corticosteroids are often an effective treatment.

Signs and symptoms
The most common symptom of eosinophilic bronchitis is a chronic dry cough lasting more than 6–8 weeks. Eosinophilic bronchitis is also defined by the increased number of eosinophils, a type of white blood cell, in the sputum compared to that of healthy people. As patients with asthma usually present with eosinophils in the sputum as well, some literature distinguish the two by classifying the condition as non-asthmatic eosinophilic bronchitis (NAEB) versus eosinophilic bronchitis in asthma. Non-asthmatic eosinophilic bronchitis is different from asthma in that it does not have airflow obstruction or airway hyperresponsiveness. Along with eosinophils, the number of mast cells, another type of white blood cell, is also significantly increased in the bronchial wash fluid of eosinophilic bronchitis patients compared to asthmatic patients and other healthy people. Asthmatic patients, however, have greater number of mast cells that go into the smooth muscle of the airway, distinguishing it from non-asthmatic eosinophilic bronchitis. The increased number of mast cells in the smooth muscle correlate with the increased hyperresponsiveness of the airway seen in asthma patients, and the difference in the mast cell infiltration of the smooth muscle may explain why eosinophilic bronchitis patients do not have airway hyperresponsiveness. Eosinophilic bronchitis has also been linked to other conditions such as COPD, atopic cough, and allergic rhinitis.

Pathophysiology
The number of eosinophils in the sputum samples of non-asthmatic eosinophilic bronchitis patients are similar to those of patients with asthma. In the sputum samples of those with NAEB, histamine and prostaglandin D2 is increased. This suggests that the superficial airways have significant mast cell activation and this may lead to the differing symptom presentation compared to asthma </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 Urethral syndrome 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 Keratolytic winter erythema and can you explain it in depth? [/INST] Keratolytic Winter erythema (also known as Oudtshoorn disease or Oudtshoorn skin) is a rare autosomal dominant skin disease of unknown cause which causes redness and peeling of the skin on the palms and soles. Onset, increased prominence and severity usually occurs during winter. It is a type of genodermatosis.The name "Oudtshoorn skin" derives from the town of Oudtshoorn in the Western Cape province of South Africa, where the disorder was first described. It is one of several genetic disorders known to be highly prevalent among the Afrikaner population.

Presentation
KWE is characterized by a number of anomalies affecting the skin. Erythema causes redness of the skin, which is generally associated with inflammation and irritation. Including erythema and hyperkeratosis (thickening of the stratum corneum), naturally occurring keratolytic peeling and scaling, with increased manifestation in winter, are prevailing features of the disorder.Erythema in KWE has been attributed to necrobiosis (cellular death) within the Malpighian layer (the innermost layer of the epidermis). Peeling and scaling are caused by spreading dissection of the stratum corneum, correlating to the underlying necrobiosis.The effects of KWE appear intermittently as patches on the skin of the palms and soles, with these patches appearing on the limbs, buttocks and torso in severe cases. Facial lesions of this type have also been reported with the disorder, though this is considered to be an extremely rare occurrence.Onset and cyclical recurrence of KWE have shown to be associated with the arrival of winter, or winter-like weather. Worsening of symptoms during this time may be considered as an indicator of recurrent onset in patients known to have the disorder, and age of initial onset can be from early childhood to young adulthood, with attenuation of symptoms sometimes happening after age 30. Patients first exhibiting the disorder at a younger age may also experience worsened symptoms. Currently, no specific correlating factor or reason for winter-related manifestation has been established, though the coldness and dryer air common to winter conditions may be suspect. Winter onset is, however, considered to be a distinguishing feature of KWE among other erythematic skin disorders.When peeling of skin occurs, the newly exposed layer of skin underneath is moist, raw and very sensitive. While this may result in minor discomfort and inconvenience, in severe cases of KWE where large areas of raw skin are present, it is often life-altering and debilitating.
KWE is inherited in an autosomal dominant manner. This means that the defective gene responsible for the disorder is located on an autosome (chromosome 8 is an autosome), and one copy of the defective gene is sufficient to cause the disorder when inherited from a parent who also has the disorder.KWE can begin as a spontaneous mutation, first appearing in an individual with no previous family history of the disorder. This may be due to a genetic predisposition for the disorder, possibly connected to the Oudtshoorn ancestral line.

Genetics
KWE is inherited in an autosomal dominant manner. This means that the defective gene responsible for the disorder is located on an autosome (chromosome 8 is an autosome), and one copy of the defective gene is sufficient to cause the disorder when inherited from a parent who also has the disorder. KWE can begin as a spontaneous mutation, first appearing in an individual with no previous family history of the disorder. This may be due to a genetic predisposition for the disorder, possibly connected to the Oudtshoorn ancestral line.

Pathophysiology
KWE is of unknown cause, as at the present time, no specific mutation of any gene has been established as the cause of the disorder. Research has shown, however, that the gene involved is located on human chromosome 8.  The function of enzymes in general are fundamentally subject to temperature.
A candidate gene is a gene that is suspected to cause a disease or disorder. In KWE, this gene is known to be located in the area between chromosome 8q22 and 8q23. Within this region, the occurrence of loss of heterozygosity (simultaneous loss of function in both alleles of a gene) has been associated with malignancy, including certain types of breast and lung cancer. During the investigation for a KWE candidate gene in this same region, twelve protein transcripts were evaluated between microsatellite markers D8S550 and D8S1759, which is a critical area shown to be the source of KWE pathogenesis </s>