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)

A 6-year-old male Yorkshire Terrier had clinical signs including intermittent vomiting and diarrhea associated with abdominal distention. Contrast radiography disclosed dilatation and decreased motility of the small intestine, with dilution of barium. Hemograms, blood chemical profiles, and results of fecal examinations and urinalyses were normal. Obstruction was not found at exploratory laparotomy, but a dilated segment of mid-jejunum was biopsied. There was hypoplasia of the tunica muscularis of the jejunum, without fibrosis, inflammation, or myenteric plexus involvement. The diagnosis was idiopathic intestinal pseudoobstruction. Post-operative care consisted solely of feeding bland foods. Three months after surgery there was progressive deterioration and emaciation due to chronic intestinal malabsorption.
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PMID:Intestinal pseudoobstruction in a dog. 65 2

Three female patients with cachexia are reported in whom a psychogenic emaciation (anorexia nervosa) had been assumed. The postpubertal onset of the disease, deliberate limitation of diet, vomiting and subsequent emaciation and--in 2 patients--amenorrhea, as well as demonstrable experience of conflict supported this. The disease ran a lethal course. Autopsy revealed serious somatic diseases (stenosis of the ileum in two cases and brain tumor in one); their symptoms had been largely overlapped by those of anorexia nervosa.
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PMID:[The differential diagnosis of anorexia nervosa. Coincidence of somatic disease and psychogenic emaciation (author's transl)]. 81 92

The paper is concerned with a description of a special form of nervous anorexia related to the presence of vomitophobia. The disease appears on the background of a somatogenic asthenia as a psychogenic reaction and leads to an expressed vomiting reaction. The vomiting reaction becomes fixated with a habitual form of reaction and eventually leads to an emaciation and a development of a special vomitophobic syndrome (vomitophobia proper, voluantary and involuntary vomiting, limitation in food as a measure against vomiting, depression, special ideas of reference).
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PMID:[Atyptical forms of anorexia nervosa]. 85 42

A 5-week-old mixed-breed dog was examined because of emaciation and depression associated with chronic anorexia, diarrhea, and vomiting. Its rectal temperature was subnormal and it died on the day of admission. At necropsy, small focal lesions were distributed through the liver. Enteric alterations included catarrhal enteritis with fluid contents, excess production of mucus, and mucosal hyperemia. Microscopically, the hepatic lesions were disseminated foci of coagulative necrosis, with little or no associated inflammatory cell response. Numerous organisms morphologically consistent with Bacillus piliformis were demonstrated within viable hepatocytes at the periphery of the necrotic foci and in the intestinal mucosa. Numerous coccidial forms were found within the epithelial cells of the intestinal mucosa, which was focally necrotic.
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PMID:Tyzzer's disease in a dog. 127 Mar 43

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

An infection with Ollulanus tricuspis was found in three cats with hypertrophic gastritis. Two cats were put down because of chronic vomiting and emaciation. The third cat died shortly after the appearance of blood in its vomit and faeces.
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PMID:[3 cases of hypertrophic gastritis associated with a Ollulanus tricuspis infection in cats]. 148 Nov 95

Four investigators conducted participative observation at 4 hamlets, representing 4 typical topography in the area, wet or dry near the river and wet or dry far from the river, in District Rambutan, South Sumatera Province, Indonesia from July 1988 up until February 1989 to study the community perception and practices on diarrheal diseases (DD). The observation was supported by focus group discussions and informal interviews. It was found that the causes of DD can be grouped into: dirty water; wrong (cold, hot, sting) food; part of the growth process; physical condition (extreme heat, cold wind and inner abnormality, inner heat, muscle strain), and supernatural. The type of DD can be grouped into: mild without vomiting named ngadi, negenteng-ngentengi, nambah kepacakan, etc which was linked to the growth process; more severe diarrhea, might be with fever (mising-mising, murus, mencret, etc); more severe diarrhea with severe vomiting (muntager, kolera); bloody/mucoid stool (disentri, mising tai angin, mising umbal). The community had also the concept of prolonged diarrhea named as menerus (literally meaning prolonged) Muntaber was more associated with bad water while the prolonged one was more associated with inner abnormality. The danger of diarrhea perceived was susut = shrinkage, lisut = emaciation. Pale and red hair with lisut were recognized as the dangers of prolonged diarrhea. The community did not associate these conditions with fluid loss. The management started by self medication using tapel (pasta of herb applied) to the stomach), decoct (daun jambu, akar teratai etc), solid oral preparation (cassava with raw sugar, rast rice, etc).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Community perceptions on diarrheal diseases: a case study in swampy lowland area of south Sumatra, Indonesia. The Diarrheal Diseases Research and Training Study Group. 185 67

The case of a young women with dysphagia, regurgitation, and weight loss, who was diagnosed as having anorexia nervosa but in whom reevaluation showed that achalasia was causing the symptoms, is presented together with related observations. Misinterpretation of esophageal symptoms may occur not only as a consequence of inadequate history taking and of being biased by a patient's emaciation, age, and gender, which leads to view certain aspects of the patient's history and behavior as suggesting a pathologic attitude towards eating and body weight, but also as a consequence of a misinterpretation of the symptoms as indicative of an eating disorder by the patients themselves. In some cases a disordered attitude toward eating and body weight may develop together or coexist with achalasia. The clinical evaluation of patients with symptoms suggestive of anorexia nervosa but also of bulimia nervosa should include the taking of a thorough history regarding swallowing and vomiting in order to recognize a possible esophageal motor disorder.
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PMID:Symptoms of achalasia in young women mistaken as indicating primary anorexia nervosa. 227 21

Acute toxicity studies of propiverine hydrochloride (P-4) were carried out in mice, rats and dogs of both sexes. 1. The LD50 values of P-4 were as follows: Mice; 410 (male) and 323 (female) mg/kg in oral route, 223 (male) and 283 (female) mg/kg in subcutaneous route and 36 (male and female) mg/kg in intravenous route, Rats; 1000 (male) and 1092 (female) mg/kg in oral route, 1632 (male) and 1411 (female) mg/kg in subcutaneous route, and 22 (male) and 25 (female) mg/kg in intravenous route. On the LD50 values, no sexual difference was apparent but the species difference between mice and rats observed to be present in oral and subcutaneous routes. The approximate lethal doses of P-4 in dogs were 987-1137 mg/kg for male and 865-894 mg/kg for female in oral route, and the values were almost same as those in rats of oral route. 2. Major toxic signs such as clonic convulsion, bradypnoea, dyspnoea, decreased spontaneous activity and hematuria were observed in mice and rats. Furthermore mydriasis in rats, and transitory salivation and/or vocalization in mice and rats were observed. In some rats, sedation, salivation, soil at hypogastrium, rale and emaciation were detected from the next day of oral administration. In dogs, toxic signs such as vomiting, tremor, tonic and/or clonic convulsion, mydriasis and gasping were observed. 3. Pathological changes observed in dead animals were congestion of lungs, liver and kidneys in all routes, congestion and hemorrhage in digestive tracts in oral route, inflammatory changes at the injection site in subcutaneous route. In addition, retention of hematuria in urinary bladder in rats of oral and subcutaneous routes, the hemorrhagic changes of heart, atonia of urinary bladder and retention of urine in dogs were observed. 4. The main cause of death seemed to be respiratory disturbance in all species and the weakness in a few rats of oral route.
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PMID:[Acute toxicity studies of propiverine hydrochloride]. 260 50

Nine dogs with primary gastrointestinal disease had clinical and laboratory findings resembling hypoadrenocorticism. The dogs had histories of anorexia, weakness or lethargy, diarrhea, vomiting, and weight loss. Hypothermia, dehydration, and emaciation also were detected on physical examination. Hyponatremia, hyperkalemia, and abnormally low Na/K ratios were found on laboratory evaluation, but results of ACTH-response tests were not compatible with hypoadrenocorticism. The primary diagnoses were trichuriasis and salmonellosis in 2 dogs, trichuriasis in 5 dogs, and perforated duodenal ulcer in 2 dogs. Most dogs responded to medical or surgical treatment of their primary gastrointestinal disease, and the original electrolyte abnormalities resolved. These findings emphasize the importance of the ACTH-response test in the diagnostic evaluation of dogs with clinicopathologic findings similar to those of hypoadrenocorticism.
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PMID:Clinicopathologic findings resembling hypoadrenocorticism in dogs with primary gastrointestinal disease. 299 Nov 78


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