Alcohol opioid interactions

THC has a variety of pharmacologic effects that resemble those of amphetamines, LSD, alcohol, sedatives, atropine, and morphine. Important opioid interactions include reduction in opioid dependence in CB1 knockout mice lacking the CB1 receptor. 

Drug interactions metaxalone may augment the effects of alcohol, opioids, benzodiazepines, barbiturates, and other CNS depressants. 

A number of psychosocial treatments for alcohol and other substance use disorders exist and are widely used. In this chapter, we discuss six of these psychotherapies as they are applied to alcohol, cocaine, and opioid dependence brief interventions, motivational enhancement therapy, cognitive-behavioral therapy, behavioral treatments (including contingency management and community reinforcement approaches), behavioral marital therapy, and 12-step facilitation. We also describe studies that examined the efficacy of a medication in combination with one or more of the six psychotherapies. In the second section of the chapter, we highlight research that directly studied the interaction between psychosocial and pharmacological treatments. 

Many studies have examined the efficacy of a variety of psychosocial treatments for alcohol, cocaine, and opioid use disorders, alone and in conjunction with pharmacotherapy. However, only a handful of studies have explored how these two treatment approaches may interact. More research is needed to further explore the ways in which psychosocial interventions may be used in conjunction with pharmacotherapy to optimize outcomes for both treatments. Providing encouragement for abstinence, greater treatment retention, medication adherence, and coping with medication side effects are some potential applications of psychosocial therapies. 

Strong evidence indicates at least a familial pattern and perhaps a hereditary basis for some types of alcoholism ( 393). More recent data show that genotype accounts for approximately 33% of the overall variance in liability ( 394). In addition, specific neurocircuitry and neurochemical systems appear to be important in the etiology of alcoholism (395). Thus, positive reinforcement may be mediated by activation of g-aminobutyric acid (GABA) receptors, release of opioid peptides and dopamine, inhibition of glutamate receptors, and interactions with the 5-HT system. Furthermore, neurobehavioral effects of alcohol and their association with these various neurotransmitters serve as potential targets for novel drug therapies. 

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. 

The interactions of benzodiazepines with other nervous system depressants, especially alcohol and other GABA-ergic drugs, have been reviewed (152). Other drugs with nervous system depressant effects (opioids, anticonvulsants, general anesthetics) also can add to, and complicate, the depressant action of benzodiazepines. 

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. 

Pharmacodynamic interactions. Many TCAs cause sedation and therefore co-prescription with other sedative agents such as opioid analgesics, antihistamines, anxiolytics, hypnotics and alcohol may lead to excessive drowsiness and daytime somnolence. The majority of TCAs can have undesirable cardiovascular effects, in particular prolongation of the QT interval. A similar risk of QT prolongation arises with many other cardiovascular drugs including amiodarone, disopyramide, procainamide, propa-... 

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. 

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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