Alcohol and Wernicke flashcards
15 high-yield MRCP Part 1 cards from the Intellect Medicos Psychiatry course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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What is the first-line drug for managing acute alcohol withdrawal?
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A reducing regimen of a long-acting benzodiazepine, usually chlordiazepoxide (diazepam is an alternative).
Why? Chronic alcohol use down-regulates GABA-A and up-regulates NMDA receptors; benzodiazepines replace the lost GABA effect and prevent seizures and delirium tremens.
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After the last drink, alcohol withdrawal seizures peak at about ______, and delirium tremens typically develops at 48–72 hours.
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36 hours
Why? Mild withdrawal starts at 6–12 hours. Knowing the timeline helps decide how long to observe and cover with benzodiazepines.
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After the last drink, alcohol withdrawal seizures peak at about 36 hours, and delirium tremens typically develops at ______.
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48–72 hours
Why? Mild withdrawal starts at 6–12 hours. Knowing the timeline helps decide how long to observe and cover with benzodiazepines.
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In suspected Wernicke's encephalopathy, which treatment must be given first, and by which route?
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IV thiamine (Pabrinex), given before any glucose.
Why? Glucose increases thiamine demand and can precipitate or worsen Wernicke's encephalopathy.
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What is the classic triad of Wernicke's encephalopathy?
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Confusion, ataxia and ophthalmoplegia (often with nystagmus).
Why? The full triad is often absent, so treat on clinical suspicion. MRI may show lesions in the mammillary bodies and medial thalamus. Untreated, it can progress to Korsakoff syndrome with amnesia and confabulation.
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After alcohol detoxification in moderate–severe dependence, which drugs are first line to help a patient maintain abstinence?
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Acamprosate or oral naltrexone, combined with a psychological intervention.
Why? Acamprosate modulates glutamate (NMDA) transmission and reduces craving. Naltrexone is an opioid antagonist that reduces the reward from drinking. Disulfiram is second line.
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What is the mechanism of action of disulfiram?
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It inhibits aldehyde dehydrogenase, so acetaldehyde builds up if alcohol is drunk.
Why? Acetaldehyde causes flushing, nausea, vomiting and palpitations, which act as a deterrent (aversion therapy). It is second line after acamprosate or naltrexone.
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What is the first-line screening tool for harmful drinking?
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AUDIT-C.
Why? It is a short 3-question version of the AUDIT questionnaire; a positive result leads on to the full AUDIT and assessment.
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Which memory features characterise Korsakoff syndrome?
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Severe anterograde amnesia (with some retrograde loss) and confabulation, in a patient with clear consciousness.
Why? It follows untreated or inadequately treated Wernicke's encephalopathy and is often irreversible.
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On MRI, Wernicke's encephalopathy classically shows symmetrical lesions in the ______ and the medial thalamus.
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mammillary bodies
Why? The periaqueductal grey matter and hypothalamus can also be affected. A normal MRI does not exclude the diagnosis; treat on clinical suspicion.
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Which class of drugs must not be taken with naltrexone, and why?
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Opioids. Naltrexone is an opioid antagonist, so it can precipitate acute opioid withdrawal and blocks opioid pain relief.
Why? Check for opioid use (prescribed or illicit) before starting naltrexone for alcohol relapse prevention.
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What is the first-line treatment for delirium tremens (NICE)?
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Oral lorazepam. If symptoms persist or oral medication is refused, give parenteral lorazepam or haloperidol.
Why? Delirium tremens is a medical emergency with confusion, hallucinations, tremor and autonomic instability, usually 48–72 hours after the last drink.
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Which drug does NICE say should not be used to treat alcohol withdrawal seizures?
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Phenytoin.
Why? Withdrawal seizures are treated with a quick-acting benzodiazepine such as lorazepam; if they occur during treatment, review the withdrawal regimen.
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Chronic alcohol use down-regulates ______ receptors and up-regulates NMDA (glutamate) receptors, so stopping suddenly causes CNS over-excitation.
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GABA-A
Why? This explains tremor, seizures and delirium tremens in withdrawal, and why benzodiazepines (GABA-A enhancers) are the treatment.
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Chronic alcohol use down-regulates GABA-A receptors and up-regulates ______ receptors, so stopping suddenly causes CNS over-excitation.
Show answer
NMDA (glutamate)
Why? This explains tremor, seizures and delirium tremens in withdrawal, and why benzodiazepines (GABA-A enhancers) are the treatment.