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Naltrexone and acamprosate matter because they help prevent relapse in alcohol dependence through two completely different mechanisms, neither of which works by punishing drinking the way disulfiram does. Naltrexone is an opioid antagonistA drug that blocks a receptor, stopping it from being activated.Read more → (a drug that blocks opioid receptors), which reduces the rewarding, pleasurable effect of alcohol and so reduces craving. Acamprosate instead modulates glutamate and GABAThe brain's main calming (inhibitory) chemical messenger, boosted by benzodiazepines and alcohol.Read more → (gamma-aminobutyric acid) systems, calming the brain's overactivity during abstinence rather than blocking reward. For example, imagine two patients who have both stopped drinking: one still craves alcohol strongly, better suited to naltrexone, while the other struggles mainly with post-withdrawal unease, better suited to acamprosate.

Naltrexone blocks opioid receptors, which reduces the euphoric, rewarding effect of alcohol and lowers craving, but because it is an opioid antagonistA drug that blocks a receptor, stopping it from being activated.Read more →, it will precipitate withdrawal in anyone currently dependent on opioids. Acamprosate instead restores the balance between excitatory glutamate and inhibitory GABAThe brain's main calming (inhibitory) chemical messenger, boosted by benzodiazepines and alcohol.Read more → signalling that becomes disrupted during prolonged alcohol use, easing the discomfort of early abstinence rather than acting on reward. Take a patient on methadone maintenance who is also drinking heavily: naltrexone would be dangerous here because it would trigger acute opioid withdrawal, so acamprosate would be the safer choice. In practice, disulfiram works completely differently again, causing an unpleasant reaction, flushing, nausea, palpitations, if alcohol is consumed, deterring drinking rather than reducing craving.

• A man is started on naltrexone for alcohol relapse prevention. What should be checked at baseline and monitored during treatment?
• A man completes opioid detoxification and starts naltrexone, then relapses two months later using his previous heroin dose. Which danger should he have been warned about?
• A trainee is asked how acamprosate is dosed. Which description matches its usual administration?
• A woman established on naltrexone is admitted after a major road traffic injury needing strong analgesia. What is the most appropriate approach to her pain relief?

• Disulfiram, works by deterrence, causing an unpleasant reaction to alcohol, unlike naltrexone and acamprosate which reduce craving or ease withdrawal discomfort instead.
• Opioid maintenance treatment (methadone/buprenorphine): naltrexone is contraindicated here, unlike acamprosate which has no opioid-receptor activity.
• Benzodiazepines, used for acute alcohol withdrawal symptoms, whereas naltrexone and acamprosate are used afterward, for relapse prevention rather than withdrawal management.
• Nalmefene, another opioid antagonistA drug that blocks a receptor, stopping it from being activated.Read more →, similar to naltrexone, but licensed specifically for reducing alcohol consumption rather than full abstinence maintenance.

• Thyroid disturbance is not a recognised effect of this drug.
• Calcium disturbance is not a recognised effect of this drug.
• That flushing reaction belongs to an alcohol relapse-prevention drug.
• The blockade is reversible rather than permanent.
• A months-long withdrawal syndrome is not the principal danger.

• Identify the drug, receptor, enzyme or pharmacokinetic change named in the stem.
• Translate it into the immediate mechanism before looking at the options.
• Use timing and the adverse-effect pattern to separate the nearest alternatives.
• Check whether the question asks for mechanism, clinical consequence, monitoring or management.