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Drug-induced vomiting

Levodopa, the metabolic precursor of dopamine, is the most effective agent in the treatment of Parkinson s disease but not for drug-induced Parkinsonism. Oral levodopa is absorbed by an active transport system for aromatic amino acids. Levodopa has a short elimination half-life of 1-3 hours. Transport over the blood-brain barrier is also mediated by an active process. In the brain levodopa is converted to dopamine by decarboxylation and both its therapeutic and adverse effects are mediated by dopamine. Either re-uptake of dopamine takes place or it is metabolized, mainly by monoamine oxidases. The isoenzyme monoamine oxidase B (MAO-B) is responsible for the majority of oxidative metabolism of dopamine in the striatum. As considerable peripheral conversion of levodopa to dopamine takes place large doses of the drug are needed if given alone. Such doses are associated with a high rate of side effects, especially nausea and vomiting but also cardiovascular adverse reactions. Peripheral dopa decarboxylase inhibitors like carbidopa or benserazide do not cross the blood-brain barrier and therefore only interfere with levodopa decarboxylation in the periphery. The combined treatment with levodopa with a peripheral decarboxylase inhibitor considerably decreases oral levodopa doses. However it should be realized that neuropsychiatric complications are not prevented by decarboxylase inhibitors as even with lower doses relatively more levodopa becomes available in the brain. [Pg.360]

J. R. Fozard (1987). S-HTj receptors and cytotoxic drug-induced vomiting. Trends Pharmacol. Sci. 8 44 5. [Pg.304]

It causes antiemetic action by blocking dopamine (D receptors and it also increases gastric motility. It is absorbed orally but bioavailability is 15% due to first pass metabolism. It is completely biotransformed and metabolites are excreted in urine. It is used in nausea and vomiting in postoperative period, drug induced, radiation, uraemia, hepatitis, peptic ulcer. It is also useful in reflex oesophagitis. [Pg.258]

Cyclizine has antimuscarinic properties and is a potent anti-emetic, effective for the control of postoperative and drug-induced nausea and vomiting. It has been used to prevent motion sickness, although diphenhydramine and promethazine are more effective. It is available in oral and parenteral formulations. In contrast to many other first-generation antihistamines sedation is not marked. It is available in tablet form as the hydrochloride and in injectable form as the lactate. Because of its anticholinergic action, blurred vision and dry mouth are associated with clinical doses. When given by rapid intravenous injection tachycardia may be a problem. Meclozine is a related drug which, like cyclizine, is used primarily for motion sickness. [Pg.242]

Approximately 30% of patients using sulfasalazine discontinue the drug because of toxicity. Common adverse effects include nausea, vomiting, headache, and rash. Hemolytic anemia and methemoglobinemia also occur, but rarely. Neutropenia occurs in 1-5% of patients, while thrombocytopenia is very rare. Pulmonary toxicity and positive double-stranded DNA are occasionally seen, but drug-induced lupus is rare. Reversible infertility occurs in men, but sulfasalazine does not affect fertility in women. The drug does not appear to be teratogenic. [Pg.809]

The side effects of mycophenolate mofetil include diarrhea, abdominal pain, constipation, nausea/vomiting, acne, dyspnea, cough, peripheral edema, increased risk of infections, drug-induced fever, dizziness, headaches, leukopenia and anemia. [Pg.97]

Side effects. The common dose-related side effects of valproate include nausea, vomiting and gastrointestinal distress weight gain is frequent (estimated as high as 30%) and may be associated with a drug-induced decrease in the beta oxidation of fatty acids. Sedation is also frequent. Alopecia is an unusual side effect of valproate, possibly caused by an abnormal metabolite. Valproate has a number of metabolically linked side... [Pg.316]

Drug-induced anorexia, nausea, vomiting, and constipation are common side effects. [Pg.106]

Freeman AJ, Cullen MH. Advances in the management of cytotoxic drug-induced nausea and vomiting. J CUn Pharm Ther 1991 16(6) 411-21. [Pg.1043]

Simpson K, Spencer CM, McClellan KJ. Tropisetron an update of its use in the prevention of chemotherapy-induced nausea and vomiting. Drugs 2000 59(6) 1297-315. [Pg.1369]

Nausea and vomiting are frequent, perhaps in as many as one-third of all cases. In about half the cases, diarrhea is induced or existing diarrhea aggravated. Melena can occur, but this seems unlikely to be drug-induced (SED-11, 594). [Pg.1905]

A number of chemicals and drugs induce nausea and vomiting by an action involving the so-called chemoreceptor trigger zone (CTZ) within the area postrema of the brain. [Pg.29]

Other people turn to a different method of forced weight loss. Individuals with bulimia, an eating disorder in which vomiting is induced after eating in order to prevent food from being absorbed by the body, sometimes use drugs as part of their illness. In particular, a medicinal syrup called ipecac causes abusers to vomit. Ipecac, an... [Pg.29]

Many cytotoxic drugs used in the treatment of malignant disease are powerful emetics, and the distress caused by drug-induced nausea and vomiting is the... [Pg.732]

Acute barbiturate toxicity is characterized by automatism, or a state of drug-induced confusion, in which patients lose track of how much medication they have taken and take more. Death results from respiratory failure. The treatment of poisoning consists of supporting respiration, prevention of hypotension, as well as diuresis, hemodialysis and, in the event of phenobarbital poisoning, the administration of sodium bicarbonate. Tolerance does not develop from lethal doses. The abrupt withdrawal from barbiturates may cause tremors, restlessness, anxiety, weakness, nausea and vomiting, seizures, delirium, and cardiac arrest. [Pg.101]


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See also in sourсe #XX -- [ Pg.330 ]

See also in sourсe #XX -- [ Pg.665 ]




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