<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Complement receptor and explain in detail? [/INST] A complement receptor is a membrane-bound receptor belonging to the complement system, which is part of the innate immune system. Complement receptors bind effector protein fragments that are produced in response to antigen-antibody complexes or damage-associated molecules. Complement receptor activation contributes to the regulation of inflammation, leukocyte extravasation, and phagocytosis; it also contributes to the adaptive immune response. Different complement receptors can participate in either the classical complement pathway, the alternative complement pathway, or both.

Expression and function
White blood cells, particularly monocytes and macrophages, express complement receptors on their surface. All four complement receptors can bind to fragments of complement component 3 or complement component 4 coated on pathogen surface, but the receptors trigger different downstream activities. Complement receptor (CR) 1, 3, and 4 function as opsonins which stimulate phagocytosis, whereas CR2 is expressed only on B cells as a co-receptor.
Red blood cells (RBCs) also express CR1, which enables RBCs to carry complement-bound antigen-antibody complexes to the liver and spleen for degradation.
a.^ B: B cell </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Laryngeal paralysis and explain in detail? [/INST] Laryngeal paralysis in animals is a condition in which the nerves and muscles that control the movements of one or both arytenoid cartilages of the larynx cease to function, and instead of opening during aspiration and closing during swallowing, the arytenoids remain stationary in a somewhat neutral position. Specifically, the muscle that causes abduction of the arytenoid cartilage, the cricoarytenoideus dorsalis muscle, ceases to function. This leads to inadequate ventilation during exercise and during thermoregulatory panting as well as incomplete protection of the airway during swallowing.
One of the most common forms of laryngeal paralysis develops in geriatric medium to large breed dogs, in particular the Labrador retriever, but also some other breeds. This had been traditionally known as idiopathic laryngeal  paralysis ("ILP": idiopathic means "of unknown cause"), and was believed to be a result of a condition affecting the nerves of the larynx (bilateral mononeuropathy of the recurrent laryngeal nerves). However investigations into ILP by two groups in Michigan and Tennessee between 2005 - 2013 showed that the condition was not limited to, or specifically a result of, dysfunction of the laryngeal nerves. Instead it was the most visible symptom of a slowly progressing polyneuropathy of old age, which also affected other nerves in the body.  This finding, now generally believed correct following further research, has led to the proposed renaming of this type of laryngeal paralysis from "Idiopathic laryngeal paralysis" ("ILP") to "Geriatric onset laryngeal paralysis polyneuropathy" ("GOLPP").
Animals affected by laryngeal paralysis have reduced tolerance for exercise and heat and an increased risk of aspiration pneumonia. The condition is not generally regarded as causing pain, other than physical distress and anxiety caused by any difficulty in breathing or emotional distress from any difficulty with physical movement.  Where laryngeal paralysis is related to a general progressive polyneuropathy, as in GOLPP, the nervous system will gradually degenerate causing increasing difficulty in management of the limbs (especially rear limbs), swallowing and breathing, and eventually in most cases euthanasia. Laryngeal paralysis is fairly common in large breed and geriatric dogs, particularly in the Labrador retriever, is rarely found in cats, and can also occur in horses where it is referred to as roaring, roarers syndrome, or medically as laryngeal hemiplegia or  recurrent laryngeal neuropathy (RLN). Laryngeal paralysis can be unilateral or bilateral depending upon dysfunction of one or both arytenoid cartilages.

Causes
In most cases, the cause of laryngeal paralysis is unknown or idiopathic.  However, the disorder may arise secondary to general neuropathies, generalized neuromuscular diseases, muscular diseases, neoplasia either in the cervical (neck) region or the cranial mediastinum, or trauma. This acquired form occurs predominantly in middle-aged to old large breed or giant breed dogs such as the Labrador Retriever, golden retriever, Siberian Husky, Newfoundland, and St. Bernard.  Usually these dogs are born with a normal larynx, but over time the nerves and muscles that control the laryngeal cartilages lose function.Laryngeal paralysis may also be congenital in some breeds (e.g. Bouvier des Flandres, Dalmatians, Siberian huskies, and bulldogs), appearing in dogs between two and six months of age. Affected puppies may have difficulty swallowing and breathing, they may gag frequently, and their bark often sounds abnormal.  In Dalmatians it is part of another condition called laryngeal paralysis-polyneuropathy complex.   Affected puppies should not be used for breeding.Choke collars are not thought to be a significant risk factor for this disorder. However, after LP is diagnosed it is usually recommended to stop using a collar or anything else around the dogs neck and to switch to a harness instead.

Signs
Signs of laryngeal paralysis include voice change (the dogs bark becomes hoarse-sounding), gagging or coughing (often during or after eating or drinking), exercise intolerance, inspiratory stridor (noisy breathing on inspiration), difficulty breathing, and in severe cases cyanosis or syncope (fainting).  Secondary problems may also occur, including aspiration or edema in the lungs, though often the problem remains an upper respiratory problem.  Affected dogs are vulnerable to heat stroke and heat exhaustion due to their limited ability to cool themselves down by panting, but the disorder itself can be mistaken for heat stroke.
Signs may occur at any time, but initially owners may only notice that their dogs bark sounds different, that their dog cant run as much as before, or that the dog has trouble in hot weather in unilateral cases because the unaffected side can compensate for the paralysed side.  However most unilateral cases will eventually progress to include both sides of the larynx, a more serious problem with symptoms appearing more often.
Signs are usually worse in hot and humid weather, during exercise, during times of stress or excitement, and in obese pets.  Acute or late-stage symptoms are usually unmistakable and require immediate emergency treatment.

Diagnosis
This condition is usually diagnosed by direct examination of the larynx under light sedation, which also allows checking for benign or malignant tumors.  Tests, such as thoracic radiographs, CT-scans, or echocardiography, are sometimes needed to rule out heart, lung, or mediastinal diseases or other possible causes of the symptoms often seen with LP.  Some vets may also recommend running a thyroid profile since LP can be a symptom or complication of hypothyroidism.

Treatment
Mild cases are managed by limiting activity, keeping a healthy body weight, and avoiding exposure to high ambient temperatures. Mild sedatives can be used to decrease anxiety and panting and therefore improve respiration. Corticosteroids may also be administered in acute cases to decrease inflammation and edema of the larynx.
Severe acute symptoms, such as difficulty breathing, hyperthermia, or aspiration pneumonia, must be stabilized with sedatives and oxygen therapy and may require steroid or antibiotic medications. Sometimes a tracheotomy is required to allow delivery of oxygen. Once the patient is stabilized, surgical treatment may be beneficial especially when paralysis occurs in both arytenoid cartilages (bilateral paralysis). The surgery (aretynoid lateralization, or a "laryngeal tieback") consists of suturing one of the aretynoid cartilages in a maximally abducted (open) position. This reduces the signs associated with inadequate ventilation (such as exercise intolerance or overheating) but may exacerbate the risk of aspiration and consequent pneumonia.  Tying back only one of the arytenoid cartilages instead of both helps reduce the risk of aspiration </s>


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Erythema multiforme and explain in detail? [/INST] Erythema multiforme (EM) is a skin condition that appears with red patches evolving into target lesions, typically on both hands.It is a type of erythema possibly mediated by deposition of immune complexes (mostly IgM-bound complexes) in the superficial microvasculature of the skin and oral mucous membrane that usually follows an infection or drug exposure. It is an uncommon disorder, with peak incidence in the second and third decades of life. The disorder has various forms or presentations, which its name reflects (multiforme, "multiform", from multi- + formis) </s>


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


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Alveolar soft part sarcoma and explain in detail? [/INST] Alveolar soft part sarcoma, abbreviated ASPS, is a very rare type of soft-tissue sarcoma, that grows slowly and whose cell of origin is unknown.
ASPS arises mainly in children and young adults and can migrate (metastasize) into other parts of the body, typically the lungs and the brain. Typically, ASPS arises in muscles and deep soft tissue of the thigh or the leg (lower extremities), but can also appear in the upper extremities (hands, neck, and head). While ASPS is a soft tissue sarcoma, it can also spread and grow inside the bones.

Etymology
The term alveolar comes from the microscopic pattern, visible during the analysis of slides of ASPS under the microscope in histopathology. The tumor cells seem to be arranged in the same pattern as the cells of the small air sacks (alveoli) in the lungs. However, this is just a structural similarity. ASPS was first described and characterized in 1952.ASPS is a sarcoma, and that indicates that this cancer initially arises from tissue of embryonic mesenchymal origin.  (The fertilized egg divides and redivides forming a sphere.  Early in embryogenesis, dimples appear in the poles of the sphere and burrow through the sphere forming an inner passage that will ultimately form the gut. Malignancies arising from cells that were originally part of the outer layer of the sphere and those that were part of the embryonic tunnel are termed carcinomas; malignancies arising from the cells between the outer layer and the inner burrow are termed sarcomas.)

Causes
Chromosomal analysis of ASPS shows the breaking and joining of two chromosomes in the tumor cells. A piece of chromosome X breaks and is joined to chromosome 17. This translocation creates a fusion between two genes named ASPL and TFE3, which results in the formation of an aberrant protein (termed fusion protein) that is not found in normal cells. Two sorts of fusions between chromosome X and chromosome 17 are found in different ASPS tumors: type one and type two.
Dr. Marc Ladanyi at Memorial Sloan-Kettering Cancer Center, in New York City, has pioneered this work </s>


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


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


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


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Diffuse leprosy of Lucio and Latapí and explain in detail? [/INST] The diffuse leprosy of Lucio and Latapí, also known as diffuse lepromatous leprosy or "pretty leprosy" is a clinical variety of lepromatous leprosy </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Fat embolism syndrome and explain in detail? [/INST] Fat embolism syndrome occurs when fat enters the blood stream (fat embolism) and results in symptoms. Symptoms generally begin within a day. This may include a petechial rash, decreased level of consciousness, and shortness of breath. Other symptoms may include fever and decreased urine output. The risk of death is about 10%.Fat embolism most commonly occurs as a result of fractures of bones such as the femur or pelvis. Other potential causes include pancreatitis, orthopedic surgery, bone marrow transplant, and liposuction. The underlying mechanism involved widespread inflammation. Diagnosis is based on symptoms.Treatment is mostly supportive care. This may involve oxygen therapy, intravenous fluids, albumin, and mechanical ventilation. While small amounts of fat commonly occur in the blood after a bone fracture, fat embolism syndrome is rare. The condition was first diagnosed in 1862 by Zenker.

Signs and symptoms
Symptoms of fat embolism syndrome (FES) can start from 12 hours to 3 days after diagnosis of the underlying clinical disease. The three most characteristic features are: respiratory distress, neurological features, and skin petechiae. Respiratory distress (present in 75% of the cases) can vary from mild distress which requires supplemental oxygen to severe distress which requires mechanical ventilation. For neurologic features, those who have FES may become lethargic, restless, with a drop in Glasgow Coma Scale (GCS) due to cerebral oedema rather than cerebral ischaemia. Therefore, neurological signs are not lateralised to one side of the body. In the severe form of cerebral odema, a person may become unresponsive. Petechiae rash usually happens in 50% of the patients. Such skin manifestation is temporary and can disappear within one day. The fat embolism syndrome can be divided into three types:
Subclinical FES - It manifests as reduced partial pressure of oxygen (PaO2) on arterial blood gas (ABG) with deranged blood parameters (reduced haemoglobin or thrombocytopenia) associated with fever, pain, discomfort, tachypnoea, tachycardia. However, there is no respiratory distress. However, it is often confused with post-operative symptoms of fever, pain, and discomfort.
Subacute FES (non-fulminant FES) - The three characteristic features of fat embolism are present: respiratory distress, neurological signs, and skin petechiae. Petechiae are seen on the chest, axilla, shoulder, and mouth. Occulsion of dermal capillaries by the fat emboli result in petechial rash. Petechiae rash occurs in 50 to 60% of the cases. Neurologic signs such as confusion, stupor, and coma may be present. These are usually temporary and do not happen on one side of the body. Respiratory distress can be mild and tends to improve on the third day. Retinal changes similar to Purtschers retinopathy may also be present. Retinal changes happens in 50% of the patients with FES. These are the cotton wool exudates and small haemorrhages along the retinal vessels and macula.
Fulminant FES - This type of FES is much rarer than the above two types. It usually happens within the first few hours of the injury. The three characteristics of FES existed in the most severe form. Cause of death is usually due to acute right heart failure.

Causes
Orthopaedic injuries especially fractures of the long bones are the most common cause of fat embolism syndrome (FES). The rates of fat embolism in long bone fractures vary from 1% to 30%. The mortality rate of fat-embolism syndrome is approximately 10–20%. However, fat globules have been detected in 67% of those with orthopaedic trauma and can reach as high as 95% if the blood is sampled near the fracture site. As the early operative fixation of long bone fractures became a common practice, the incidence of FES has been reduced to between 0.9% and 11%.

Other rare causes of fat embolism syndrome are:
Severe burns
Liver injury
Closed chest cardiac massage (during cardiopulmonary resuscitation)
Bone marrow transplantation
Liposuction
Parenteral lipid infusion
Decompression sickness
Extracorporeal circulation
Acute haemorrhagic pancreatitis
Alcoholic liver disease
Prolonged corticosteriod therapy
Sickle cell disease
Carbon tetrachloride poisoning
Osteomyelitis

Pathophysiology
Once fat emboli enter the blood circulation, they can lodge at various sites of the body, most commonly in the lungs (up to 75% of cases). However, it can also enter the brain, skin, eyes, kidneys, liver, and heart circulation, causing capillary damage, and subsequently cause organ damage in these areas. There are two theories that describe the formation of a fat embolus:
Mechanical theory - Following trauma, fat is released directly from the bone marrow into the circulation. This is because after trauma, an elevated pressure in the medullary cavity (central cavity of the bone where the bone marrow are stored) causes the release of fat globules into the venous system supplying the bone. Since venous blood returns to the right heart and is pumped to the lungs for reoxygenation, the fat globules often get lodged in the pulmonary circulation. Fat globules may also pass through lung circulation back into the left ventricle of the heart to be pumped throughout the body in the systemic circulation. They may also reach the systemic circulation through a patent foramen ovale (a hole communicating the right atrium directly to the left atrium of the heart). If fat globules obstruct 80% of the lung capillary network, the resulting back pressure on the right heart increases workload and causes right heart dilatation through cor pulmonale, leading to acute right heart failure.
Biochemical theory - Following trauma, an inflammation causes bone marrow to liberate fatty acids into the venous circulation. This is achieved through the increased activity of lipoprotein lipase which break down triglycerides into free fatty acids. Both the release of fatty acids and the inflammation causes damage to the capillary beds of the lungs and other organs, causing interstitial lung disease, chemical pneumonitis, and acute respiratory distress syndrome (ARDS). This theory can help to explain non-traumatic causes of fat embolism.

Diagnosis
Fat embolism is presence of fat particles in the micro-circulation of the body. Meanwhile, fat embolism syndrome is the clinical manifestation as the result of fat particles lodging in the body micro-circulation. There are three major diagnostic criteria proposed for fat embolism syndrome, however, none of them are validated and accepted universally. However, Gurd and Wilsons criteria for fat embolism become more commonly used when compared to the other two diagnostic criteria.

Gurd and Wilsons criteria
Major criteria
Axillary or subconjunctival petechiae
Hypoxaemia PaO2 <60 mm Hg, FIO2 = 0.4
Central nervous system depression disproportionate to hypoxaemia
Pulmonary oedemaMinor criteria
Tachycardia more than 110 beats per minute
Pyrexia more than 38.5 °C
Fat globules present in urine
Changes in renal function (reduced urine output)
Drop in haemoglobin values (more than 20% of the value upon admission)
Drop in haematocrit values
Drop in platelet values (more than 50% of the value upon admission)
Increasing erythrocyte sedimentation rate (ESR) (greater than 71 mm per hour)
Fat globules present in the sputum
Emboli present in the retina on fundoscopyA least two positive major criteria plus one minor criteria or four positive minor criteria are suggestive of fat embolism syndrome. Fat embolism syndrome is a clinical diagnosis. There are no laboratory tests sensitive or specific enough to diagnose FES. Such laboratory tests are only used to support the clinical diagnosis only. Chest X-ray may show diffuse interstitial infiltrates while chest CT scan will show diffuse vascular congestion and pulmonary oedema. Bronchoalveolar lavage has been proposed to look for fat droplets in alveolar macrophages however it is time-consuming and is not specific to fat embolism syndrome. Looking for fat globules in sputum and urine is also not specific enough to diagnose FES.

Prevention
For those treated conservatively with immobilisation of long bone fractures, the incidence of FES  is 22%. Early operative fixation of long bone fractures can reduce the incidence of FES especially with the usage of internal fixation devices. Patients undergoing urgent fixation of long bone fractures has a rate of 7% of acute respiratory distress syndrome (ARDS) when compared to those undergoing fixation after 24 hours (39% with ARDS). However, movement of the fracture ends of the long bones during the operative fixation can cause transient increase of fat emboli in the blood circulation. Cytokines are persistently elevated if the long bone fractures is treated conservatively using immobilisation. The cytokine levels would return to normal after operative fixation. Although ream nailing increases pressure in the medullary cavity of the long bones, it does not increase the rates of FES. Other methods such as drilling of holes in the bony cortex, lavaging bone marrow prior to fixation, and the use of tourniquets to prevent embolisation have not been shown to reduce the rates of FES.Corticosteroid therapy such as methylprednisolone (6 to 90 mg/kg) has been proposed for the treatment of FES, however, it is controversial. Corticosteroid can be used to limit free fatty acid levels, stabilising membranes, and inhibit leukocyte aggregation. A meta-analysis conducted in 2009 reported prophylactic corticosteroids can reduce the risk of FES by 77%. However, there is no difference in mortality, infection, and avascular necrosis when compared to the control group. However, a randomised trial conducted in 2004 reported no differences in FES incidence when comparing treatment with the control group. Administration of corticosteroids for 2 to 3 days is not associated with increased rates of infection. However, there is insufficient data to support the use of methyprednisolone once FES is established.Heparin has been used in the prevention of venous thrombosis in post-operative patients; however its regular use in those with FES has been contraindicated due to increase risk of bleeding in those with polytrauma. Placement of inferior vena cava filters has been proposed to reduce the amount of emboli going into the lung vascular system, however, this method has not been studied in detail.

Treatment
Once FES develops,  the person should be admitted into intensive care unit (ICU), preferably with central venous pressure (CVP) monitoring. CVP monitoring would be helpful to guide the volume resuscitation. Supportive treatment is the only proven treatment method. Supplemental oxygen can be given if a person has mild respiratory distress. However, if a person has severe respiratory distress, either continuous positive pressure ventilation (CPAP), or mechanical ventilation using positive end-expiratory pressure (PEEP) may be indicated. Fluid replacement is required to prevent shock. Volume resuscitation with human albumin is recommended because it can restore blood volume in the circulatory system while also binds to free fatty acids in order to reduce lung injuries. In severe cases, dobutamine should be used to support the right ventricular failure </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Atonic seizure and explain in detail? [/INST] An atonic seizure (also called drop seizure, akinetic seizure,  astatic seizure, or drop attack) is a type of seizure that consists of partial or complete loss of muscle tone that is caused by temporary alterations in brain function. These seizures are brief – usually less than fifteen seconds. They usually begin in childhood and may persist into adulthood. The seizure itself causes no physical injury, but the loss of control, predominantly in trunk muscles, can result in direct injury from falling </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Idiopathic pulmonary haemosiderosis and explain in detail? [/INST] Idiopathic pulmonary haemosiderosis (IPH) is a lung disease of unknown cause that is characterized by alveolar capillary bleeding and accumulation of haemosiderin in the lungs. It is rare, with an incidence between 0.24 and 1.23 cases per million people.

Pathophysiology
Being idiopathic, IPH by definition has an unknown cause. It is thought to be an immune-mediated disease. The lung bleeding causes accumulation of iron, which in itself causes additional lung damage. Meanwhile, there is insufficient iron for inclusion into the haemoglobin molecules inside red blood cells which carry oxygen to body tissues for cellular respiration.Idiopathic pulmonary haemosiderosis can occur either as a primary lung disorder or as the sequela to other pulmonary, cardiovascular or immune system disorder.

PH1 involves PH with circulating anti-GBM antibodies.
PH2 involves PH with immune complex disease such as systemic lupus erythematosus, SLE.
PH3 involves no demonstrable immune system involvement.A distinct subset of patients with pulmonary hemosiderosis has hypersensitivity to cows milk which result in formation of IgG antibodies against basement membrane. This is called Heiner syndrome. Mechanism of haemorrhage is similar to that observed in Goodpasture syndrome.

Related or similar conditions
There are many pulmonary problems that may seem to mimic haemosiderosis but do not necessarily include the deposits of iron into the lung. The deposition of iron in the lungs, occurring in the form of haemosiderin, is the defining characteristic of this illness. These other conditions may occur separately or together with haemosiderosis.
Pulmonary fibrosis
Adult respiratory distress syndrome (ARDS)
Immune complex disease
intra-alveolar bleeding

Diagnosis
Clinically, IPH manifests as a triad of haemoptysis, diffuse parenchymal infiltrates on chest radiographs, and iron deficiency anaemia. It is diagnosed at an average age of 4.5 plus or minus 3.5 years, and it is twice as common in females. The clinical course of IPH is exceedingly variable, and most of the patients continue to have episodes of pulmonary haemorrhage despite therapy. Death may occur suddenly from acute pulmonary haemorrhage or after progressive pulmonary insufficiency resulting in chronic respiratory failure.

Treatment
Corticosteroids are the mainstay of treatment of IPH, though they are controversial and lack clear evidence in their favour </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Phlegmasia alba dolens and explain in detail? [/INST] Phlegmasia alba dolens (also colloquially known as milk leg or white leg; not to be confused with phlegmasia cerulea dolens) is part of a spectrum of diseases related to deep vein thrombosis. Historically, it was commonly seen during pregnancy and in mothers who have just given birth.  In cases of pregnancy, it is most often seen during the third trimester, resulting from a compression of the left common iliac vein against the pelvic rim by the enlarged uterus.  Today, this disease is most commonly (40% of the time) related to some form of underlying malignancy.  Hypercoagulability (a propensity to clot formation) is a well-known state that occurs in many cancer states. The incidence of this disease is not well reported.

Cause
The disease presumably begins with a deep vein thrombosis that progresses to total occlusion of the deep venous system.  It is at this stage that it is called phlegmasia alba dolens.  It is a sudden (acute) process.  The leg, then, must rely on the superficial venous system for drainage.  The superficial system is not adequate to handle the large volume of blood being delivered to the leg via the arterial system.  The result is edema, pain and a white appearance (alba) of the leg </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Comedo and explain in detail? [/INST] A comedo is a clogged hair follicle (pore) in the skin. Keratin (skin debris) combines with oil to block the follicle. A comedo can be open (blackhead) or closed by skin (whitehead) and occur with or without acne. The word "comedo" comes from the Latin comedere, meaning "to eat up", and was historically used to describe parasitic worms; in modern medical terminology, it is used to suggest the worm-like appearance of the expressed material.The chronic inflammatory condition that usually includes comedones, inflamed papules, and pustules (pimples) is called acne. Infection causes inflammation and the development of pus. Whether a skin condition classifies as acne depends on the number of comedones and infection. Comedones should not be confused with sebaceous filaments.
Comedo-type ductal carcinoma in situ (DCIS) is not related to the skin conditions discussed here. DCIS is a noninvasive form of breast cancer, but comedo-type DCIS may be more aggressive, so may be more likely to become invasive.

Causes
Oil production in the sebaceous glands increases during puberty, causing comedones and acne to be common in adolescents. Acne is also found premenstrually and in women with polycystic ovarian syndrome. Smoking may worsen acne.Oxidation rather than poor hygiene or dirt causes blackheads to be black. Washing or scrubbing the skin too much could make it worse, by irritating the skin. Touching and picking at comedones might cause irritation and spread infection. What effect shaving has on the development of comedones or acne is unclear.Some skin products might increase comedones by blocking pores, and greasy hair products (such as pomades) can worsen acne. Skin products that claim to not clog pores may be labeled noncomedogenic or nonacnegenic. Make-up and skin products that are oil-free and water-based may be less likely to cause acne. Whether dietary factors or sun exposure make comedones better, worse, or neither is unknown.A hair that does not emerge normally, an ingrown hair, can also block the pore and cause a bulge or lead to infection (causing inflammation and pus).Genes may play a role in the chances of developing acne. Comedones may be more common in some ethnic groups. People of Latino and recent African descent may experience more inflammation in comedones, more comedonal acne, and earlier onset of inflammation.

Pathophysiology
Comedones are associated with the pilosebaceous unit, which includes a hair follicle and sebaceous gland. These units are mostly on the face, neck, upper chest, shoulders, and back. Excess keratin combined with sebum can plug the opening of the follicle. This small plug is called a microcomedo.  Androgens increase sebum (oil) production. If sebum continues to build up behind the plug, it can enlarge and form a visible comedo.A comedone may be open to the air ("blackhead") or closed by skin ("whitehead"). Being open to the air causes oxidation, which turns it black. Cutibacterium acnes is the suspected infectious agent in acne. It can proliferate in sebum and cause inflamed pustules (pimples) characteristic of acne. Nodules are inflamed, painful, deep bumps under the skin.Comedones that are 1 mm or larger are called macrocomedones. They are closed comedones and are more frequent on the face than neck.Solar comedones (sometimes called senile comedones) are related to many years of exposure to the sun, usually on the cheeks, not to acne-related pathophysiology.

Management
Using nonoily cleansers and mild soap may not cause as much irritation to the skin as regular soap. Blackheads can be removed across an area with commercially available pore-cleansing strips (which can still damage the skin by leaving the pores wide open and ripping excess skin) or the more aggressive cyanoacrylate method used by dermatologists.Squeezing blackheads and whiteheads can remove them, but  can also damage the skin. Doing so increases the risk of causing or transmitting infection and scarring, as well as potentially pushing any infection deeper into the skin </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Monkeypox and explain in detail? [/INST] Monkeypox is an infectious viral disease that can occur in humans and some other animals. Symptoms include fever, swollen lymph nodes, and a rash that forms blisters and then crusts over. The time from exposure to onset of symptoms ranges from five to twenty-one days. The duration of symptoms is typically two to four weeks. There may be mild symptoms, and it may occur without any symptoms being known. The classic presentation of fever and muscle pains, followed by  swollen glands, with lesions all at the same stage, has not been found to be common to all outbreaks. Cases may be severe, especially in children, pregnant women or people with suppressed immune systems.The disease is caused by the monkeypox virus, a zoonotic virus in the genus Orthopoxvirus. The variola virus, the causative agent of smallpox, is also in this genus. Of the two types in humans, clade II (formerly West African clade) causes a less severe disease than the Central African (Congo basin) type. It may spread from infected animals by handling infected meat or via bites or scratches. Human-to-human transmission can occur through exposure to infected body fluids or contaminated objects, by small droplets, and possibly through the airborne route. People can spread the virus from the onset of symptoms until all the lesions have scabbed and fallen off; with some evidence of spread for more than a week after lesions have crusted. Diagnosis can be confirmed by testing a lesion for the viruss DNA.There is no known cure. A study in 1988 found that the smallpox vaccine was around 85% protective in preventing infection in close contacts and in lessening the severity of the disease. A newer smallpox and monkeypox vaccine based on modified vaccinia Ankara has been approved, but with limited availability. Other measures include regular hand washing and avoiding sick people and animals. Antiviral drugs, cidofovir and tecovirimat, vaccinia immune globulin and the smallpox vaccine may be used during outbreaks. The illness is usually mild and most of those infected will recover within a few weeks without treatment. Estimates of the risk of death vary from 1% to 10%, although few deaths as a consequence of monkeypox have been recorded since 2017.Several species of mammals are suspected to act as a natural reservoir of the virus. Although it was once thought to be uncommon in humans, the quantity and severity of outbreaks has significantly increased since the 1980s, possibly as a result of waning immunity since the stopping of routine smallpox vaccination. The first cases in humans were found in 1970 in the Democratic Republic of the Congo (DRC). There have been sporadic cases  in Central and West Africa, and it is endemic in the DRC.   The 2022 monkeypox outbreak represents the first incidence of widespread community transmission outside of Africa, which was initially identified in the United Kingdom in May 2022, with subsequent cases confirmed in at least 74 countries in all continents except Antarctica. On 23 July 2022, the World Health Organization (WHO) declared the outbreak a Public Health Emergency of International Concern (PHEIC) with more than 53,000 reported cases in 75 countries and territories.

Signs and symptoms
It is possible for a person to be infected with monkeypox without showing any symptoms. Monkeypox symptoms tend to begin 5 to 21 days after infection, with early symptoms including headache, muscle pains, fever and fatigue, initially resembling influenza. Within a few days of the fever, lesions characteristically appear on the face before appearing on the trunk then elsewhere such as palms of the hands and soles of the feet. The disease can resemble chickenpox, measles and smallpox but is distinguished by the presence of swollen glands which may appear behind the ear, below the jaw, in the neck or in the groin, before the onset of the rash. Many cases in the 2022 monkeypox outbreak presented with genital and peri-anal lesions, fever, swollen lymph nodes, and pain when swallowing, with  some patients manifesting only single sores from the disease.Three-quarters of affected people have lesions on the palms and soles, more than two-thirds in the mouth, a third on the genitals and one in five have lesions in the eyes. They begin as small flat spots, before becoming small bumps which then fill with at first clear fluid and then yellow fluid, which subsequently burst and scab over, persisting for around ten days. There may be a few lesions or several thousand, sometimes merging to produce large lesions. After healing, the lesions may leave pale marks before becoming dark scars.An unwell person may remain so for two to four weeks.

Complications
Complications include secondary infections, pneumonia, sepsis, encephalitis, and loss of vision with severe eye infection. If infection occurs during pregnancy, still birth or birth defects may occur. The disease may be milder in people vaccinated against smallpox in childhood. Patel and colleagues, in the BMJ, demonstrate that this virus can produce severe symptoms, particularly in HIV-positive people. The  descriptive case series reveal that symptoms can be so severe that hospitalization is required in 10% of cases. The study also shows that 75% of patients (15 out of 20 participants) admitted to the hospital were HIV-positive individuals. Overall, the study depict a new variety of clinical manifestations including proctitis and rectal perforation. The pictures of genital lesions published in the BMJ show the severity of monkeypox, which is often described as causing moderate symptoms.

In other animals
The disease has also been reported in dormice, tree squirrels, rope squirrels and non human primates. Rodents such as rats and mice are likely susceptible but not known.
Signs and symptoms in animals vary among different species. Monkeypox infected Gambian pouched rats may have mild symptoms. During the 2003 US outbreak, affected prairie dogs presented with fever, cough, sore eyes, poor feeding and rash. Non-human primates present similarly. They may have breathing problems, facial swelling, mouth ulcers and swollen glands. In cynomolgus monkeys, the time from exposure to symptoms was noted to be around a week. Rabbits and rodents typically present with fever, cough, runny nose, sore eyes and swollen glands. They develop small bumps that fill with yellow fluid and may have patches of hair loss and pneumonia.
Spread among animals occurs via the fecal-oral route and through the nose, through wounds and eating infected meat. Death is more likely in baby monkeys. The CDC recommend that animals exposed to monkeypox be quarantined for six weeks.

Causes
Monkeypox in both humans and animals is caused by infection with the monkeypox virus – a double-stranded DNA virus in the genus Orthopoxvirus, family Poxviridae. The virus was first identified in captive monkeys and is found mainly in tropical rainforest regions of Central and West Africa. The two subtypes of virus are clade I and clade II (formerly Congo Basin and West African clades, matching the geographical areas).In addition to monkeys, the virus has been identified in Gambian pouched rats (Cricetomys gambianus), dormice (Graphiurus spp.) and African squirrels (Heliosciurus, and Funisciurus). The use of these animals as food may be an important source of transmission to humans.

Transmission
Humans can be infected by an animal via a bite or scratch, bush meat preparation, or by contact with an infected animal’s bodily fluids or lesion material. The virus is thought to enter the body through broken skin, the respiratory tract, or the mucous membranes of the eyes, nose, or mouth.Once a human is infected, transmission to other humans is common, with family members and hospital staff at particularly high risk of infection. The virus can spread by respiratory (airborne) contact or by direct contact with an infected persons bodily fluids  or during pregnancy from mother to fetus. There are indications that transmission can occur during sexual contact, with infectious monkeypox virus able to be isolated from semen samples. Prolonged shedding in seminal fluids has raised the possibility of a genital reservoir for monkeypox virus. It is not known if the virus can spread through vaginal fluids.The virus can also spread via fomites or through indirect contact with lesion material, such as through contaminated bedding, even with standard personal protective equipment, likely through inhalation. Risk factors for transmission include sharing a bed or room, or using the same utensils as an infected person. Increased transmission risk is associated with factors involving the introduction of virus to the oral mucosa. It is not yet known if people without symptoms of monkeypox can spread the virus.Further research about the transmission of the strain responsible for the 2022 outbreak is ongoing, but it is not thought to be different from other strains of the clade II.

People living with HIV
According to a CDC report, 41% of cases of monkeypox were among HIV-positive patients (136 out of 334 patients) between May and July 2022. The New England Journal of Medicine (NEJM) also looked at more than 500 cases from different countries and found that 41% of them were among HIV patients. In addition, a study published in The Lancet that looked at nearly 200 cases in Barcelona and Madrid discovered that 40% were HIV-positive.  Patel and colleagues observed 197 patients from sexual health centres in south London between May and July 2022. They reported 35.5% patients had HIV-1 co-infection. 91.4% of these participants were receiving antiretroviral therapy and 78.6% had an undetectable HIV-1 viral load (<200 copies). The median CD4 count was 664 cells (interquartile range 522-894 cells). The proportion of HIV-positive individuals in these reports is significantly higher than the HIV rate among men who have sex with other men. The reasons for this heavy overrepresentation of men living with HIV among monkeypox cases are not fully understood yet.

Diagnosis
Clinical differential diagnosis must consider other rash illnesses, such as chickenpox, measles, bacterial skin infections, scabies, syphilis and medication-associated allergies. Lymphadenopathy during the prodromal stage of illness can distinguish monkeypox from chickenpox or smallpox. Diagnosis can be verified by testing for the virus.Polymerase chain reaction (PCR) testing of samples from skin lesions is the preferred laboratory test. PCR blood tests are usually inconclusive because the virus remains in blood only a short time. To interpret test results, information is required on date of onset of fever, date of onset of rash, date of specimen collection, current stage of rash, and patient age.

Prevention
Vaccination against smallpox is assumed to protect against human monkeypox infection because they are closely related viruses, and the vaccine protects animals from experimental lethal monkeypox challenges. This has not been conclusively demonstrated in humans because routine smallpox vaccination was discontinued following the eradication of smallpox.Smallpox vaccine has been reported to reduce the risk of monkeypox among previously vaccinated persons in Africa. The decrease in immunity to poxviruses in exposed populations is a factor in the prevalence of monkeypox. It is attributed to waning cross-protective immunity among those vaccinated before 1980, when mass smallpox vaccinations were discontinued, and to the gradually increasing proportion of unvaccinated individuals.The United States Centers for Disease Control and Prevention (CDC) recommends that persons investigating monkeypox outbreaks and involved in caring for infected individuals or animals should receive a smallpox vaccination to protect against monkeypox. Persons who have had close or intimate contact with individuals or animals confirmed to have monkeypox should also be vaccinated. However, the CDC does not recommend pre-exposure vaccination for unexposed veterinarians, veterinary staff, or animal control officers, unless such persons are involved in field investigations. No smallpox or monkeypox vaccine has been approved for use during pregnancy. The CDC recommends that healthcare providers don a full set of personal protective equipment (PPE) before caring for an infected person. This includes a gown, mask, goggles, and a disposable filtering respirator (such as an N95). An infected person should be isolated in preferably a negative air pressure room or at least a private exam room to keep others from possible contact.Monkeypox prevention cannot be simplified to just providing a vaccine. There are more pressing challenges to address, such as access to treatment, veracity and availability of information, and quality of health care. Public health messaging is perhaps the most important challenge. The multiple levels of interconnectivity and negotiated social meanings inherent to the disease require cooperation between medical professionals and patients to achieve correct public health communication. Therefore, Scalvini argues in the BMJ that it is necessary a "new ethic of shared responsibility" to educate people about dangers and give people from underprivileged groups the tools they need to make better decisions.

Treatment
In the European Union and the United States, tecovirimat is approved for the treatment of several poxviruses, including monkeypox. BMJ Best Practice recommends tecovirimat or the smallpox treatment brincidofovir as the first line antiviral treatment if required, alongside supportive care (including antipyretic, fluid balance and oxygenation). Empirical antibiotic therapy or aciclovir may be used if secondary bacterial or varicella zoster infection is suspected, respectively.

Outcome
After healing, the scabs may leave pale marks before becoming darker scars. The risk of death in those infected ranges from 0% to 11%, depending on the type of monkeypox and location in the world. Fatality rates have been reported as around 3.6% in West Africa and 10.6% in Central Africa. Most reported deaths have occurred in young children and people with HIV infection.

Epidemiology
In 1970, monkeypox was first associated with an illness as a disease in humans in the Democratic Republic of the Congo (formerly Zaire), in the town of Basankusu, Équateur Province.
Although it was once thought to be uncommon in humans, cases increased since the 1980s, possibly as a result of waning immunity since the stopping of routine smallpox vaccination.Between 1981 and 1986  WHO surveillance in DRC/Zaire recorded 338 confirmed cases and 33 deaths (CFR 9.8%). In 1996–1997, a second outbreak of human illness was identified in DRC/Zaire and between 1991 and 1999, 511 cases were reported in DRC/Zaire. Clade I of disease remains endemic in DRC and has a higher CFR than the other genetic clade in Western Africa.By May 2022, the case fatality rate (CFR) of past outbreaks was around 3%–6%, while the CFR of the 2022 outbreak remains below 1%. No human-to-human transmission was documented until the 2022 monkeypox outbreak in Europe. Clade II had an outbreak – the first outbreak of monkeypox outside of Africa – in Midwestern United States among owners of pet prairie dogs in 2003. Seventy-one people were reportedly infected, of whom none died.As of 2018, monkeypox was traditionally restricted to the ecology of tropical rainforests. although the pattern was broken in 2005, when 49 cases were reported in Sudan (areas now South Sudan), with no fatalities. The genetic analysis suggested that the virus did not originate in Sudan but was imported, most likely from DRC.Many more monkeypox cases have been reported in Central and West Africa, and in the Democratic Republic of Congo in particular: 2000 cases per year are known between 2011 and 2014. The collected data is often incomplete and unconfirmed, which hinders realistic estimations of the number of cases of monkeypox over time. Nevertheless, it was suggested that the number of reported monkeypox cases had increased and the geographical occurrence broadened as of 2018.

2003 U.S. outbreak
In May 2003, a young child became ill with fever and rash after being bitten by a prairie dog purchased at a local swap meet near Milwaukee, Wisconsin. In total, 71 cases of monkeypox were reported through June 20, 2003. All cases were traced to Gambian pouched rats imported from Accra, Ghana, in April 2003 by a Texas exotic animal distributor. No deaths resulted. Electron microscopy and serologic studies were used to confirm that the disease was human monkeypox.People with monkeypox typically experienced prodromal symptoms of fever, headaches, muscle aches, chills, and drenching sweats. Roughly one-third of infected people had nonproductive coughs. This prodromal phase was followed 1–10 days later by the development of a papular rash that typically progressed through stages of vesiculation, pustulation, umbilication, and crusting. In some people, early lesions had become ulcerated.Rash distribution and lesions occurred on head, trunk, and extremities. Many of the people had initial and satellite lesions on palms, soles, and extremities. Rashes were generalized in some people. After onset of the rash, people generally manifested rash lesions in different stages. Everyone affected reported direct or close contact with prairie dogs, later found to be infected with the monkeypox virus.

2017–2019 Nigeria outbreak
According to the Nigeria Centre for Disease Control (NCDC), between 1971 and 1978, only 10 human monkeypox infections were reported in the country.In September 2017, human monkeypox re-emerged in Nigeria, 39 years since it had been last reported. The subsequent 2017–18 Nigerian human monkeypox outbreak was, at that time, the largest ever outbreak of clade II of the virus, with 118 confirmed cases. Unlike previous outbreaks of this clade, infection was predominantly among young male adults and human-to-human transmission appears to have readily occurred. Seven deaths (5 male, 2 female, case fatality rate of 6%) were reported, including a baby and four HIV/AIDS patients. Additionally, a pregnant woman in her second trimester had a spontaneous miscarriage due to monkeypox infection.The Niger Delta University Teaching Hospital reported that a substantial number of its young adult cases had concomitant genital ulcers, syphilis and HIV infection.
Monkeypox spread around southeast and south Nigeria with some states and the federal government of Nigeria seeking ways to contain it. By December 2017 it spread to Akwa Ibom, Abia, Bayelsa, Benue, Cross River, Delta, Edo, Ekiti, Enugu, Imo, Lagos, Nasarawa, Oyo, Plateau, Rivers and Federal Capital Territory. The outbreak started in September 2017 and remained ongoing across multiple states as of May 2019.
The Centers for Disease Control and Prevention reported cases of American travelers contracting Monkeypox upon return from Lagos and Ibadan. Agam Rao, a medical officer in the Division of Pathogens and High Consequence Pathology at the CDC, said that since 2018 all cases reported outside Africa have come from Nigeria.In a 2021 article Oyewale Tomori pointed out that the number of monkeypox infections in Nigeria through 2021 was likely to be under-represented, because much of the Nigerian population had been avoiding healthcare facilities due to fear of contracting COVID-19.In May 2022, the Nigerian government released a report stating that between 2017 and 2022, 558 cases were confirmed across 32 states and the Federal Capital Territory. The Rivers State was the most affected by monkeypox followed by Bayelsa and Lagos. There were 8 deaths reported, making for a 3.5% Case Fatality Ratio. In 2022, NCDC implemented a National Technical Working Group for reporting and monitoring infections, strengthening response capacity.

2018 and 2019 United Kingdom cases
In September 2018, the United Kingdoms first case of monkeypox was recorded. The person, a Nigerian national, is believed to have contracted monkeypox in Nigeria before travelling to the United Kingdom. According to Public Health England, the person was staying in a naval base in Cornwall before being moved to the Royal Free Hospitals specialised infectious disease unit. People who had been in contact with the person since he contracted the disease were contacted.A second case was confirmed in the town of Blackpool, with a further case that of a medical worker who cared for the case from Blackpool. A fourth case occurred on 3 December 2019, when monkeypox was diagnosed in a person in south west England. They were travelling to the UK from Nigeria.

2019 Singapore case
On 8 May 2019, a 38-year-old man who travelled from Nigeria was hospitalised in an isolation ward at the National Centre for Infectious Diseases in Singapore, after being confirmed as the countrys first case of monkeypox. As a result, 22 people were quarantined. The case may have been linked to a simultaneous outbreak in Nigeria.

2021 cases in United Kingdom, United States
On 24 May in the UK, three cases of monkeypox from a single household were identified by Public Health Wales. The cases were also announced by Health Secretary Matt Hancock while addressing MPs. The index case was diagnosed on 24 May after traveling from Nigeria. The second case was reported on 2 June, and the third on 24 June. One of the three patients, an adult female, was treated with tecovirimat. On day 7 of tecovirimat, she was discharged from hospital to complete her second week of treatment at home.On 14 July in the US, an American returning from a trip in Nigeria was diagnosed with monkeypox. Subsequent testing identified the virus as belonging to clade II. The patient was hospitalized and treated with tecovirimat and was discharged after 32 days, at which time monkeypox virus DNA could no longer be detected in residual skin lesions.

2022 outbreak
History
Monkeypox was first identified as a distinct illness in 1958 among laboratory monkeys in Copenhagen, Denmark.
The first documented cases in humans was in 1970, in six unvaccinated children during the smallpox eradication efforts; the first being a 9-month old boy in the Democratic Republic of the Congo (formerly Zaire). The others, including three who were playmates, were in Liberia and Sierra Leone. It was noted to be less easily transmissible than smallpox. From 1981 to 1986, over 300 cases of human monkeypox were reported in the DRC, the majority being due to contact with animals. In 1996, the disease reemerged in the DRC with 88% of cases resulting from human-to-human transmission. Small viral outbreaks with a death rate in the range of 10% and a secondary human-to-human infection rate of about the same amount occur routinely in equatorial Central and West Africa </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Macrophagic myofasciitis and explain in detail? [/INST] Macrophagic myofasciitis (MMF) is a histopathological finding involving inflammatory microphage formations with aluminium-containing crystal inclusions and associated microscopic muscle necrosis in biopsy samples of the deltoid muscle. Based on the presence of aluminium and the common practice of administering vaccines into the deltoid, it has been proposed that the abnormalities are a result of immunisation with aluminium adjuvant-containing vaccines. The findings were observed in a minority of persons being evaluated for "diffuse myalgias, arthralgias or muscle weakness" who underwent deltoid muscle biopsies. The individuals had a history of receiving aluminium-containing vaccines, administered months to several years prior to observation of MMF histopathology, however this link is tenuous and unsustainable </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Tonsil carcinoma and explain in detail? [/INST] Carcinoma of the tonsil is a type of squamous cell carcinoma. The tonsil is the most common site of squamous cell carcinoma in the oropharynx. It comprises 23.1% of all malignancies of the oropharynx. The tumors frequently present at advanced stages, and around 70% of patients present with metastasis to the cervical lymph nodes.
. The most reported complaints include sore throat, otalgia or dysphagia. Some patients may complain of feeling the presence of a lump in the throat. Approximately 20% patients present with a node in the neck as the only symptom.Main risk factors of developing carcinoma tonsil include tobacco smoking and regular intake of high amount of alcohol. It has also been linked to human papilloma virus (HPV type HPV16). Other risk factors include poor maintenance of oral hygiene, a genetic predisposition leading to inclination towards development of throat cancer, immunocompromised states (such as post solid-organ transplant), and chronic exposure to agents such as asbestos and perchloroethylene in certain occupations, radiation therapy and dietary factors.

Signs and symptoms
The early lesions are usually asymptomatic. The patients presenting with an advanced stage of the disease comprises around 66–77% of the cases.
The most important signs include a lump in the neck when palpated and weight loss.
People may also present with fatigue as a symptom.The primary tumor does not have readily discernible signs or symptoms as they grow within the tonsillar capsule. It is difficult to notice anything suspicious on examination of the tonsil other than slight enlargement or the development of firmness around the area.
The carcinoma may occur in one or more sites deep within the tonsillar crypts. It may be accompanied by the enlargement of the tonsil. The affected tonsil grows into the oropharyngeal space making it noticeable by the patient in the form of a neck mass mostly in the jugulodigastric region.
As the tonsils consist of a rich network of lymphatics, the carcinoma may metastasize to the neck lymph nodes which many are cystic.
Extension of tumor to skull or mediastinum can occur.
The additional symptoms include a painful throat, dysphagia, otalgia (due to cranial nerve involvement), foreign body sensation, bleeding, fixation of tongue (infiltration of deep muscles) and trismus (if the pterygoid muscle is involved in the parapharyngeal space).On the other hand, the tumor may also present as a deep red or white fungating wound growing outwards, breaking the skin surface with a central ulceration. This wound-like ulcer fails to heal (non-healing) leading to bleeding and throat pain and other associated symptoms.During biopsy, the lesion may show three signs: gritty texture, firmness and cystification owing to keratinization, fibrosis and necrosis respectively.Cervical lymphydenopathy may be present.

Cause
Smoking and alcohol abuse are the major risk factors. Viral causes have recently been taken under consideration as one of the risk factors. Viruses such as Epstein-Barr virus (EBV) (majorly involved in causing nasopharyngeal carcinoma) and human papilloma virus are included in this category. Chewing of betel nut (Areca catechu) quid has been directly associated to cause oral cancers. It has also been stated under the FDA poisonous plant data base by the U.S Food and Drug Administration
An unbalanced diet, deficit in fruits and vegetables has shown to increase the risk of cancer.

Pathophysiology
Metastasis to regional lymphnodes is common as the tonsil has a rich supply of lymphatics giving way to the tumor cells to metastasis to other lymph nodes (commonly the lymph nodes of neck) and cause lymphydenopathy. The cervical lyphydenopathy can be ipsilateral (70% or more patients) or bilateral (30% and fewer patients). The carcinoma of tonsil usually spreads through the cervical lymph node levels II, III, IV, V, and retropharyngeal lymph nodes.The fourth edition of WHO s classification of head and neck tumors subdivides squamous cell carcinoma of the tonsil into two types: HPV positive or negative. HPV positive tumors arise from the deep lymphoid tissue of the tonsillar crypts and are non-keratinizing. On the other hand HPV negative tumors develop from the tonsillar surface epithelium and hence have keratinizing dysplasia.

Routes of metastasis
Metastasis is common in tonsillar carcinoma. It largely depends on the stage of the cancer and the route through with the cancer cells metastasize.
The cancer cells may spread to adjacent structures, to lymphatics or to distant locations in the body producing secondary tumors.

Local
The tumor may spread locally to soft palate and pillars, base of tongue, pharyngeal wall and hypopharynx. It may invade pterygoid muscles and mandible, resulting in pain and trismus. Parapharyngeal space may also get invaded.

Lymphatic
50% of patients have initial cervical node involvement at the time of presentation. Jugulardigastric nodes are the first to be involved.

Distant metastasis
The occurrence of distant metastasis varies extensively, ranging between 4–31% in clinical studies.
Factors influencing the incidence of distant metastasis are:
Location of primary tumor.
Initial staging
Histological differentiation
Loco-regional control of the primary tumor.The records of 471 male patients with tonsillar carcinoma seen at the Veterans Administration Medical Center, Hines, Illinois, have been reviewed to establish the incidence and site of distant metastasis. All the patients were histological diagnosed and proven cases of tonsillar carcinoma. 72 (15%) out of 471 patients and 33 (29%) of 155 autopsied patients were reported to have distant metastasis.
Squamous cell carcinoma was the most common reported cell type (88%); cases with Lymphoepithelioma had the highest incidence of distant metastasis. The most common anatomical sites of incidence of distant metastasis include lung, liver and bones.
Thorough investigation of these organs is highly recommended before treatment as well as during follow ups.

Diagnosis
The first step to diagnosing tonsil carcinoma is to obtain an accurate history from the patient. The physician will also examine the patient for any indicative physical signs. A few tests then, maybe conducted depending on the progress of the disease or if the doctor feels the need for. The tests include:
Fine needle aspiration, blood tests, MRI, x-rays and PET scan.

Staging
The staging of a tumor mass is based on TNM staging.T staging is the based on the tumor mass. The N staging is based on the extent of spread of cancer to the lymph nodes. Finally, the M stage indicates if the cancer has spread beyond the head and neck or not.

T Staging
The basis of deciding the T stage depends on physical examination and imaging of the tumor.

N staging
This stage is decided through the assessment of the lymph nodes.

M staging
Based on the examination of the entire body.

FInally, the stage is decided by concluding the above results and referring the following chart:

Treatment
The treatment for tonsil carcinoma includes the following methods:

Radiotherapy
Early radio-sensitive tumors are treated by radiotherapy along with irradiation of cervical nodes. The radiation uses high-energy X-rays, electron beams, or radioactive isotopes to destroy cancer cells.

Chemotherapy
Induction chemotherapy is the treatment adapted for shrinking the tonsil tumor. It is given prior to other treatments, hence, the term induction. After the therapy is completed, the patient is asked to rest and is evaluated over a period of time. Then the patient is given chemo-radiation therapy (a combination of chemotherapy and radiation) to completely destroy the tumor cells.

Surgery
If radiation and chemotherapy are unable to destroy the tumor, surgical intervention is considered. Excision of the tonsil can be done for early superficial lesions. Large lesions and those which invade bone require wide surgical excision with hemimandibulectomy and neck dissection (Commando operation)

Combination therapy
Surgery may be combined with pre- or post operative radiation.
Chemotherapy may be given as an adjunct to surgery or radiation.

Prognosis
Prognosis is determined by various factors such as stage, Human Papilloma Virus (HPV) status, Lymph infiltration of cancer cells, spread of cancer cells beyond the lymph node capsule, margins of the tumor and the extent of metastasis.
Many factors are unique to each individual patient and may affect the chances of success of the treatment.
Factors determining the prognosis of tonsillar carcinoma are as follows:

HPV status
Tonsillar carcinoma can be either HPV related or HPV unrelated. It is shown that cases which are HPV positive have a better prognosis than those with HPV negative oropharyngeal cancer.

Stage
The stage at which the cancer presents itself affects the type of definitive treatment, chance of cure, recurrence of cancer and survival rate of the patient. Generally the patient presents very late due to the lack of definitive symptoms in the early stages of the disease. Nearly three fourths of the patients present in Stage III or later.The stages of oropharyngeal cancer are as follows:
• Stage 0 (carcinoma in situ): This stage indicates a good prognosis as most patients with stage 0 survive for a long period without the requirement of an intensive treatment. Although, the patient must cease smoking as it can increase the risk of developing a new cancer.• Stage I and II: Most patients presenting at this stage receive successful treatment, showing a good prognosis. The modes of treatment for this stage include chemotherapy, surgery, radiation therapy or chemoradiation. The main treatment at this stage is radiation, targeting the tumor and the cervical lymph nodes. Surgical removal of the tumor and lymphadenectomy of the cervical (neck) lymph nodes can also be taken up at the main treatment method instead of radiation. And remaining cancer cells post surgery are treated with chemoradiation.• Stage III and IVA: In this stage the cancer cells metastasize into the local tissues and cervical lymph nodes. The treatment used in these cases is chemo radiation </s>