Acamprosate Mechanism — MRCPsych Paper B MCQ

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HardSubstance MisuseAcamprosate MechanismMRCPsych Paper B

A 30-year-old woman with alcohol dependence has remained abstinent for 3 months following assisted withdrawal. She takes acamprosate 666 mg three times daily for relapse prevention. Which pharmacodynamic action best accounts for its therapeutic effect in maintaining abstinence?

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Correct answer: D — Modulation of glutamatergic (NMDA) transmission, dampening withdrawal-related hyperexcitability

Explanation lettering: D = shown as A · A = shown as B · B = shown as C · C = shown as D

C is correct. Chronic alcohol exposure upregulates excitatory glutamatergic (NMDA) transmission; during abstinence this produces a hyperglutamatergic state associated with craving and relapse. Acamprosate's principal proposed action is modulation of NMDA receptor-mediated glutamatergic transmission—antagonising excitatory amino acids and reducing brain glutamate—with possible indirect enhancement of GABAergic inhibition, thereby restoring the disturbed excitatory–inhibitory balance (eMC SmPC section 5.1; Plosker 2013). A describes naltrexone, the other licensed relapse-prevention agent, and is the closest distractor. B describes baclofen, which reduces glutamate release via GABA-B agonism but is not acamprosate's mechanism. D describes antipsychotics, and E describes SSRIs; neither underlies acamprosate's effect. Note that acamprosate is renally excreted and does not undergo hepatic metabolism, but it is contraindicated in severe hepatic impairment (Child-Pugh C), so blanket claims of safety in liver disease are inaccurate.

Reference: electronic Medicines Compendium (eMC), Acamprosate 333 mg Gastro-resistant Tablets, Summary of Product Characteristics, section 5.1 Pharmacodynamic properties. https://www.medicines.org.uk/emc/product/2729/smpc