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)

The most common cause of hypoadrenocorticism in dogs is idiopathic immune-mediated destruction of the adrenal cortex. Other causes include anterior pituitary insufficiency, pituitary or adrenal neoplasia, acute withdrawal of exogenous corticosteroids, and mitotane toxicity. Females are affected more often than males; only 1 feline case has been documented. Animals 2-5 years old are most commonly affected. Clinical signs include lethargy, weakness, weight loss, anorexia, vomiting, diarrhea and bradycardia. Hematologic and biochemical changes can include eosinophilia, lymphocytosis, anemia, hyperkalemia, hyponatremia and hypercalcemia. Diagnosis is by finding negligible resting levels of plasma cortisol and no response to ACTH administration, and a serum Na:K ratio of 20:1 or less. Treatment involves restoring fluid volume, correcting acidosis, and supplementing salt and glucocorticoids. Daily oral use of prednisone at 0.05 mg/kg can safely maintain most affected dogs. Some dogs only require glucocorticoids in stressful situations. Iatrogenic secondary adrenocortical insufficiency (iatrogenic Cushing's disease) may result from a single injection of long-acting glucocorticoids or from long-term use. Clinical signs are the same as for natural hyperadrenocorticism, but endogenous cortisol release is suppressed. Treatment is gradual withdrawal of the offending glucocorticoid and elimination of the cause that initially prompted glucocorticoid therapy.
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PMID:Diseases of the adrenal cortex of dogs and cats. 674 17

The analgesic agent butorphanol was evaluated for its ability to block cisplatin-induced emesis in ferrets and dogs. In ferrets, butorphanol (0.15, 0.3, or 0.45 mg/kg; expressed in terms of the tartrate salt) administered sc 30 minutes prior to cisplatin (8 mg/kg iv) reduced the number of emetic episodes but did not eliminate them. When these doses of butorphanol were administered 30 minutes before and 30 and 90 minutes after cisplatin, they caused a dose-related reduction in the number of emetic episodes; there was complete protection at a dose of 0.45 mg/kg/injection. In dogs, butorphanol (0.185 or 0.37 mg/kg/injection, expressed in terms of the tartrate salt) was administered sc on the same multiple-dose schedule used in the ferrets; this caused a nearly complete elimination of the emetic response to cisplatin (3 mg/kg iv). Butorphanol caused some sedation in both species at effective antiemetic doses but had no effect on the antitumor activity of cisplatin against murine L1210 leukemia. Naloxone blocked the antiemetic effect of butorphanol in ferrets, indicating the involvement of opiate receptors. The results of these studies suggest that butorphanol may be useful clinically in mitigating the emetic effects of cisplatin.
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PMID:Antiemetic activity of butorphanol against cisplatin-induced emesis in ferrets and dogs. 688 14

In a randomized double-blind trial, infants with mild or moderate diarrhoeal dehydration were rehydrated orally either with a simple solution containing table sugar and salt (without potassium or bicarbonate) or with a complete glucose/electrolyte formula. All 32 given glucose/electrolyte solution and 27 (93%) of 29 infants given sugar/salt were successfully rehydrated with similar improvement in metabolic acidosis and rapidity of rehydration. The drawbacks to oral therapy with simple sugar/salt solution were the frequent development of hypokalaemia and greater volume of vomiting during treatment. Carefully prepared sugar/salt solution, if accompanied by adequate potassium supplementation, may be used as an alternative to the preferred glucose/electrolyte formula when the latter is unavailable.
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PMID:Comparison of simple sugar/salt versus glucose/electrolyte oral rehydration solutions in infant diarrhoea. 702 4

L-Alanosine is an antitumor antibiotic that inhibits adenine synthesis. It showed significant activity in animal tumor systems. Using a daily x 3 dose schedule every 3 weeks, we performed a phase I study to determine toxicity in man. Doses of 8-375 mg/m2/day x 3 were administered to 49 patients in 117 courses. The dose-limiting toxic effect was mucositis. Vomiting, infrequent myelosuppression, fever, headache, malaise, and blood pressure changes were detected at higher dose levels. No antitumor activity was noted. Toxicity with this regimen is acceptable. A phase II study with doses of 250 mg/m2/day x 3 every 3 weeks is feasible.
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PMID:Phase I study of L-alanosine using a daily x 3 schedule. 705 69

Pilocarpine, a parasympathomimetic drug used in the treatment of glaucoma, produces a variety of ocular and systemic adverse reactions. Ocular side effects include miosis, accommodative spasm, frontal headaches, twitching lids, conjunctival injection, cataractous changes, allergic reactions, iris cysts, retinal detachment, increased permeability of the blood-aqueous barrier, anterior chamber narrowing, and the potential for inducing an acute angle-closure attack. Systemic side effects include nausea, vomiting, tenesmus, abdominal spasm, salivation, lacrimation, sweating, pulmonary edema, and bronchial spasm. The systemic side effects can best be minimized initially through proper use of the medication and nasolacrimal occlusion. The Ocusert, a long-acting pilocarpine-incorporated ocular insert, is a recent advance in delivery technique that offers an adequate hypotensive action with fewer side effects. Pilopex is a promising new experimental pilocarpine polymer salt presently being studied in Israel. Photomydriasis, a process involving the use of a laser to enlarge miotic pupils also offers help for these patients. N-demethylated carbachol is a new parasympathomimetic drug currently under study for glaucoma therapy. Initial results show that it may have considerable ocular hypotensive action with fewer adverse effects.
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PMID:Miotics: side effects and ways to avoid them. 707 Jul 79

The toxicology of a potentially useful antitumor agent, 2,4-diamino-5-adamantyl-6-methylpyrimidine (DAMP), and its ethanesulfonate salt has been studied in beagle dogs after 1 to 20 doses. Two types of toxicity could be discerned: the acute central nervous system toxicity manifested by vomiting, convulsions, and minor hypothermia; and the antiproliferative toxicity, similar to that of other folate antagonists, manifested by diarrhea, anorexia, loss of body weight, and hematological changes as well as changes in blood chemistry. There is evidence of a cumulative effect of the drug with respect to antiproliferative toxicity. Characteristically, the animals could be protected against the antiproliferative toxicity by simultaneous administration of folinic acid. The pharmacokinetics of the ethanesulfonate salt of DAMP was studied after i.v. administration of sublethal doses (5 mg/kg) of tritium-labeled drug. Sixty-three % of the administered dose was excreted in the urine and 10% was excreted in the feces within 48 hr after drug administration. Thus, about 27% of the drug was not recovered, and it is possible that it persists in the tissues for a period of several days. Analysis of the plasma and urine revealed that DAMP was metabolized rapidly. At least 2 metabolites were found in plasma and urine, one lipophilic and one hydrophilic, the latter being the predominant form. Pharmacokinetic data were successfully fitted to a model consisting of central and peripheral DAMP compartments and a DAMP metabolite compartment. DAMP was very rapidly sequestered in the peripheral compartment with a rapid phase half-life of 23 sec. The slower phase of DAMP plasma disappearance had a half-life of 3 hr. The short plasma half-life and rapid metabolism distinguished this drug from other lipophilic antifolates.
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PMID:Toxicity and pharmacokinetics of a new antifolate, 2,4-diamino-5-adamantyl-6-methylpyrimidine, in dogs. 707 98

A 27-year old female received about 1 kg of salt in about 600 ml of water as an emetic after a self-poisoning attempt. Vomiting did not occur and massive necrosis of gastric, duodenal, and jejunal mucosa resulted in a severe and prolonged illness which required 31 weeks of continuous hospital care and 31 laparotomies over a period of 16 months. The dangers of salt emesis are emphasized.
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PMID:Extensive gastrointestinal damage following a saline emetic. 711 77

The management of diarrhea is mostly dependent on parenteral administration of fluids and electrolytes, yet for the majority of India's population such facilities are practically unavailable. In addition there are several serious limitations to the use of this technique. These include prohibitive cost, the fact that it can only be administered by trained personnel, and that it brings undue distress to both patients and parents. Such procedures should be reserved only for those patients who have severe dehydration, impending shock, electrolyte imbalance, or persistent vomiting. For the others, the majority, oral rehydration therapy should be the treatment of choice. The implementation of oral rehydration therapy in the Infectious Diseases Hospital, Calcutta alone, has resulted in an annual saving of much money. Another benefit is that the family members can participate in the therapy and can continue it at home. The process of water and solute absorption is accelerated in the presence of glucose and sodium, and its effectiveness has been proven and documented. There are various types of oral multi-electrolyte-glucose powders available in India. The mixture recommended by the World Health Organization seems to be the most suitable, and this mixture can be prepared at home by the addition of 3-1/2 grams of common salt, 2-1/2 grams of baking soda, 1-1/2 grams of potassium chloride, and 20 grams of glucose in 1 liter of water. Instructions for the use of oral rehydration therapy are outlined, and other types of rehydration therapy are described.
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PMID:Oral rehydration therapy. 722 9

Oral rehydration therapy (ORT) has simplified treatment of diarrheal dehydration. Hospitals in India have diarrheal treatment and training units (DTUs) to help manage the many diarrheal cases. DTU staff keep children for 4-6 hours to correct the dehydration with ORT and feeding. Health personnel undergo training in diarrhea management at DTUs. ORT is the preferred treatment in almost all cases of acute diarrhea. It is not best for diarrheal cases which exhibit shock, profuse vomiting (3 times/hour), glucose malabsorption, abdominal distension or paralytic ileus, and high rate of purging (15 ml/kg body weight/hour). ORT successfully treats 95% cases of infantile diarrhea, even Rotavirus-caused diarrhea. Health workers should begin treating cases of severe dehydration with intravenous (IV) therapy and then administer ORT 3-4 hours later for infants and 1-2 hours later for adults. If IV therapy is not possible, the patient should receive oral rehydration solution (ORS) nasogastrically and then referred to a facility with IV therapy. WHO's ORS formula is safe for newborns and young infants. ORT is appropriate even when diarrheal cases are vomiting. ORT tends to stop vomiting 1-2 hours after initial ORS administration because it corrects acidosis. The glucose in WHO's ORS facilitates absorption of adequate sodium across the intestinal mucous membrane. ORS also restores the loss potassium ions and HCO3/citrate. If ORS is not available, sugar salt solution can be used. To achieve the optimum concentration, the amount of sucrose has to be twice that of glucose. ORS should be stored in a cool place, be covered, and used for no more than 24 hours. Antiemetics should not be given during ORT. Most diarrheas do not require any antibiotic. Sterile water is not necessary to prepare ORS. Rice gruel, coconut water, and pulse water are home available fluids which can treat dehydration. Breast feeding and regular feeding should continue during diarrheal episodes.
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PMID:Answers to questions in relation to oral rehydration therapy. 783 4

Sodium chloride deficiency (SCD) was observed within the 1st year of life in 12 of 46 cystic fibrosis (CF) patients between July 1989 and September 1992. All patients showed sweating, loss of appetite, fever, vomiting, irritation, dehydration, weakness, and cyanosis during an attack. Mean plasma sodium, potassium and chloride levels were 122.9 (range 106-135), 2.5 (range 1.6-3.5), and 73.3 (range 60-90) mEq/l respectively. Alkalosis and elevated plasma renin activity were detected in all patients. Of the patients, 50% showed microscopic haematuria, and hypercalciuria was detected in two out of four patients. Low urinary sodium and high urinary potassium were observed in the four examined patients. Increased creatinine, BUN and uric acid values returned to normal with treatment. All the patients were treated initially with intravenous fluids and electrolyte solutions. All patients were less than 7 months of age during the first attack, five received only breast milk and the others breast milk with formula milk. Their oral salt supplement was 2-4 mEq/kg per day, which is recommended for CF patients, but could be deficient in excessively sweating infants. The genotype of these patients might be cause of high salt losses. F508 is the most common mutation with the frequency of 38% in our CF patients with SCD, but the frequency of unknown mutations is high (54%).
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PMID:Sodium chloride deficiency in cystic fibrosis patients. 784 98


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