<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 Crush syndrome and can you explain it in depth? [/INST] Crush syndrome (also traumatic rhabdomyolysis or Bywaters syndrome) is a medical condition characterized by major shock and kidney failure after a crushing injury to skeletal muscle. Crush injury is compression of the arms, legs, or other parts of the body that causes muscle swelling and/or neurological disturbances in the affected areas of the body, while crush syndrome is localized crush injury with systemic manifestations. Cases occur commonly in catastrophes such as earthquakes, to individuals that have been trapped under fallen or moving masonry.
People with crushing damage present some of the greatest challenges in field medicine, and may need a physicians attention on the site of their injury. Appropriate physiological preparation of the injured is mandatory. It may be possible to free the patient without amputation; however, field amputations may be necessary in drastic situations.

Pathophysiology
Seigo Minami, a Japanese physician, first reported the crush syndrome in 1923.  He studied the pathology of three soldiers who died in World War I due to kidney failure. The renal changes were due to the buildup of excess myoglobin, resulting from the destruction of muscles from lack of oxygen. These changes can also be seen in persons who are buried alive. The progressive acute kidney failure is because of acute tubular necrosis.
The syndrome was later described by British physician Eric Bywaters in patients during the 1941 wartime bombing of London (the Blitz).  It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release into the bloodstream of muscle breakdown products—notably myoglobin, potassium and phosphorus—that are the products of rhabdomyolysis (the breakdown of skeletal muscle damaged by ischemic conditions).
The specific action on the kidneys is not understood completely, but may be due partly to nephrotoxic metabolites of myoglobin.
The most devastating systemic effects can occur when the crushing pressure is suddenly released, without proper preparation of the patient, causing reperfusion syndrome. In addition to tissue directly suffering the crush mechanism, tissue is then subjected to sudden reoxygenation in the limbs and extremities. Without proper preparation, the patient, with pain control, may be cheerful before recovery, but die shortly thereafter. This sudden failure is called the "smiling death".These systemic effects are caused by a traumatic rhabdomyolysis. As muscle cells die, they absorb sodium, water and calcium; the rhabdomyolysis releases potassium, myoglobin, phosphate, thromboplastin, creatine and creatine kinase.Crush syndrome can directly come from compartment syndrome, if the injury is left untreated. Symptoms include the 5 Ps: pain, pallor, paresthesias (pins and needles), paralysis, and pulselessness.

Treatment
There is no distinct treatment option that can undo the effects and damage from rhabdomyolysis because it is a necrosis. However, the rate of the pathology that can lead to more complications can be decreased by acting early and consistently. Overall treatment depends on preventing kidney failure (renal failure) which is done by rehydrating the patient. It also depends on making urine have a more basic pH (alkalinization of urine).

Immediate untreated crush syndrome death is caused by severe head injury, torso injury with damaged abdominal organs, and asphyxia (excessive loss of oxygen). Early untreated crush syndrome death is caused by hyperkalemia and by hypovolemic shock. Late untreated crush syndrome death is caused by renal failure, coagulopathy and hemorrhage, and sepsis.Due to the risk of crush syndrome, current recommendation to nonprofessional first-aiders (in the UK) is to not release those with a crush injury who have been trapped for more than 15 minutes. Treatment consists of not releasing the tourniquet, overloading the patient with fluid using Dextran 4000 IU, and slow release of pressure. If pressure is released during first aid, then fluid is restricted and an input-output chart for the patient is maintained, and proteins are decreased in the diet.

Field management
As mentioned, permissive hypotension (restrictive fluid therapy) is unwise. Careful fluid overload and administration of intravenous sodium bicarbonate is wise, especially if the crushing weight is on the patient for more than 4 hours, but often if it persists more than one hour. The San Francisco emergency services protocol calls for a basic adult dose of a 2 L bolus of normal saline followed by 500 mL/h, limited for "pediatric patients and patients with history of cardiac or renal dysfunction."Use of a tourniquet can stall the life-threatening consequences of a crush related injury and can be a second option if the person cannot immediately have the fluids that were lost be medically replaced back into the body. Tourniquet measures should be taken if the person has been entrapped for more than 2 hours.

Initial hospital management
The clinician must protect the patient against hypotension, kidney failure, acidosis, hyperkalemia and hypocalcemia. Admission to an intensive care unit, preferably one experienced in trauma medicine, may be appropriate; even well-seeming patients need observation </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 Vascular tumor and can you explain it in depth? [/INST] A vascular tumor is a tumor of vascular origin; a soft tissue growth that can be either benign or malignant, formed from blood vessels or lymph vessels. Examples of vascular tumors include hemangiomas, lymphangiomas, hemangioendotheliomas, Kaposis sarcomas, angiosarcomas, and hemangioblastomas. An angioma refers to any type of benign vascular tumor.Some vascular tumors can be associated with serious blood-clotting disorders, making correct diagnosis critical.A vascular tumor may be described in terms of being highly vascularized, or poorly vascularized, referring to the degree of blood supply to the tumor.

Classification
Vascular tumors make up one of the classifications of vascular anomalies. The other grouping is vascular malformations. Vascular tumors can be further subclassified as being benign, borderline or aggressive, and malignant. Vascular tumors are described as proliferative, and vascular malformations as nonproliferative.

Types
A vascular tumor typically grows quickly by the proliferation of endothelial cells. Most are not birth defects.

Benign
The most common type of benign vascular tumors are hemangiomas, most commonly infantile hemangiomas, and less commonly congenital hemangiomas.

Infantile hemangioma
Infantile hemangiomas are the most common type of vascular tumor to affect babies, accounting for 90% of hemangiomas. They are characterised by the abnormal proliferation of endothelial cells and of deviant blood vessel formation or architecture. Hypoxic stress seems to be a major trigger for this. Infantile hemangiomas are easily diagnosed, and little if any aggressive treatment is needed. They are characterised by rapid growth in the first few months, followed by spontaneous regression in early childhood.

Congenital hemangioma
Congenital hemangiomas are present and fully formed at birth, and only account for 2% of the hemangiomas. They do not have the postnatal phase of proliferation common to infantile hemangiomas. There are two main variants of congenital hemangioma: non-involuting, and rapidly involuting (beginning in the first year of life). A third variant is also recognised as partially involuting. Congenital hemangiomas can also be distinguished from infantile hemangiomas in that neither variant of congenital hemangioma expresses the glucose transporter GLUT 1.Some cases have been associated with a mild form of thrombocytopenia. Rare cases have been associated with heart failure.

Hemangioblastoma
Hemangioblastomas are vascular tumors of the central nervous system.

Pyogenic granuloma
A range of benign vascular tumors are described as reactive proliferative lesions that grow in response to a stimulus, such as trauma, or a local thrombosis. They can also form infrequently during pregnancy as a hormonal reaction affecting the gums.The most common type of reactive proliferative tumors are pyogenic granulomas also known as lobular capillary hemangiomas, that are more often found in children and young adults. These granulomas are well defined growths of less than a centimetre across. They are bright red due to being highly vascularised, and bleed and ulcerate easily. Their colouring fades with age.

Tufted angioma
Tufted angiomas are hereditary hemangiomas found in infants from birth to five years of age, however they may occur in adults. They are found on the neck, shoulders, and trunk as rounded nodules. Tufted angiomas are usually poorly defined lesions of purple colouration. The tumors are of tufts of capillary-sized vessels in lobules that are scattered in the skin, and that sometimes reach into the subcutaneous tissue, and have lymph vessels on the periphery. Their growth is slow to begin with, and progresses to a stable size. They show a high rate of spontaneous regression, particularly in congenital and early-onset cases </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 Cyclopia and can you explain it in depth? [/INST] Cyclopia (named after the Greek mythology character cyclopes) is the most extreme form of holoprosencephaly and is a congenital disorder (birth defect) characterized by the failure of the embryonic prosencephalon to properly divide the orbits of the eye into two cavities. Its incidence is 1 in 16,000 in born animals and 1 in 200 in miscarried fetuses.

Signs and symptoms
Typically, the nose is either missing or not functional. This deformity (called proboscis) forms above the center eye and is characteristic of a form of cyclopia called rhinencephaly or rhinocephaly. Most such embryos are either naturally aborted or are stillborn upon delivery.
Although cyclopia is rare, several cyclopic human babies are preserved in medical museums (e.g. The Vrolik Museum, Amsterdam, Trivandrum Medical College).Some extreme cases of cyclopia have been documented in farm animals (horses, sheep, pigs, and sometimes chickens). In such cases, the nose and mouth fail to form, or the nose grows from the roof of the mouth, obstructing airflow and resulting in suffocation shortly after birth.

Causes
Genetic defects or toxins can misdirect the embryonic forebrain-dividing process. One highly teratogenic alkaloid toxin that can cause cyclopia is cyclopamine or 2-deoxyjervine, found in the plant Veratrum californicum (also known as corn lily or false hellebore). Grazing animals are most likely to ingest this plant and induce cyclopia in offspring. People sometimes accidentally ingest false hellebore while pregnant, thinking it is hellebore, an unrelated plant which does not even resemble false hellebore, being recommended as a "natural" treatment for vomiting, cramps, and poor circulation, three conditions which may be present in the early stages of pregnancy. Cyclopia occurs  when certain proteins are inappropriately expressed, causing the brain to stay whole, rather than developing two distinct hemispheres. This leads to the fetus having one optic lobe and one olfactory lobe, resulting in the eye and nose malformations of cyclopia.The Sonic Hedgehog (SHH) gene regulator is involved in the separation of the single eye field into two bilateral fields.
Although not proven, it is thought that SHH emitted from the prechordal plate suppresses Pax6, which causes the eye field to divide into two. If the SHH gene is mutated, the result is cyclopia, a single eye in the center of the face (Gilbert, 2000).

Notable cases
A British description from 1665 of a colt apparently suffering from cyclopia reads:First, That it had no sign of any Nose in the usual place, nor had it any, in any other place of the Head, unless the double Bagg CC that grew out of the midst of the forehead, were some rudiment of it. Next, That the two Eyes were united into one Double Eye which was placed just in the middle of the Brow.
In October 1766, an infant in France was born with cyclopia, living for only a few hours. Reports of the case were made in the Mercure de France and an illustration of the infant was made by Marie Bihéron. The case was also mentioned in Volume IV of Buffons LHistoire Naturelle.
On 1 March 1793, a 46-year-old woman in Boalts Torp, Glimåkra, Sweden gave birth to a child with cyclopia that died after two hours. The child was 35 cm long, its face without nose and nostrils, and its lidless eye with no eyebrow sat raised on the middle of its forehead like a large blueberry. The wrists were somewhat crooked as well as the right foot which was completely crooked and bent inwards. It was not clear whether it was a boy or a girl, but it was believed to be the former.
On December 28, 2005, a kitten with cyclopia, "Cy", was born in Redmond, Oregon, United States and died about one day after birth.
In 2006, a baby girl in India with cyclopia was born. Her only eye was in the center of her forehead </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 Lethal midline granuloma 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 Reye syndrome and can you explain it in depth? [/INST] Reye syndrome is a rapidly worsening brain disease. Symptoms of Reye syndrome may include vomiting, personality changes, confusion, seizures, and loss of consciousness. While liver toxicity typically occurs in the syndrome, jaundice usually does not. Death occurs in 20–40% of those affected with Reye syndrome, and about a third of those who survive are left with a significant degree of brain damage.The cause of Reye syndrome is unknown. It usually begins shortly after recovery from a viral infection, such as influenza or chickenpox. About 90% of cases in children are associated with aspirin (salicylate) use. Inborn errors of metabolism are also a risk factor. The syndrome is associated with changes on blood tests such as a high blood ammonia level, low blood sugar level, and prolonged prothrombin time. Often, the liver is enlarged in the syndrome.Prevention is typically by avoiding the use of aspirin in children. When aspirin was withdrawn for use in children in the US and UK in the 1980s, a decrease of more than 90% in rates of Reye syndrome was seen. Early diagnosis of the syndrome improves outcomes. Treatment is supportive; mannitol may be used to help with the brain swelling.The first detailed description of Reye syndrome was in 1963 by Australian pathologist Douglas Reye. The syndrome most commonly affects children. It affects fewer than one in a million children a year. The general recommendation to use aspirin in children was withdrawn because of Reye syndrome, with use only recommended in Kawasaki disease.

Signs and symptoms
Reye syndrome progresses through five stages:
Stage I
Vasoconstrictive rash on palms of hands and feet
Persistent, heavy vomiting that is not relieved by not eating
Generalized lethargy
Confusion
Nightmares (possible symptom)
No fever usually present
Headaches
Stage II
Stupor
Hyperventilation
Fatty liver (found on biopsy)
Hyperactive reflexes
Stage III
Continuation of Stage I and II symptoms
Possible coma
Possible cerebral edema
Rarely, respiratory arrest
Stage IV
Deepening coma
Dilated pupils with minimal response to light
Minimal but still present liver dysfunction
Stage V
Very rapid onset following stage IV
Deep coma
Seizures
Multiple organ failure
Flaccidity
Hyperammonemia (above 300 mg/dL of blood)
Death

Causes
The cause of Reye syndrome is unknown. It usually begins shortly after recovery from a viral infection, such as influenza or chickenpox. About 90% of cases in children are associated with aspirin (salicylate) use. Inborn errors of metabolism are also a risk factor.The association with aspirin has been shown through epidemiological studies. The diagnosis of Reye syndrome greatly decreased in the 1980s, when genetic testing for inborn errors of metabolism was becoming available in developed countries. A retrospective study of 49 survivors of cases diagnosed as Reye syndrome showed that the majority of the surviving patients had various metabolic disorders, particularly a fatty-acid oxidation disorder medium-chain acyl-CoA dehydrogenase deficiency.

Aspirin
There is an association between taking aspirin for viral illnesses and the development of Reye syndrome, but no animal model of Reye syndrome has been developed in which aspirin causes the condition.The serious symptoms of Reye syndrome appear to result from damage to cellular mitochondria, at least in the liver, and there is a number of ways that aspirin could cause or exacerbate mitochondrial damage. A potential increased risk of developing Reye syndrome is one of the main reasons that aspirin has not been recommended for use in children and teenagers, the age group for which the risk of lasting serious effects is highest.In some countries, oral mouthcare product Bonjela (not the form specifically designed for teething) has labeling cautioning against its use in children, given its salicylate content. There have been no cases of Reye syndrome following its use, and the measure is a precaution.  Other medications containing salicylates are often similarly labeled as a precaution.The Centers for Disease Control and Prevention (CDC), the U.S. Surgeon General, the American Academy of Pediatrics (AAP) and the Food and Drug Administration (FDA) recommend that aspirin and combination products containing aspirin not be given to children under 19 years of age during episodes of fever-causing illnesses. Hence, in the United States, it is advised that the opinion of a doctor or pharmacist should be obtained before anyone under 19 years of age is given any medication containing aspirin (also known on some medicine labels as acetylsalicylate, salicylate, acetylsalicylic acid, ASA, or salicylic acid).Current advice in the United Kingdom by the Committee on Safety of Medicines is that aspirin should not be given to those under the age of 16 years, unless specifically indicated in Kawasaki disease or in the prevention of blood clot formation.

Diagnosis
Differential diagnosis
Causes for similar symptoms include
Various inborn metabolic disorders
Viral encephalitis
Drug overdose or poisoning
Head trauma
Liver failure due to other causes
Meningitis
Kidney failure
Shaken baby syndrome

Treatment
Treatment is supportive. Mannitol may be used to help with the brain swelling.

Prognosis
Documented cases of Reye syndrome in adults are rare. The recovery of adults with the syndrome is generally complete, with liver and brain function returning to normal within two weeks of onset.In children, mild to severe permanent brain damage is possible, especially in infants.  Over thirty percent of the cases reported in the United States from 1981 through 1997 resulted in fatality.

Epidemiology
Reye syndrome occurs almost exclusively in children.  While a few adult cases have been reported over the years, these cases do not typically show permanent neural or liver damage. Unlike in the United Kingdom, the surveillance for Reye syndrome in the United States is focused on people under 18 years of age.In 1980, after the CDC began cautioning physicians and parents about the association between Reye syndrome and the use of salicylates in children with chickenpox or virus-like illnesses, the incidence of Reye syndrome in the United States began to decline, prior to the FDAs issue of warning labels on aspirin in 1986. In the United States between 1980 and 1997, the number of reported cases of Reye syndrome decreased from 555 cases in 1980 to about two cases per year since 1994. During this time period 93% of reported cases for which racial data were available occurred in whites and the median age was six years. In 93% of cases a viral illness had occurred  in the preceding three-week period. For the period 1991–1994, the annual rate of hospitalizations due to Reye syndrome in the United States was estimated to be between 0.2 and 1.1 per million population less than 18 years of age.During the 1980s, a case-control study carried out in the United Kingdom also demonstrated an association between Reye syndrome and aspirin exposure. In June 1986, the United Kingdom Committee on Safety of Medicines issued warnings against the use of aspirin in children under 12 years of age and warning labels on aspirin-containing medications were introduced. United Kingdom surveillance for Reye syndrome documented a decline in the incidence of the illness after 1986. The reported incidence rate of Reye syndrome decreased from a high of 0.63 per 100,000 population less than 12 years of age in 1983–1984 to 0.11 in 1990–1991.From November 1995 to November 1996 in France, a national survey of pediatric departments for children under 15 years of age with unexplained encephalopathy and a threefold (or greater) increase in serum aminotransferase and/or ammonia led to the identification of nine definite cases of Reye syndrome (0.79 cases per million children) </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 Classification of pneumonia and can you explain it in depth? [/INST] Pneumonia can be classified in several ways, most commonly by where it was acquired (hospital versus community), but may also by the area of lung affected or by the causative organism. There is also a combined clinical classification, which combines factors such as age, risk factors for certain microorganisms, the presence of underlying lung disease or systemic disease and whether the person has recently been hospitalized.

By location acquired
Community-acquired
Community-acquired pneumonia (CAP) is infectious pneumonia in a person who has not recently been hospitalized. CAP is the most common type of pneumonia. The most common causes of CAP vary depending on a persons age, but they include Streptococcus pneumoniae, viruses, the atypical bacteria, and Haemophilus influenzae. Overall, Streptococcus pneumoniae is the most common cause of community-acquired pneumonia worldwide. Gram-negative bacteria cause CAP in certain at-risk populations. CAP is the fourth most common cause of death in the United Kingdom and the sixth in the United States. The term "walking pneumonia" has been used to describe a type of community-acquired pneumonia of less severity (because the sufferer can continue to "walk" rather than requiring hospitalization). Walking pneumonia is usually caused by the atypical bacterium, Mycoplasma pneumoniae.

Hospital-acquired
Hospital-acquired pneumonia, also called nosocomial pneumonia, is pneumonia acquired during or after hospitalization for another illness or procedure with onset at least 72 hrs after admission. The causes, microbiology, treatment and prognosis are different from those of community-acquired pneumonia. Up to 5% of patients admitted to a hospital for other causes subsequently develop pneumonia. Hospitalized patients may have many risk factors for pneumonia, including mechanical ventilation, prolonged malnutrition, underlying heart and lung diseases, decreased amounts of stomach acid, and immune disturbances. Additionally, the microorganisms a person is exposed to in a hospital are often different from those at home. Hospital-acquired microorganisms may include resistant bacteria such as MRSA, Pseudomonas, Enterobacter, and Serratia. Because individuals with hospital-acquired pneumonia usually have underlying illnesses and are exposed to more dangerous bacteria, it tends to be more deadly than community-acquired pneumonia. Ventilator-associated pneumonia (VAP) is a subset of hospital-acquired pneumonia. VAP is pneumonia which occurs after at least 48 hours of intubation and mechanical ventilation.

By cause
Pneumonia has historically been characterized as either typical or atypical depending on the presenting symptoms and thus the presumed underlying organism. Attempting to make this distinction based on symptoms, however, has not been found to be accurate, and The American Thoracic Society does not recommend its use.

Bronchiolitis obliterans organizing pneumonia
Bronchiolitis obliterans organizing pneumonia (BOOP) is caused by inflammation of the small airways of the lungs. It is also known as cryptogenic organizing pneumonitis (COP).
Eosinophilic pneumonia
Eosinophilic pneumonia is invasion of the lung by eosinophils, a particular kind of white blood cell. Eosinophilic pneumonia often occurs in response to infection with a parasite or after exposure to certain types of environmental factors.

Chemical pneumonia
Chemical pneumonia (usually called chemical pneumonitis) is caused by chemical toxicants such as pesticides, which may enter the body by inhalation or by skin contact. When the toxic substance is an oil, the pneumonia may be called lipoid pneumonia.

Aspiration pneumonia
Aspiration pneumonia (or aspiration pneumonitis) is caused by aspirating foreign objects which are usually oral or gastric contents, either while eating, or after reflux or vomiting which results in bronchopneumonia. The resulting lung inflammation is not an infection but can contribute to one, since the material aspirated may contain anaerobic bacteria or other unusual causes of pneumonia. Aspiration is a leading cause of death among hospital and nursing home patients, since they often cannot adequately protect their airways and may have otherwise impaired defenses.

Dust pneumonia
Dust pneumonia describes disorders caused by excessive exposure to dust storms, particularly during the Dust Bowl in the United States. With dust pneumonia, dust settles all the way into the alveoli of the lungs, stopping the cilia from moving and preventing the lungs from ever clearing themselves.

Necrotizing pneumonia
Necrotizing pneumonia (NP), also known as cavitary pneumonia or cavitatory necrosis, is a rare but severe complication of lung  parenchymal infection. In necrotizing pneumonia, there is a substantial  liquefaction following death of the lung tissue, which may lead to gangrene formation in the lung. In most cases patients with NP have fever, cough and bad breath, and those with more indolent infections have weight loss. Often patients clinically present with acute respiratory failure. The most common pathogens responsible for NP are Streptococcus pneumonia, Staphylococcus aureus, Klebsiella pneumoniae.

Opportunistic pneumonia
People with weakened immune defense, such as HIV/AIDS patients, are highly susceptible to opportunistic infections affecting the lungs. Most common pathogens are Pneumocystis jiroveci, Mycobacterium avium-intracellulare complex, Streptococcus pneumoniae, Haemophilus species. Less frequent pathogens are Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis, cytomegalovirus (CMV), and Toxoplasma gondii.
Chemotherapy-induced immunodeficiency may lead to severe lung infections. Pathogens commonly associated with lung infectioins are bacteria (like Pseudomonas aeruginosa, Stenotrophomonas maltophilia, and Nocardia species), viruses (eg, respiratory syncytial virus, parainfluenza virus, influenza virus A and influenza B, and cytomegalovirus), and fungi (eg, Aspergillus, Fusarium, and Mucorales species, and Pneumocystis jirovecii).

Double pneumonia (bilateral pneumonia)
This is a historical term for acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). However, the term was and, especially by lay people, still is used to denote pneumonia affecting both lungs. Accordingly, the term double pneumonia is more likely to be used to describe bilateral pneumonia than it is ALI or ARDS.

Severe acute respiratory syndrome
Severe acute respiratory syndrome (SARS) is a highly contagious and deadly type of pneumonia which first occurred in Nov-2002 after initial outbreaks in China caused by SARS-CoV/SARS-CoV-1,which almost disappeared by the month of May-2004. The second outbreak of SARS-CoV-2 started in December 2019 from Wuhan, China and was declared pandemic by WHO on 11 March 2020. SARS is caused by the SARS coronavirus, a previously unknown pathogen.

By area of lung affected
Initial descriptions of pneumonia focused on the anatomic or pathologic appearance of the lung, either by direct inspection at autopsy or by its appearance under a microscope.

A lobar pneumonia is an infection that only involves a single lobe, or section, of a lung. Lobar pneumonia is often due to Streptococcus pneumoniae (though Klebsiella pneumoniae is also possible.)
Multilobar pneumonia involves more than one lobe, and it often causes a more severe illness.
Bronchial pneumonia affects the lungs in patches around the tubes (bronchi or bronchioles).
Interstitial pneumonia involves the areas in between the alveoli, and it may be called "interstitial pneumonitis." It is more likely to be caused by viruses or by atypical bacteria.The discovery of x-rays made it possible to determine the anatomic type of pneumonia without direct examination of the lungs at autopsy and led to the development of a radiological classification. Early investigators distinguished between typical lobar pneumonia and atypical (e.g </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 Delayed hemolytic transfusion reaction 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 Hyperoxia and can you explain it in depth? [/INST] Hyperoxia occurs when cells, tissues and organs are exposed to an excess supply of oxygen (O2) or  higher than normal partial pressure of oxygen.In medicine, it refers to excess oxygen in the lungs or other body tissues, which can be caused by breathing air or oxygen at pressures greater than normal atmospheric pressure. This kind of hyperoxia can lead to oxygen toxicity, caused from the harmful effects of breathing molecular oxygen at elevated partial pressures. Hyperoxia is the opposite of hypoxia; hyperoxia refers to a state in which oxygen supply is excessive, and hypoxia refers to a state in which oxygen supply is insufficient.
In the environment, it refers to excess oxygen in a body of water or other habitat.

Signs and symptoms
Associated with hyperoxia is an increased level of reactive oxygen species (ROS), which are chemically reactive molecules containing oxygen. These oxygen containing molecules can damage lipids, proteins, and nucleic acids, and react with surrounding biological tissues. The human body has naturally occurring antioxidants to combat reactive molecules, but the protective antioxidant defenses can become depleted by abundant reactive oxygen species, resulting in oxidation of the tissues and organs.The symptoms produced from breathing high concentrations of oxygen for extended periods have been studied in a variety of animals, such as frogs, turtles, pigeons, mice, rats, guinea pigs, cats, dogs and monkeys. The majority of these studies reported the occurrence of irritation, congestion and edema of the lungs, and even death following prolonged exposures.

Oxygen toxicity
The supplementation of oxygen can lead to oxygen toxicity, also known as oxygen toxicity syndrome, oxygen intoxication, and oxygen poisoning. There are two main types of oxygen toxicity: central nervous system (CNS) toxicity, and pulmonary and ocular toxicity.Temporary exposure to high partial pressures of oxygen at greater than atmospheric pressure can lead to central nervous system toxicity (CNS). An early but serious sign of CNS oxygen toxicity is a grand-mal seizure, also known as a generalized tonic-clonic seizure. This type of seizure consists of a loss of consciousness and violent muscle contractions. Signs and symptoms of oxygen toxicity are usually prevalent, but there are no standard warning signs that a seizure is about to ensue. The convulsion caused by oxygen toxicity does not lead to hypoxia, a side effect common to most seizures, because the body has an excess amount of oxygen when the convulsion begins. The seizures can lead to drowning, however, if the convulsion is suffered by a diver still in the water.Prolonged exposure to higher oxygen levels at atmospheric pressure can lead to pulmonary and ocular toxicity. Symptoms of oxygen toxicity may include disorientation, respiratory problems, myopia, or accelerated development of cataracts. Prolonged exposure to higher than normal partial pressures of oxygen can result in oxidative damage to cell membranes. Signs of pulmonary (lung) oxygen toxicity begin with slight irritation in the trachea. A mild cough usually ensues, followed by greater irritation and a worse cough until breathing becomes quite painful and the cough becomes uncontrollable. If supplementation of oxygen is continued, the individual will notice tightness in the chest, difficulty breathing, shortness of breath, and if exposure is continued, fatality due to lack of oxygen.

Cause
Oxygen supplied at greater than atmospheric pressure has been known to damage plants, animals, and aerobic bacteria such as Escherichia coli. The damaging effects vary depending on the specimen used, its age, physiological state, and diet.The supplementation of oxygen has been a common procedure of prehospital treatment for many years. Guidelines include cautions about chronic obstructive pulmonary disease (COPD). These guidelines stress the use of 28% oxygen masks and caution the dangers of hyperoxia. Long-term use of supplemental oxygen improves survival in patients with COPD, but can lead to lung injury.An additional cause of hyperoxia is related to underwater diving with breathing apparatus </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 Ankylosis 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 Postpartum blues and can you explain it in depth? [/INST] Postpartum blues, also known as baby blues and maternity blues, is a very common but self-limited condition that begins shortly after childbirth and can present with a variety of symptoms such as mood swings, irritability, and tearfulness. Mothers may experience negative mood symptoms mixed with intense periods of joy. Up to 85% of new mothers are affected by postpartum blues, with symptoms starting within a few days after childbirth and lasting up to two weeks in duration. Treatment is supportive, including ensuring adequate sleep and emotional support. If symptoms are severe enough to affect daily functioning or last longer than two weeks, the individual should be evaluated for related postpartum psychiatric conditions, such as postpartum depression and postpartum anxiety. It is unclear whether the condition can be prevented, however education and reassurance are important to help alleviate patient distress.

Signs and symptoms
Symptoms of postpartum blues can vary significantly from one individual to another, and from one pregnancy to the next. Many symptoms of postpartum blues overlap both with normal symptoms experienced by new parents and with postpartum depression. Individuals with postpartum blues have symptoms that are milder and less disruptive to their daily functioning compared to those with postpartum depression. Symptoms of postpartum blues include, but are not limited to:
Tearfulness or crying "for no reason"
Mood swings
Irritability
Anxiety
Questioning ones ability to care for the baby
Difficulty making choices
Loss of appetite
Fatigue
Difficulty sleeping
Difficulty concentrating
Negative mood symptoms interspersed with positive symptoms

Onset
Symptoms of postpartum blues generally begin within a few days of childbirth and often peak by day four or five.

Duration
Postpartum blues may last a few days up to two weeks. If symptoms last more than two weeks, the individual must be evaluated for postpartum depression.

Causes
The causes of postpartum blues have not been clearly established. Most hypotheses regarding the etiology of postpartum blues and postpartum depression center on the intersection of the significant biological and psychosocial changes that occur with childbirth.

Psychosocial causes
Pregnancy and postpartum are significant life events that increase a womans vulnerability for postpartum blues. Even with a planned pregnancy, it is normal to have feelings of doubt or regret, and it takes time to adjust to having a newborn. Feelings commonly reported by new parents and lifestyle changes that may contribute to developing early postpartum mood symptoms include:
Fatigue after labor and delivery
Caring for a newborn that requires 24/7 attention
Sleep deprivation
Lack of support from family and friends
Marital or relationship strain
Changes in home and work routines
Financial stress
Unrealistic expectations of self
Societal or cultural pressure to "bounce back" quickly after pregnancy and childbirth
Overwhelmed and questioning ability to care for baby
Anger, loss, or guilt, especially for parents of premature or sick infants

Risk factors
Most risk factors studied have not clearly and consistently demonstrated an association with postpartum blues. These include sociodemographic factors, such as age and marital status, obstetric factors, such as delivery complications or low birth weight.Factors most consistently shown to be predictive of postpartum blues are personal and family history of depression. This is of particular interest given of the bidirectional relationship between postpartum blues and postpartum depression: a history of postpartum depression appears to be a risk factor for developing postpartum blues, and postpartum blues confers a higher risk of developing subsequent postpartum depression.

Pathophysiology
Estrogen and progesterone
After delivery of the placenta, mothers experience an abrupt decline of gonadal hormones, namely estrogen and progesterone. Major hormonal changes in the early postpartum period may trigger mood symptoms similarly to how more minor hormonal shifts cause mood swings prior to menstrual periods.Studies have not detected a consistent association between hormone concentrations and development of postpartum mood disorders. Some investigators believe the discrepant results may be due to variations in sensitivity to hormonal shifts across different subgroups of women. Therefore, development of mood symptoms may be related to a womans sensitivity, based on genetic predisposition and psychosocial stressors, to changes in hormones rather than absolute hormonal levels.

Other
The association between postpartum blues and a variety of other biological factors, including cortisol and the HPA axis, tryptophan, prolactin, thyroid hormone, and others have been assessed over the years with inconclusive results.Emerging research has suggested a potential association between the gut microbiome and perinatal mood and anxiety disorders.

Diagnosis
Classification
The proper diagnostic classification of postpartum blues has not been clearly established. Postpartum blues has long been considered to be the mildest condition on the spectrum of postpartum psychiatric disorders, which includes postpartum depression and postpartum psychosis. However, there exists some discussion in the literature of the possibility that postpartum blues may be an independent condition.

Criteria
There are no standardized criteria for the diagnosis of postpartum blues. Unlike postpartum depression, postpartum blues is not a diagnosis included in the Diagnostic and Statistical Manual of Mental Disorders.
Investigators have employed a variety of diagnostic tools in prospective and retrospective studies of postpartum blues, including repurposing screening tools, such as the Edinburgh Postnatal Depression Scale (EPDS) and Beck Depression Index (BDI), as well as developing blues-specific scales. Examples of blues-specific scales include the Maternity Blues Questionnaire and the Stein Scale.

Differential diagnosis:-
Although symptoms of postpartum blues present in a majority of mothers and the condition is self-limited, it is important to keep related psychiatric conditions in mind as they all have overlap in presentation and similar period of onset.

Postpartum anxiety
Symptoms of anxiety and irritability are often predominant in the presentation of postpartum blues. However, compared to postpartum anxiety, symptoms of postpartum blues are less severe, resolve on their own, and last fewer than two weeks.
Postpartum depression
Postpartum depression and postpartum blues may be indistinguishable when symptoms first begin. However, symptoms of postpartum blues are less severe, resolve on their own, and last fewer than two weeks. Mothers who experience severe postpartum blues appear to be at increased risk of developing depression.
Postpartum psychosis
Although both conditions can cause periods of high and low moods, the mood swings in postpartum psychosis are significantly more severe and may include mania, hallucinations, and delusions. Postpartum psychosis is a rare condition, affecting 1-2 per 1000 women. Postpartum psychosis is classified as a psychiatric emergency and requires hospital admission.Additionally, a variety of medical co-morbidities can mimic or worsen psychiatric symptoms.

Prevention
Screening
There are no specific screening recommendations for postpartum blues. Nonetheless, a variety of professional organizations recommend routine screening for depression and/or assessment of emotional well-being during pregnancy and postpartum. Universal screening provides an opportunity to identify women with sub-clinical psychiatric conditions during this period and those at higher risk of developing more severe symptoms. Specific recommendations are listed below:

American College of Obstetrics and Gynecology (ACOG): In 2018, ACOG recommended universal screening for depression and anxiety using a validated tool at least once during pregnancy or postpartum, in addition to a full assessment of mood and well-being at the postpartum visit. This is in addition to existing recommendations for annual depression screening in all women.
American Academy of Pediatrics (AAP): In 2017, the AAP recommended universal screening of mothers for postpartum depression at the 1-, 2-, 4-, and 6-month well child visits.
United States Preventative Services Task Force (USPSTF): In 2016, the USPSTF recommended depression screening in the general adult population, including pregnant and postpartum women. Their recommendations did not include guidelines for frequency of screening.

Primary prevention
Given the mixed evidence regarding causes of postpartum blues, it is unclear whether prevention strategies would be effective in decreasing the risk of developing this condition. However, educating women during pregnancy about postpartum blues may help to prepare them for these symptoms that are often unexpected and concerning in the setting of excitement and anticipation of a new baby. Mothers who develop postpartum blues often have significant shame or guilt for feelings of anxiety or depression during a time is expected to be joyful. It is important to reassure new parents that low mood symptoms after childbirth are common and transient. Obstetric providers may recommend that patients and their families prepare ahead of time to ensure the mother will have adequate support and rest after the delivery. Additionally, they should provide education and resources to family and friends about red flags of more severe perinatal psychiatric conditions that may develop, such as postpartum depression and postpartum psychosis.

Treatment
Postpartum blues is a self-limited condition. Signs and symptoms are expected to resolve within two weeks of onset without any treatment. Nevertheless, there are a number of recommendations to help relieve symptoms, including:
Getting enough sleep
Taking time to relax and do activities that you enjoy
Asking for help from family and friends
Reaching out to other new parents
Avoiding alcohol and other drugs that may worsen mood symptoms
Reassurance that symptoms are very common and will resolve on their ownIf symptoms do not resolve within two weeks or if they interfere with functioning, individuals are encouraged to contact their healthcare provider. Early diagnosis and treatment of more severe postpartum psychiatric conditions, such as postpartum depression, postpartum anxiety, and postpartum psychosis, are critical for improved outcomes in both the parent and child.

Prognosis
Most mothers who develop postpartum blues experience complete resolution of symptoms by two weeks. However, a number of prospective studies have identified more severe postpartum blues as an independent risk factor for developing subsequent postpartum depression </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 Chalazion and can you explain it in depth? [/INST] A chalazion (; plural chalazia or chalazions) or meibomian cyst is a cyst in the eyelid usually due to a blocked meibomian gland,  typically in the middle of the eyelid, red, and not painful. They tend to come on gradually over a few weeks.A chalazion may occur following a stye or from hardened oils blocking the gland. The blocked gland is usually the meibomian gland, but can also be the gland of Zeis.A stye and cellulitis may appear similar. A stye, however, is usually more sudden in onset, painful, and occurs at the edge of the eyelid. Cellulitis is also typically painful.Treatment is initiated with warm compresses. In addition, antibiotic/corticosteroid eyedrops or ointment may be used. If this is not effective, injecting corticosteroids into the lesion may be tried. If large, incision and drainage may be recommended. While relatively common, the frequency of the condition is unknown. It is most common in people 30–50 years of age, and equally common in males and females. The term is from the Greek khalazion (χαλάζιον) meaning "small hailstone".

Signs and symptoms
Painless swelling on the eyelid
Eyelid tenderness typically none-to-mild
Increased tearing
Heaviness of the eyelid
Redness of conjunctiva

Complications
A large chalazion can cause astigmatism due to pressure on the cornea.As laser eye surgery involves shaping the cornea by burning parts of it away, weakening its structure, post-operation people can be left predisposed to deformation of the cornea from small chalazia.Complications of corticosteroid injection include hypopigmentation and fat atrophy which is less likely to occur in conjunctival approach of injection.A chalazion that reoccurs in the same area may rarely be a symptom of sebaceous carcinoma.

Diagnosis
A chalazion or meibomian cyst can sometimes be mistaken for a stye.

Differential diagnosis
Sebaceous gland adenoma
Sebaceous gland carcinoma
Sarcoid granuloma
Foreign body granuloma

Treatment
General treatment
Chalazia will often disappear without further treatment within a few months, and virtually all will resorb within two years.Healing can be facilitated by applying a moist warm compress to the affected eye for approximately 10–15 minutes, 4 times per day. This promotes opening, drainage, and healing by softening the hardened oil that is occluding the duct. In addition, it is helpful to scrub the lid margin (at the base of the eyelashes) with a washcloth and mild (baby) shampoo, which removes oily debris.Topical antibiotic eye drops or ointment (e.g., chloramphenicol or fusidic acid) are sometimes used for the initial acute infection, but are otherwise of little value in treating a chalazion.If they continue to enlarge or fail to settle within a few months, smaller lesions can be injected with a corticosteroid.
Larger ones can be surgically removed using local anesthesia. This is usually done from underneath the eyelid to avoid a scar on the skin. If the chalazion is located directly under the eyelids outer tissue, however, an excision from above may be more advisable so as not to inflict any unnecessary damage on the lid itself. Eyelid epidermis usually mends well, without leaving any visible scar. Depending on the chalazions texture, the excision procedure varies: while fluid matter can easily be removed under minimal invasion, by merely puncturing the chalazion and exerting pressure upon the surrounding tissue, hardened matter usually necessitates a larger incision, through which it can be scraped out. Any residual matter should be metabolized in the course of the subsequent healing process, generally aided by regular appliance of dry heat. The excision of larger chalazia may result in visible hematoma around the lid, which will wear off within three or four days, whereas the swelling may persist for longer. Chalazion excision is an ambulant treatment and normally does not take longer than fifteen minutes. Nevertheless, owing to the risks of infection and severe damage to the eyelid, such procedures should only be performed by a medical professional.
Chalazia may recur, and they will usually be biopsied to rule out the possibility of a tumour.

Antibiotic/corticosteroid eyedrops or ointment
A limited course of topical antibiotic/corticosteroid combination eyedrops or ointment such as tobramycin/dexamethasone may be effective in treating a chalazion.

Surgery
Chalazion surgery is a simple procedure that is generally performed as a day operation, and the person does not need to remain in the hospital for further medical care. The eyelid is injected with a local anesthetic, a clamp is put on the eyelid, then the eyelid is turned over, an incision is made on the inside of the eyelid, and the chalazion is drained and scraped out with a curette. A scar on the upper lid can cause discomfort as some people feel the scar as they blink. As surgery damages healthy tissue (e.g., by scarring tissue or possibly even causing blepharitis), given other options, less invasive treatment is preferable.Chalazion removal surgery is performed under local or general anesthesia. Commonly, general anesthesia is administered in children to make sure they stay still and no injury to the eye occurs. Local anesthesia is used in adults and it is applied with a small injection into the eyelid. The discomfort of the injection is minimized with the help of an anesthetic cream, which is applied locally.
The chalazion can be removed in two ways, depending on the size of cyst. Relatively small chalazia are removed through a small cut at the back of the eyelid. The surgeon lifts the eyelid to access the back of its surface and makes an incision of approximately 3mm just on top of the chalazion. The lump is then removed, and pressure is applied for a few minutes to stop any oozing of blood that may occur because of the operation. Surgery of small chalazia does not require stitches, as the cut is at the back of the eyelid and therefore the cut cannot be seen, and the cosmetic result is excellent.
Larger chalazia are removed through an incision in front of the eyelid. Larger chalazia usually push on the skin of the eyelid, and this is the main reason why doctors prefer removing them this way. The incision is not usually larger than 3mm and it is made on top of the chalazion. The lump is removed and then pressure is applied to the incision to prevent oozing. This type of surgery is closed with very fine stitches. They are hardly visible and are usually removed within a week after the surgery has been performed. Although chalazia are rarely dangerous, it is common to send the chalazion or part of it to a laboratory to screen for cancer.When surgery for a chalazion is considered, people who take aspirin or any other blood-thinning medications are advised to stop taking them one week prior to the procedure as they may lead to uncontrollable bleeding.In rare cases, people are kept overnight in the hospital after chalazion surgery. This includes cases in which complications occurred and the person needs to be closely monitored. In most cases, however, people are able to go home after the operation has ended.
The recovery process is easy and quite fast. Most people with chalazion experience some very minor discomfort in the eye, which can be easily controlled by taking painkilling medication. People are, however, recommended to avoid getting water in the eye for up to 10 days after surgery. They may wash, bathe, or shower, but they must be careful to keep the area dry and clean. Makeup may be worn after at least one month post-operatively. People are recommended to not wear contact lenses in the affected eye for at least eight weeks to prevent infections and potential complications.Commonly, people receive eye drops to prevent infection and swelling in the eye and pain medication to help them cope with the pain and discomfort in the eyelid and eye </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 Plasmacytoma and can you explain it in depth? [/INST] Plasmacytoma is a plasma cell dyscrasia in which a plasma cell tumour grows within soft tissue or within the axial skeleton.
The International Myeloma Working Group lists three types: solitary plasmacytoma of bone (SPB); extramedullary plasmacytoma (EP), and multiple plasmacytomas that are either primary or recurrent. The most common of these is SPB, accounting for 3–5% of all plasma cell malignancies. SPBs occur as lytic lesions within the axial skeleton and extramedullary plasmacytomas most often occur in the upper respiratory tract (85%), but can occur in any soft tissue. Approximately half of all cases produce paraproteinemia. SPBs and extramedullary plasmacytomas are mostly treated with radiotherapy, but surgery is used in some cases of extramedullary plasmacytoma. The skeletal forms frequently progress to multiple myeloma over the course of 2–4 years.Due to their cellular similarity, plasmacytomas have to be differentiated from multiple myeloma. For SPB and extramedullary plasmacytoma the distinction is the presence of only one lesion (either in bone or soft tissue), normal bone marrow (<5% plasma cells), normal skeletal survey, absent or low paraprotein and no end organ damage.

Signs and symptoms
For SPB the most common presenting symptom is that of pain in the affected bone. Back pain and other consequences of the bone lesion may occur such as spinal cord compression or pathological fracture. Around 85% of extramedullary plasmacytoma presents within the upper respiratory tract mucosa, causing possible symptoms such as epistaxis, rhinorrhoea and nasal obstruction. In some tissues it may be found as a palpable mass.

Diagnosis
The diagnosis of plasmacytoma uses a diverse range of interdisciplinary techniques including serum protein electrophoresis, bone marrow biopsy, urine analysis for Bence Jones protein and complete blood count, plain film radiography, MRI and PET-CT.Serum protein electrophoresis separates the proteins in the liquid part of the blood (serum), allowing the analysis of antibodies. Normal blood serum contains a range of antibodies and are said to be polyclonal, whereas serum from a person with plasmacytoma may show a monoclonal spike. This is due to an outgrowth of a single type of plasma cell that forms the plasmacytoma and produces a single type of antibody. The plasma cells are said to be monoclonal and the excessively produced antibody is known as monoclonal protein or paraprotein.  Paraproteins are present in 60% of SPB and less than 25% of extramedullary plasmacytoma.Bone marrow biopsies are performed to ensure the disease is localised; and in SPB or extramedullary plasmacytoma there will not be an increase of monoclonal plasma cells. Tissue biopsies of SPB and extramedullary plasmacytoma are used to assess the phenotype of the plasma cells. Histological analyses can be performed on these biopsies to see what cluster of differentiation (CD) markers are present and to assess monoclonality of the cells. CD markers can aid in the distinction of extramedullary plasmacytoma from lymphomas.Skeletal surveys are used to ensure there are no other primary tumors within the axial skeleton. MRI can be used to assess tumor status and may be advantageous in detecting primary tumors that are not detected by plain film radiography. PET-CT may also be beneficial in detecting extramedullary tumours in individuals diagnosed with SPB. CT imaging may be better than plain film radiography for assessing bone damage.An important distinction to be made is that a true plasmacytoma is present and not a systemic plasma cell disorder, such as multiple myeloma. The difference between plasmacytoma and multiple myeloma is that plasmacytoma lacks increased blood calcium, decreased kidney function, too few red blood cells in the bloodstream, and multiple bone lesions (collectively termed CRAB).

Classification
Plasmacytoma is a tumor of plasma cells. The cells are identical to those seen in multiple myeloma, but they form discrete masses of cells in the skeleton (solitary plasmacytoma of bone; SPB) or in soft tissues (extramedullary plasmacytoma; EP). They do not present with systemic disease, which would classify them as another systemic plasma cell disorder.The International Myeloma Working Group (IMWG) has published criteria for the diagnosis of plasmacytomas. They recognise three distinct entities: SPB, extramedullary plasmacytoma and multiple solitary plasmacytomas (+/- recurrent). The proposed criteria for SPB is the presence of a single bone lesion, normal bone marrow (less than 5% plasma cells), small or no paraprotein, no related organ involvement/damage and a normal  skeletal survey (other than the single bone lesion). The criteria for extramedullary plasmacytoma are the same but the tumor is located in soft tissue. No bone lesions should be present. Criteria for multiple solitary plasmacytomas (+/- recurrent) are the same except either multiple solitary bone or soft tissue lesions must be present. They may occur as multiple primary tumors or as a recurrence from a previous plasmacytoma.

Association with the Epstein–Barr virus
Rarely, the Epstein–Barr virus (EBV) is associated with multiple myeloma and plasmacytomas, particularly in individuals who have an immunodeficiency due to e.g. HIV/AIDS, organ transplantation, or a chronic inflammatory condition such as rheumatoid arthritis. EBV-positive multiple myeloma and plasmacytoma are classified together by the World Health Organization (2016) as Epstein–Barr virus-associated lymphoproliferative diseases and termed Epstein–Barr virus-associated plasma cell myeloma. EBV-positivity is more common in plasmacytoma than multiple myeloma. The tissues involved in EBV+ plasmacytoma typically show foci of EBV+ cells with the appearance of rapidly proliferating immature or poorly differentiated plasma cells. These cells express products of EBV genes such as EBER1 and EBER2. EBV-positive plasmacytoma(s) is more likely to progress to multiple myeloma than EBV-negative plasmacytoma(s) suggesting that the virus may play a role in the progression of plasmacytoma to multiple myeloma.

Treatment
Radiotherapy is the main choice of treatment for both SPB and extramedullary plasmacytoma, and local control rates of >80% can be achieved. This form of treatment can be used with curative intent because plasmacytoma is a radiosensitive tumor. Surgery is an option for extramedullary plasmacytoma, but for cosmetic reasons it is generally used when the lesion is not present within the head and neck region. Another option is the possible combination of radiotherapy with anti-multiple myeloma treatment. In a study that included 68 patients, a group of 8 patients who were treated with radio- and chemotherapy (with or without surgery) were less likey to have a relapse of plasmacytoma, progress to multiple myeloma, or die compared with patients who were treated with radiotherapy and/or surgery alone [progression free survival (PFS), overall median: not reached vs. 48.0 months; respectively] </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 Angiodysplasia and can you explain it in depth? [/INST] In medicine (gastroenterology), angiodysplasia is a small vascular malformation of the gut. It is a common cause of otherwise unexplained gastrointestinal bleeding and anemia.  Lesions are often multiple, and frequently involve the cecum or ascending colon, although they can occur at other places. Treatment may be with colonoscopic interventions, angiography and embolization, medication, or occasionally surgery.

Signs and symptoms
Although some cases present with black, tarry stool (melena), the blood loss can be subtle, with the anemia symptoms predominating.

Pathophysiology
Histologically, it resembles telangiectasia and development is related to age and strain on the bowel wall. It is a degenerative lesion, acquired, probably resulting from chronic and intermittent contraction of the colon that is obstructing the venous drainage of the mucosa. As time goes by the veins become more and more tortuous, while the capillaries of the mucosa gradually dilate and precapillary sphincter becomes incompetent. Thus is formed an arteriovenous malformation characterized by a small tuft of dilated vessels.Although angiodysplasia is probably quite common, the risk of bleeding is increased in disorders of coagulation. A classic association is Heydes syndrome (coincidence of aortic valve stenosis and bleeding from angiodysplasia).
In this disorder, von Willebrand factor (vWF) is proteolysed due to high shear stress in the highly turbulent blood flow around the aortic valve. vWF is most active in vascular beds with high shear stress, including angiodysplasias, and deficiency of vWF increases the bleeding risk from such lesions.Warkentin et al. argue that apart from aortic valve stenosis, some other conditions that feature high shear stress might also increase the risk of bleeding from angiodysplasia.

Diagnosis
Fecal occult blood testing is positive when bleeding is active.  If bleeding is intermittent the test may be negative at times.Diagnosis of angiodysplasia is often accomplished with endoscopy, either colonoscopy or esophagogastroduodenoscopy (EGD).  Although the lesions can be notoriously hard to find, the patient usually is diagnosed by endoscopy.  A new technique, pill enteroscopy, has been a major advance in diagnosis, especially in the small bowel which is difficult to reach with traditional endoscopy.  With this technique a pill that contains a video camera and radio transmitter is swallowed, and pictures of the small intestine are sent to a receiver worn by the patient. Recently, multiphase CT angiography (without positive oral contrast) has been shown to play a promising role in the diagnoses of small and large bowel angiodysplasia, especially when associated with active hemorrhage.Angiodysplasiae in the small bowel can also be diagnosed and treated with double-balloon enteroscopy, a technique involving a long endoscopic camera and overtube, both fitted with balloons, that allow the bowel to be accordioned over the camera.In cases with negative endoscopic findings and high clinical suspicion, selective angiography of the mesenteric arteries is sometimes necessary, but this allows for interventions at time of the procedure. An alternative is scintigraphy with red blood cells labeled with a radioactive marker; this shows the site of the bleeding on a gamma camera but tends to be unhelpful unless the bleeding is continuous and significant.

Treatment
If the anemia is severe, blood transfusion is required before any other intervention is considered. Endoscopic treatment is an initial possibility, where cautery or argon plasma coagulation (APC) treatment is applied through the endoscope </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 Nail disease and can you explain it in depth? [/INST] A nail disease or onychosis is a disease or deformity of the nail.  Although the nail is a structure produced by the skin and is a skin appendage, nail diseases have a distinct classification as they have their own signs and symptoms which may relate to other medical conditions. Some nail conditions that show signs of infection or inflammation may require medical assistance.

Diseases
Onychia is an inflammation of the nail folds (surrounding tissue of the nail plate) of the nail with formation of pus and shedding of the nail.  Onychia results from the introduction of microscopic pathogens through small wounds.
Onychocryptosis, commonly known as "ingrown nails" (unguis incarnatus), can affect either the fingers or the toes.  In this condition, the nail cuts into one or both sides of the nail bed, resulting in inflammation and possibly infection. The relative rarity of this condition in the fingers suggests that pressure from the ground or shoe against the toe is a prime factor. The movements involved in walking or other physical disturbances can contribute to the problem.  Mild onychocryptosis, particularly in the absence of infection, can be treated by trimming and rounding the nail.  More advanced cases, which usually include infection, are treated by surgically excising the ingrowing portion of the nail down to its bony origin and thermally or chemically cauterizing the matrix, or root, to prevent recurrence.  This surgery is called matrixectomy. The best results are achieved by cauterizing the matrix with phenol. The Vandenbos Procedure is a highly effective method that focuses on excision of excessive nail fold tissue without affecting the healthy nail and nail matrix. The Vandenbos Procedure is showing high success rates in eliminating onychocryptosis without altering the normal nail. Another, much less effective, treatment is excision of the matrix, sometimes called a cold steel procedure.
Onychodystrophy is a deformation of the nails that can result from cancer chemotherapy which includes bleomycin, hydroxyurea, or 5-fluorouracil. It can include discoloration of the nail, or dyschromia.
Onychogryposis, also called "rams-horn nail", is a thickening and increase in curvature of the nail.  It is usually the result of injury to the matrix.  It may be partially hereditary and can also occur as a result of long-term neglect.  It is most commonly seen in the great toe but may be seen in other toes as well as the fingernails.  An affected nail has many grooves and ridges, is brownish in color, and grows more quickly on one side than on the other.  The thick curved nail is difficult to cut, and often remains untrimmed, exacerbating the problem.
Onycholysis is a loosening of the exposed portion of the nail from the nail bed, usually beginning at the free edge and continuing to the lunula.  It is frequently associated with an internal disorder, trauma, infection, nail fungi, allergy to nail enhancement products, or side effects of drugs.
Onychomadesis is the separation and falling off of a nail from the nail bed. Common causes include localized infection, minor injury to the matrix bed, or severe systemic illness. It is sometimes a side effect of chemotherapy or x-ray treatments for cancer. A new nail plate will form once the cause of the disease is removed.
Onychomycosis, also known as tinea unguium, is a contagious infection of the nail caused by the same fungal organisms which cause ringworm of the skin (Trichophyton rubrum or T. mentagrophytes, rarely other trichophyton species or Epidermophyton floccosum ). It can result in discoloration, thickening, chalkiness, or crumbling of the nails and is often treated by powerful oral medications which, rarely, can cause severe side effects including liver failure. Mild onychomycosis sometimes responds to a combination of topical antifungal medication, sometimes applied as special medicinal nail lacquer, and periodic filing of the nail surface. For advanced onychomycosis, especially if more than one nail is infected, systemic medication (pills) is preferred. Home remedies are often used, although their effectiveness is disputed.
Onychophosis is a growth of horny epithelium in the nail.
Onychoptosis is the periodic shedding of one or more nails, in whole or part. This condition may follow certain diseases such as syphilis, or can result from fever, trauma, systemic upsets or adverse reaction to drugs.
Onychorrhexis also known as brittle nails, is brittleness with breakage of fingernails or toenails.
Paronychia is a bacterial or fungal infection where the nail and skin meet.
Koilonychia is when the nail curves upwards (becomes spoon-shaped) due to an iron deficiency </s>