Which pharmacotherapies are FDA-approved for alcohol use disorder, and what are their main mechanisms?

• A. Acamprosate — opioid receptor antagonist; Naltrexone — NMDA receptor modulator; Disulfiram — inhibits monoamine oxidase.
• B. Disulfiram — opioid receptor antagonist; Acamprosate — dopamine reuptake inhibitor; Naltrexone — aldehyde dehydrogenase inhibitor.
• C. Naltrexone — opioid receptor antagonist; Acamprosate — modulates glutamatergic activity; Disulfiram — inhibits aldehyde dehydrogenase.
• D. Naltrexone — NMDA receptor antagonist; Acamprosate — aldehyde dehydrogenase inhibitor; Disulfiram — GABA agonist.

Answer: (C)

The main idea tested is understanding which medications are FDA-approved for alcohol use disorder and how they work in the brain. Naltrexone is an opioid receptor antagonist, which blocks the receptors that opioids act on and blunts the rewarding effects of alcohol. This reduces craving and the likelihood of relapse by dampening the dopamine-driven reward pathway that alcohol normally activates.

Acamprosate helps people maintain abstinence by modulating glutamatergic activity in the brain, stabilizing neural communication during early withdrawal and reducing withdrawal-related discomfort and cravings. It’s not an opioid blocker and doesn’t act on dopamine directly.

Disulfiram works by inhibiting aldehyde dehydrogenase, so if alcohol is consumed, acetaldehyde builds up and produces unpleasant symptoms (flushing, nausea, tachycardia). This creates a learned aversive reaction to drinking, deterring use.

The other choices mix up these mechanisms or assign actions that aren’t how these FDA-approved agents work (for example, acamprosate is not an opioid receptor antagonist, disulfiram is not a MAO inhibitor, naltrexone is not an NMDA antagonist, and disulfiram is not a GABA agonist).