Poisons, antidotes & recreational drugs flashcards
18 high-yield MRCP Part 1 cards from the Intellect Medicos Clinical Pharmacology & Toxicology 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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Which test confirms carbon monoxide poisoning?
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Carboxyhaemoglobin level measured by co-oximetry on a blood gas sample.
Why? Pulse oximetry cannot tell carboxyhaemoglobin from oxyhaemoglobin, so SpO2 reads falsely normal.
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What is the first-line treatment for carbon monoxide poisoning?
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100% high-flow oxygen via a tight-fitting non-rebreathe (reservoir) mask.
Why? High-concentration oxygen greatly shortens the half-life of carboxyhaemoglobin. Discuss hyperbaric oxygen with NPIS in severe cases (e.g. loss of consciousness, neurological features, myocardial ischaemia or arrhythmia, COHb >20%) or pregnancy.
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What is the mechanism of cyanide toxicity?
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Inhibition of cytochrome c oxidase (complex IV of the respiratory chain).
Why? Cells cannot use oxygen, so there is a severe lactic acidosis despite normal oxygen delivery.
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A man rescued from a house fire is comatose and hypotensive with a lactate of 14 mmol/L. His carboxyhaemoglobin is only mildly raised. Which antidote should be given?
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IV hydroxocobalamin (for presumed cyanide poisoning from smoke inhalation).
Why? Burning plastics release cyanide. Hydroxocobalamin binds cyanide to form cyanocobalamin, which is excreted in urine; sodium thiosulfate can be added.
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Methanol is metabolised to ______, which damages the optic nerve; folinic acid is given to speed up its breakdown.
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formic acid
Why? Methanol poisoning causes a high anion gap acidosis and 'snowfield' blurred vision that can progress to blindness.
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Methanol is metabolised to formic acid, which damages the optic nerve; ______ is given to speed up its breakdown.
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folinic acid
Why? Methanol poisoning causes a high anion gap acidosis and 'snowfield' blurred vision that can progress to blindness.
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Fomepizole, the antidote for methanol and ethylene glycol, inhibits ______; disulfiram inhibits aldehyde dehydrogenase.
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alcohol dehydrogenase
Why? Blocking alcohol dehydrogenase stops toxic acid metabolites being formed. Ethanol is an alternative antidote because it competes for the same enzyme. Haemodialysis removes the parent alcohol and acids.
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Fomepizole, the antidote for methanol and ethylene glycol, inhibits alcohol dehydrogenase; disulfiram inhibits ______.
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aldehyde dehydrogenase
Why? Blocking alcohol dehydrogenase stops toxic acid metabolites being formed. Ethanol is an alternative antidote because it competes for the same enzyme. Haemodialysis removes the parent alcohol and acids.
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What does urine microscopy classically show in ethylene glycol poisoning?
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Calcium oxalate crystals.
Why? Ethylene glycol (antifreeze) is metabolised to oxalic acid, which binds calcium, causing hypocalcaemia, renal stones and acute kidney injury.
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Which blood test 'gap' is raised early in toxic alcohol poisoning, before the anion gap rises?
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The osmolar gap.
Why? The parent alcohol is osmotically active. As it is metabolised to acids, the osmolar gap falls and the anion gap rises.
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Name three drugs that can cause methaemoglobinaemia.
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Any three: nitrates/nitrites, local anaesthetics (prilocaine, benzocaine), dapsone, primaquine, sulphonamides.
Why? These oxidise haem iron from Fe2+ to Fe3+, which cannot carry oxygen, giving cyanosis unresponsive to oxygen and chocolate-brown blood.
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A farmer is brought in after a suspected deliberate ingestion. He has pinpoint pupils, profuse sweating, salivation, diarrhoea, bradycardia, wheeze and muscle fasciculations. What is the first-line drug treatment?
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IV atropine, repeated until the chest is dry and heart rate and BP are adequate (after decontamination and ABC).
Why? Organophosphates irreversibly inhibit acetylcholinesterase. Atropine blocks muscarinic effects; pralidoxime is second-line to reactivate the enzyme, ideally before 'ageing'.
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What is the antidote for inorganic mercury poisoning?
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Unithiol (DMPS).
Why? This chelator binds mercury for excretion. Mercury causes tremor, gingivitis, neuropsychiatric change and renal tubular damage.
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Which nail finding and breath odour are classic of arsenic poisoning?
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Mees' lines (transverse white nail bands) and a garlic odour on the breath.
Why? Arsenic also causes a stocking–glove neuropathy and hypotension; chelation (e.g. DMSA/succimer) is given on NPIS advice.
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Which two haem synthesis enzymes does lead inhibit?
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ALA dehydratase and ferrochelatase.
Why? This causes a microcytic anaemia with basophilic stippling and raised free protoporphyrin.
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What is the first-line treatment for cocaine-induced agitation, hypertension and chest pain?
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IV benzodiazepines (then nitrates for chest pain; PCI if there is an STEMI).
Why? Benzodiazepines reduce the central sympathetic drive that causes tachycardia, hypertension and coronary vasospasm.
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Which electrolyte abnormality is classic in ecstasy (MDMA) toxicity?
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Hyponatraemia (from SIADH and excess water drinking).
Why? It can cause confusion and seizures. MDMA also causes hyperthermia, bruxism and sweating.
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Which toxidrome causes hot, dry, flushed skin, dilated pupils, urinary retention, absent bowel sounds and agitated confusion?
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The anticholinergic toxidrome (e.g. tricyclics, atropine, antihistamines, datura).
Why? 'Hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter.'
More Clinical Pharmacology & Toxicology topics
- Pharmacokinetics, receptors & pharmacogenetics
- Autonomic, dopamine, serotonin & antiemetic drugs
- CYP450 & drug interactions
- Drug & therapeutic level monitoring
- Pregnancy, breastfeeding & contraception
- Antimicrobial mechanisms & toxicity
- Cardiovascular, immunosuppressant & anaesthetic drugs
- Overdose of common drugs
- Adverse drug reactions: drugs causing X