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)

Clinical reports on 430 children with acute codeine intoxication are evaluated. Of 234 children who had taken more than 5 mg/kg body-weight, 8 had respiratroy arrest necessitating intubation and artificial ventilation; 2 of them died. In all other cases the intoxication produced one or more of the following symptoms: somnolence, ataxia, miosis, vomiting, rash, swelling, and itching of the skin, but no life-threatening side-effects. Close supervision of respiration is the main principle of management when more than 2 mg codeine/kg body-weight has been taken. Gastric voiding may be useful if done soon after ingestion. Charcoal and purgatives should be given in all cases.
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PMID:Codeine intoxication in childhood. 5 70

Of 488 children with central nervous system neoplasms, 43 (8.8%) had glioblastomas, 22 of which were in the cerebral hemispheres, 16 in the brain stem, two in the cerebellum, and three in the spinal cord. The male to female ratio was 3:2. Glioblastoma multiforme of the cerebral hemispheres occurred at a mean age of 12.7 years, and the frontal lobe was the most commonly involved. Main presenting symptoms included headache (85%), nausea or vomiting (65%), and seizures (35%). Papilledema (45%) was the most common physical finding. The longest survivals were achieved by a combination of operation and radiation (22 months). Brain stem glioblastomas occurred at a mean age of 6.7 years, with the pons as the most frequent site. Nausea or vomiting (50%) and headache (36%) were the main presenting symptoms; the major physical findings were ataxia (43%), cranial nerve palsies (28%), and paresis (28%). The length of survival was greatest with radiation alone (10.5 months). The period of survival of children with glioblastoma multiforme was significantly increased with steroid therapy. Glioblastoma multiforme behaves similarly in children and adults. Intracranial glioblastomas have a more rapidly fatal course than that of other similarly situated gliomas in childhood.
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PMID:Glioblastoma multiforme in children. 17 31

The purpose of this paper is to describe 2 siblings who had a generalized neurological disease which presented as intestinal pseudoobstruction. The siblings had 40-year histories of abdominal pain, distention, and vomiting as well as gait ataxia, small, irregular, poorly reactive pupils, dysarthria, absent deep tendon reflexes, and impaired vibratory and position senses. Compared with age-matched controls, they had inappropriate blood pressure responses to phenylephrine, the Valsalva maneuver, and upright posture, lack of sweating on warming, and pupillary denervation hypersensitivity. Radiographs revealed hyperactive, nonpropulsive contractions of a dilated esophagus and small intestine and extensive colonic diverticulosis. Esophageal manometry recorded repetitive, spontaneous, nonperistaltic waves and positive Mechyolyl tests. Postmortem examinations showed degeneration of the myenteric plexuses of the esophagus, small intestine, and colon of both patients. Myenteric plexus neurons were significantly reduced in number compared with 7 controls. About one-third of the siblings' neurons contained round, eosinophilic intranuclear inclusions, which, by histochemistry, were composed of protein by lacked RNA, DNA, carbohydrate, and fat. By electron microscopy the inclusions consisted of an irregular array of nonviral, nonmembrane-bounded filaments. Neurons and glial cells of the brain, spinal cord, dorsal root, and celiac plexus ganglia contained identical intranuclear inclusions. Intestinal smooth muscle was normal. These 2 siblings represent a unique disease in which degeneration of the myenteric plexus resulted in hyperactive but uncoordinated smooth muscle activity and the clinical syndrome of intestinal pseudoobstruction, the presenting manifestation of their neurological disease.
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PMID:A familial neuronal disease presenting as intestinal pseudoobstruction. 21 42

In 7 years snake bite was diagnosed in 80 dogs. Sporting breeds figured prominently. The average was 3.6 years. The commonest presenting signs were salivation, vomiting, dilated pupils, absence of the pupillary light reflex, depression and generalised muscle weakness, hindlimb ataxia and respiratory distress. Sixty-seven cases (84%) occurred in 6 warmer months on the year. Fifty-one dogs (64%) were seen either to be bitten or in contact with a snake. Tiger and Brown snakes were implicated on 32 and 3 occasions respectively. An overall recovery rate of 87% was obtained for patients receiving antivenene, fluid and support therapy. The period from treatment-to-full recovery was shorter for cases in which the bite-to-treatment period was one hour or less (24 hours) when compared with the recovery time for all cases (36 hours). The prognosis was poor for dogs presenting with the triad of complete flaccid paralysis, dyspnoea and a sub-normal temperature.
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PMID:Snake bite in dogs. 44 66

Ingestion of marijuana by three dogs in unrelated incidents resulted in depression-type toxicosis in each case. The most evident clinical signs were central nervous system depression and ataxia. Emesis and hypothermia were noted in two of the cases. Symptomatic and supportive treatment was accompanied by clinical improvement. In two cases, recovery was slow, with clinical signs apparent for 36 to 48 hours after onset. In the third case, clinical signs were apparent for only 3 hours.
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PMID:Acute oral marijuana poisoning in the dog. 52 54

Signs of a central nervous system disorder were observed following 2 instances of accidental ingestion of glucocorticoid in a young female Doberman Pinscher. The signs included transient aggressive and paranoid behavior, amaurosis, disorientation, ataxia with circling backward, and depression. Vomiting, weight loss, and abnormal drinking behavior persisted for several weeks following recovery from the acute illness.
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PMID:Central nervous system depression associated with glucocorticoid ingestion in a dog. 56 44

Clinical observations on ciguatera were collected between 1964 and 1977 on 3,009 patients from several South Pacific island groups. Patients generally presented with neurologic symptoms such as parasthesia, vertigo, and ataxia, in addition to gastrointestinal symptoms such as diarrhea, abdominal pain, nausea, and vomiting. Patients with this illness usually became symptomatic less than 24 hours after ingestion of the fish and most patients (76.8%) developed symptoms in less than 12 hours. Significant differences in certain symptoms were noted between Melanesian and Polynesian ethnic groups, suggesting a susceptibility difference, or a difference in the nature of the toxin found in different areas of the Pacific. Being poisoned multiple times appeared to result in a clinically more severe illness than disease observed in patients experiencing ciguatera for the first time.
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PMID:Clinical observations on 3,009 cases of ciguatera (fish poisoning) in the South Pacific. 57 66

Clinical and histological findings are presented as occurring in a male aged 24 years suffering from relapsing polychondritis (r. p.) of 7 years duration. The presenting symptoms were fever, ataxia, vertigo and vomiting. During the later relapses there also occurred episcleritis, paresis of the glottic muscle and hypertrophic bronchitis. At the age of 22 the patient had had a tracheostomy because of acute respiratory insufficiency. The patient has a typical saddle nose and drooping auricles. Tissues obtained from the auricles showed destructive alterations of the cartilage with fragmentation and homobenization of the elestic fibres. The perichondrium showed fibrosis and a massive round-celled inflammatory infiltration.
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PMID:[Recurrent polychondritis]. 61 34

In 6 years snake bite was diagnosed in 41 cats, with an average age of 20 months. The commonest presenting signs were dilated pupils, absence of the pupillary light reflex, depression and generalised muscle weakness. Other frequent findings were vomiting, dyspnoea, hindlimb ataxia and complete flaccid paralysis. Thirty-seven cases (90%) occurred in the 6 warmer months of the year. Tiger snakes were positively identified in 7 cases. A recovery rate of 89% was obtained in cases receiving 3000 units Tiger snake antivenene, fluid therapy and nursing. Cases presenting with a complete flaccid paralysis and sub-normal temperatures were poor prognostic risks.
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PMID:Snake bite in cats. 74 57

Twenty-seven dogs with lead poisoning were admitted to the University of Pennsylvania Veterinary Hospital from July, 1963, to April, 1975. The major source of the lead was paint. A common history was ingestion of plaster or paint scrapings during room renovation. Most of the dogs were less than 1 year old and had clinical signs referable to the gastrointestinal or the nervous system, or both. The gastrointestinal signs, in order of frequency, were vomiting, anorexia, tender abdomen, diarrhea, and constipation. The neurologic signs, in order of frequency, were hysteria, convulsions, ataxia, blindness, and mydriasis. The finding of many nucleated erythrocytes without severe anemia was nearly pathognomonic for lead poisoning. Of 14 affected dogs subjected to abdominal radiography, 9 had evidence of ingested radiopaque material. A mean blood lead concentration of 18.8 mug/100 ml, with a range of 0 to 50 mug/100 ml, was found for 26 dogs that were hospitalized for problems unrelated to lead poisoning. Of the 27 dogs with lead poisoning, 22 had their blood analyzed for lead. This group had blood lead values ranging from 40 to 530 mug/100 ml. Seven of the affected dogs were monitored throughout their period of treatment with calcium ethylenediaminetetraacetate. The concentration of lead in the blood decreased quickly after the initiation of treatment but leveled off after 2 or 3 days. The initial rapid phase probably corresponded to the removal of weakly bound or extracellular lead, whereas the slow phase probably corresponded to strongly bound or intracellular lead.
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PMID:Lead poisoning in dogs at the University of Pennsylvania Veterinary Hospital. 81 31


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