Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There are three clinical presentations of anthrax in humans: cutaneous (>95% of cases), orogastric and inhalational. The infectious form, the spore, enters the body and is thought to germinate within macrophages either at the site of inoculation (cutaneous or orogastric) or in the regional lymph node (inhalational). The bacillus then synthesizes its antiphagocytic capsule and the lethal and oedema toxins which interfere with the non-specific host defences leading to the characteristic locally destructive lesion and spread by lymphatics to the systemic circulation and other organs. The cutaneous form begins as a papule which progresses over several days to a vesicle and then ulcerates. There is often oedema, sometimes massive, probably due to the oedema toxin that surrounds the lesions which then develop a characteristic black eschar. The patient may be febrile with mild to severe systemic symptoms of malaise, headache and toxicity. Oropharyngeal anthrax presents with severe sore throat or an ulcer in the oropharyngeal cavity associated with neck swelling, fever, toxicity and dysphagia. Gastrointestinal anthrax begins with anorexia, nausea, vomiting and abdominal pain which may be similar to an acute abdomen. There may be diarrhoea and ascites, both of which may be haemorrhagic. Inhalational anthrax begins with non-specific symptoms of malaise, fever, myalgia and non-productive cough. After a period of 2-3 days, this is followed by a sudden onset of severe respiratory distress associated with diaphoresis, cyanosis and increased chest pain. There may be a widened mediastinum and pleural effusions on chest X-ray. Death follows in 24-36 h from respiratory failure, sepsis and shock. The diagnosis of anthrax is easy if it is considered. The organism is readily observed by Gram or Wright stain in local lesions or blood smear and can be easily cultured from the blood and other body fluids. However, because of its rarity, it is not often included in the differential diagnosis and in inhalational disease the diagnosis is rarely made until the patient is moribund. More rapid diagnostic tests are under development. Penicillin, combined with supportive care, remains the mainstay of treatment, although the organism is susceptible in vitro to many antibiotics. In recent years, there have been significant advances in our knowledge of the organism and its toxins and it is anticipated that similar progress will be made in the future in developing more rapid diagnostic tests and new modalities of treatment.
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PMID:Clinical aspects, diagnosis and treatment of anthrax 1047 74

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

This report describes the clinical presentation of two Cavalier King Charles spaniels with different eosinophilic diseases. The first case presented with dyspnoea and a non-productive cough, and investigations demonstrated eosinophilic bronchopneumonopathy. The second dog was referred for the investigation of haemorrhagic vomiting and diarrhoea and was eventually diagnosed with eosinophilic enteritis. Both dogs had concurrent eosinophilic stomatitis, and both responded completely to immunosuppressive glucocorticoid therapy. This report is the first to describe the concurrence of eosinophilic stomatitis and systemic eosinophilic disease in Cavalier King Charles spaniels, and suggest that this breed may be predisposed to eosinophilic syndromes.
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PMID:Eosinophilic diseases in two Cavalier King Charles spaniels. 1248 41

A 22-year-old woman presented with a 3-day history of worsening epigastric pain, non-productive cough and vomiting. On examination she was pale and had abdominal tenderness predominant in the right upper quadrant. Abdominal ultrasound excluded the presence of gall stones, but was unable to rule out free fluid in the abdomen. CT demonstrated extensive high-density ascites; however, no source of bleeding could be demonstrated. Clinically the patient's condition deteriorated, and an exploratory laparotomy was performed. In theatre the splenic capsule was found to have detached from the splenic body and emergency splenectomy was performed. Virology serology later demonstrated acute cytomegalovirus (CMV) infection, although tissue microscopy and CMV staining were negative. No other cause of rupture was found. The interesting aspects of this case include the poor correlation between initial presenting symptoms and subsequent diagnosis, the difficulty encountered in making a firm diagnosis and the atypical cause of rupture.
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PMID:An unusual diagnosis of splenic rupture. 2529 83

Anti-glomerular basement membrane disease has been reported to coexist with anti-neutrophil cytoplasmic antibody (ANCA) positive vasculitis. Seronegative anti-GBM disease has been previously described and mostly blamed for the relative insensitivity of earlier serologic assays. A 58-year-old male was transferred to our facility for acute kidney injury. Prior to his hospital admission, the patient had a 2 week history of progressive fatigue, fevers, anorexia, vomiting, decreased urine output, sinus congestion, and non-productive cough. His creatinine reached 13 mg/dL. P-ANCA was positive, anti GBM antibody was negative twice, and urinalysis showed hematuria. Chest x-ray demonstrated diffuse opacities, concerning for pulmonary hemorrhage. Renal biopsy showed a severe necrotizing and crescentic glomerulonephritis with circumferential crescents. There was bright linear glomerular basement membrane staining with IgG consistent with anti-GBM disease. Given these findings, the patient was started on oral cyclophosphamide (160 mg daily), in addition to pulse dose methylprednisolone. He was also initiated on therapeutic plasma exchange. Due to worsening renal function, hemodialysis was started. The patient was discharged from the hospital and completed a course of treatment with cyclophosphamide and prednisone but remains oligo-anuric and hemodialysis dependent at 150 days since presentation. This case highlights the importance of tissue diagnosis in situations similar to this.
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PMID:Seronegative anti-GBM Disease with Coexistent ANCA Positivity. 2598 56