Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a double-blind randomised study, 100 women who underwent induced abortion under midazolam anaesthesia were given the benzodiazepine antagonist Ro 15-1788 or placebo after termination of anaesthesia. Recovery was assessed by means of a modified Steward coma scale. Following incremental doses of Ro 15-1788, 56% of the patients were fully awake within 3 minutes and 92% after 5 minutes, which was significant compared to the placebo group. The median duration of amnesia was 91 minutes after Ro 15-1788 compared to 121 minutes in the placebo group (p less than 0.001). The median dose of Ro 15-1788 was 0.4 mg. A slight positive correlation between total dose of Ro 15-1788 and total amount of midazolam was found. Nausea and/or vomiting were found to be more frequent in the Ro 15-1788 group, but otherwise we found no differences between groups with regard to either side effects or cardiorespiratory function. Ro 15-1788 is evidently an effective antagonist to the sedation induced by midazolam.
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PMID:Ro 15-1788 for postoperative recovery. A randomised clinical trial in patients undergoing minor surgical procedures under midazolam anaesthesia. 309 31

Of 61 cases of ibuprofen overdosage reported consecutively to the Rocky Mountain Poison and Drug Center from September 1985 through April 1986, 16 were excluded because of incomplete follow-up or concurrent medication ingestion. A toxic reaction developed in 7 (16%) of the remaining 45 patients. Nausea, vomiting, abdominal cramps, mild central nervous system depression, coma, tachycardia, apnea, metabolic acidosis with or without respiratory alkalosis, hematemesis, and oliguric renal failure were noted. Two of six adults had a toxic reaction, and one died. Among pediatric patients, 5/39 (13%) had a toxic reaction. Of patients whose ibuprofen ingestion was less than 104 mg per kg, none became ill. All patients in whom the time of ingestion was known (six of seven) and who had a toxic reaction did so within four hours of ingestion. An ibuprofen overdose, although usually benign, can occasionally produce serious toxicity.
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PMID:Ibuprofen overdose--a prospective study. 317 71

Extradural haematoma (EDH) is generally a condition of young adult males. It represents only a small percentage of the total number of head injuries admitted to a neurosurgical service, but it must be differentiated from simple concussion, and this means that it is considered in a large number of patients. EDH has the potential for a low mortality rate because of its extraaxial location, but in practice it is approximately 10%. Our results show that about 40% of EDH present with vomiting or nausea and no focal neurological signs. Skull X-ray does not aid in the diagnosis as approximately 35% are reported as being normal. There is a place for conservative treatment of EDH but only if the shift of the midline is minimal (less than 5 mm). A score has been developed to predict accurately a patient's outcome after suffering an EDH. This score includes the Glasgow Coma Scale, pupillary reaction and initial CT scan appearance, and has an accuracy of 88%.
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PMID:Outcome prediction in extradural haematomas. 322 7

The toxicities of antimalarial drugs vary because of the differences in the chemical structures of these compounds. Quinine, the oldest antimalarial, has been used for 300 years. Of the 200 to 300 compounds synthesised since the first synthetic antimalarial, primaquine in 1926, 15 to 20 are currently used for malaria treatment, most of which are quinoline derivatives. Quinoline derivatives, particularly quinine and chloroquine, are highly toxic in overdose. The toxic effects are related to their quinidine-like actions on the heart and include circulatory arrest, cardiogenic shock, conduction disturbances and ventricular arrhythmias. Additional clinical features are obnubilation, coma, convulsions, respiratory depression. Blindness is a frequent complication in quinine overdose. Hypokalaemia is consistently present, although apparently self-correcting, in severe chloroquine poisoning and is a good index of severity. Recent toxicokinetic studies of quinine and chloroquine showed good correlations between dose ingested, serum concentrations and clinical features, and confirmed the inefficacy of haemodialysis, haemoperfusion and peritoneal dialysis for enhancing drug removal. The other quinoline derivatives appear to be less toxic. Amodiaquine may induce side effects such as gastrointestinal symptoms, agranulocytosis and hepatitis. The main feature of primaquine overdose is methaemoglobinaemia. No cases of mefloquine and piperaquine overdose have been reported. Overdose with quinacrine, an acridine derivative, may result in nausea, vomiting, confusion, convulsion and acute psychosis. The dehydrofolate reductase inhibitors used in malaria treatment are sulfadoxine, dapsone, proguanil (chloroguanide), trimethoprim and pyrimethamine. Most of these drugs are given in combination. Proguanil is one of the safest antimalarials. Convulsion, coma and blindness have been reported in pyrimethamine overdose. Sulfadoxine can induce Lyell and Stevens-Johnson syndromes. The main feature of dapsone poisoning is severe methaemoglobinaemia which is related to dapsone and to its metabolites. Recent toxicokinetic studies confirmed the efficacy of oral activated charcoal, haemodialysis and haemoperfusion in enhancing removal of dapsone and its metabolites. No overdose has been reported with artemesinine, a new antimalarial tested in the People's Republic of China. The general management of antimalarial overdose include gastric lavage and symptomatic treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and management of poisoning due to antimalarial drugs. 330 66

Literature data on current methods of induced abortion during the 2nd trimester are reviewed with special emphasis on the use of intraamniotic administration of hypertonic saline solution. A 20% saline is injected during amniocentesis either intra-abdominally or through the vagina; the optimum time period for pregnancy termination is 21-23 weeks of gestation. In the majority of patients, miscarriage occurs within 24-36 hours. The incidence of complications after administration of 20% saline ranges from 1.7-2.18%. Complications include hypernatremia, hemolysis, anuria, coma, seizures, incomplete abortion, hemorrhage, and inflammatory pelvic disease. Contraindications for pregnancy termination using hypertonic saline include cardiovascular diseases, central nervous system diseases, kidney diseases, late pregnancy toxemias, presence of postoperative cicatrix on the uterus, and placenta previa. The mechanism of abortifacient action of hypertonic saline may be associated with stimulation of the synthesis of endogenous prostaglandins (PG). The findings that PG can stimulate uterine contractions prompted clinical trials of PG as abortifacient agents. Longterm iv administration of PGF2 alpha and PGE during 2nd trimester was found to be associated with serious complications (nausea, vomiting, diarrhea, phlebitis at the site of vein puncture). For this reason, the method of iv administration of PG was abandoned. Intra-amniotic administration of PGF2 alpha (40-50 mg) was shown to induce abortion in 82-91% of the patients within 48 hours after injection. The incidence of hemorrhage and rupture of the cervix uteri after PG administration was significantly greater than that after saline injection. The intramuscular and vaginal administration of synthetic PG alone or in combination with Laminaria was shown to provide the most effective and safe method of induced abortion during the 2nd trimester.
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PMID:[Artificial termination of pregnancy in late periods]. 332 84

A 43-year-old alcoholic presented in coma with ketoacidosis, after three days of nausea and feeling generally unwell, which had been preceded by a prolonged three-week period of heavy alcohol consumption with poor dietary intake. The acidosis responded rapidly to intravenous dextrose. This is the first Scottish report of a case of alcoholic ketoacidosis.
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PMID:Alcoholic ketoacidosis: a case report. 344 46

Cerebral symptoms were registered in a multicenter study including 64 patients with severe hypertension, diastolic blood pressure (DBP) greater than or equal to 135 mmHg, and more or less pronounced hypertensive encephalopathy. The symptoms were: headache (70%), dizziness (35%), consciousness disturbances (28%), nausea (27%), paresis (23%), blurred vision (22%), paraesthesia (21%) and vomiting (14%). None had convulsions or coma. Initial treatment was furosemide i.v., and if DBP was greater than or equal to 125 mmHg after one hour, patients were randomized to treatment with either i.v. diazoxide (bolus injections of 75-150 mg) or i.m. dihydralazine (bolus injections of 6-12.5 mg). A gradual fall in blood pressure (BP) was obtained in all three groups. Along with BP reduction a substantial regression of neurological symptoms was registered. After 5 hours only minor cerebral symptoms were present without significant difference between diazoxide and dihydralazine. None developed cerebral complications. The study failed to show a significant correlation between BP reduction and regression of neurological symptoms graded semiquantitatively. Reduction of BP by titration using small repeated bolus injections is recommended, but oral treatment should be considered in the patients who are able to ingest peroral medication in spite of neurological symptoms.
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PMID:Reversibility of cerebral symptoms in severe hypertension in relation to acute antihypertensive therapy. Danish Multicenter Study. 353 94

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

In a double-blind randomized study of three groups of 18 patients scheduled for major abdominal surgery the efficacy and side effects of sublingual buprenorphine were tested and compared to intramuscular meperidine and buprenorphine. Single doses of either 75 mg of meperidine, 0.4 mg of sublingual buprenorphine, or 0.3 mg of intramuscular buprenorphine were used. Patients given buprenorphine as sublingual tablets were significantly more conscious in the immediate postoperative period (Glasgow Coma Scale) than when given buprenorphine or meperidine intramuscularly. Median pain intensity differences (PID) showed equal pain relief, whereas the summarized pain intensity differences (SPID) were significantly higher in the intramuscular buprenorphine group compared to the meperidine group. Three cases of respiratory acidosis in the meperidine group required IPPV treatment, and one case in the intramuscular buprenorphine group required treatment. Sedation and nausea were the most common side effects in all three groups. We conclude that sublingual buprenorphine is useful for relief of postoperative pain and exhibited administrative advantages, when the patients were able to cooperate.
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PMID:Pain relief after major abdominal surgery: a double-blind controlled comparison of sublingual buprenorphine, intramuscular buprenorphine, and intramuscular meperidine. 354 57

A case of phenytoin-induced hepatitis with mononucleosis is reported, and syndromes associated with phenytoin hypersensitivity reactions are discussed. A 23-year-old black woman with a two-month history of seizure disorder was admitted to a hospital with nausea, vomiting, fever, lymphadenopathy, diffuse maculopapular rash, left-upper-quadrant tenderness, and hepatomegaly. She was receiving phenytoin sodium 300 mg/day; carbamazepine 200 mg four times daily had been discontinued four days before admission because of leukopenia. Phenytoin was discontinued after admission; however, phenytoin 1 g i.v. was given for a tonic-clonic seizure two days after admission, after which swelling of the face and legs and pruritus developed. Over the next few days, signs and symptoms of hepatotoxicity progressed, and she became comatose. Seizures were treated with diazepam. She began to recover after 10 days of supportive therapy and was discharged several weeks later on primidone therapy. Serious phenytoin hypersensitivity reactions may appear as dermatologic, lymphoid, or hepatic syndromes. Fever, rash, and lymphadenopathy often accompany hepatic injury. Encephalopathy and death may occur. Proposed mechanisms for phenytoin hypersensitivity include antigen-antibody reactions, alteration of lymphocyte function, and an enzyme abnormality causing the production of toxic metabolites. Treatment is supportive; phenobarbital and carbamazepine may be used with caution as alternate anticonvulsant therapy. The possibility of phenytoin hypersensitivity reactions should be considered when patients receiving phenytoin have unusual symptoms, particularly fever, rash, and lymphadenopathy.
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PMID:Phenytoin-induced hypersensitivity reactions. 367 71


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