Tricyclic antidepressants alcohol interactions

Drugs that may interact with disulfiram include alcohol, benzodiazepines, caffeine, chlorzoxazone, cocaine, hydantoins, isoniazid, metronidazole, theophylline, tricyclic antidepressants, and warfarin. 

In contrast, acute alcohol use can inhibit metabolism of other drugs because of decreased enzyme activity or decreased liver blood flow. Phenothiazines, tricyclic antidepressants, and sedative-hypnotic drugs are the most important drugs that interact with alcohol by this pharmacokinetic mechanism. 

Drugs and chemicals are known to cause activated interaction. The depressant action of opioid drugs is enhanced by drugs acting on the central nervous system (CNS) such as alcohol, anesthetics, anxiolytics, hypnotics, tricyclic antidepressants, and antipsychotics. Concomitant administration of opioid analgesics and monoamine oxidase inhibitors (MAOIs) should be avoided, or extra care should be taken if such a therapy is inevitable. Fatal reactions are reported when treated along with selegiline. Interactions also are reported with cyclizine, cimetidine, mexiletine, cisapride, metoclopramide, or domperidone. 

Interactions. Morphine (also pethidine and possibly other opioids) is potentiated by monoamine oxidase inhibitors. Any central nervous system depressant (including alcohol) will have additive effects. Patients recently exposed to neuromuscular blocking agents (unless this is adequately reversed, e.g. by neostigmine) are particularly at risk from the respiratory depressant effects of morphine. The effect of diuretic drugs may be reduced by release of antidiuretic hormone by morphine. Useful interactions include the potientating effect on pain relief of tricyclic antidepressants and of dexamfetamine. 

Clinically important, potentially hazardous interactions with alcohol, barbiturates, hypnotics, narcotic analgesics, sedatives, tranquilizers, tricyclic antidepressants... 

Clinically important, potentially hazardous interactions with acyclovir, alcohol, amphetamines, barbiturates, CNS depressants, fluoxetine, furazolidone, general anesthetics, glycopyrrolate, glycopyrronium, isocarboxazid, linezolid, lithium, MAO inhibitors, moclobemide, phenelzine, phenobarbital, phenothiazines, rasagiline, ritonavir, selegiline, sibutramine, SSRIs, tranquilizers, tranylcypromine, tricyclic antidepressants, val acyclovir... 

Administered as a single, daily dose on an empty stomach Monoamine oxidase inhibitors drug-food interactions with tyramine-rich foods such as red wines, dark beers, aged cheeses, yogurt may precipitate hypertensive crisis drug interactions tricyclic antidepressants and SSRIs, sympathomimetics disulfiram-like reaction with alcohol... 

Chronic abuse of alcohol can lead to enhanced activity of cytochrome P450 enzymes and a consequent decrease in tricyclic antidepressant (TCA) serum levels. Central receptor interactions between alcohol and TCAs can cause impaired motor abilities (evident with amitriptyline, clomipramine, doxepin, and nortriptyline). 

Additive CNS depression This occurs when sedative-hypnotics are used with other drugs in the class as well as with alcoholic beverages, antihistamines, antipsychotic drugs, opioid analgesics, and tricyclic antidepressants. This is the most common type of drug interaction involving sedative-hypnotics. Additive CNS depression with buspirone is uncommon. 

Examples (1) A plethora of drug substances , for instance muscle relaxants, sedatives-hypnotics, tricyclic antidepressants, antipsychotic, antihistaminics, and alcohols are observed to interact with opiate analgesics to augment and accelerate their overlapping pharmacological activities, namely anticholinergic effects and respiratory depression. 

Neither cimetidine nor rifampicin had any clinically relevant effect on the pharmacokinetics of nicorandil. Nicorandil did not alter the anticoagulant effects of acenocoumarol. Although animal studies surest antagonism of effects, a study in patients found no pharmacodynamic interaction between nicorandil and glibenclamide. Nicorandil may potentiate the hypotensive effects of other vasodilators, tricyclic antidepressants and alcohol. 

While drug interactions based on pharmacokinetics do occur with sedative-hypnotics, the most common drug interaction is additive CNS depression. Additive effects can be predicted with concomitant use of alcoholic beverages, anticonvulsants, opioid analgesics and phenothiazines. Less obvious but equally important is enhanced CNS depression with many antihistamines, antihypertensives, and antidepressants of the tricyclic class. The answer is (A). 

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