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Pharmacology · Autonomic: pralidoxime and carbamates
Sample itemA farm worker is poisoned with carbaryl, a carbamate insecticide, and has mild cholinergic features. Why is pralidoxime generally not needed?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Carbamate inhibition of cholinesterase is spontaneously reversible, and there is no aged phosphorylated enzyme to reactivate
Carbamylated cholinesterase regenerates spontaneously within hours, so oximes are usually unnecessary, and some data suggest possible harm with carbaryl. Atropine remains the mainstay for muscarinic symptoms. Pralidoxime is valuable in organophosphate poisoning before ageing.
Option by option
A. Carbamate inhibition of cholinesterase is spontaneously reversible, and there is no aged phosphorylated enzyme to reactivate (correct)
Correct. Carbamate inhibition is short lived and reversible.
B. Pralidoxime is only effective if given after 48 hours
Oximes work best early, before enzyme ageing, not after 48 hours.
C. Pralidoxime worsens carbamate toxicity by crossing the blood-brain barrier
Pralidoxime does not cross the blood-brain barrier well and is not contraindicated for that reason.
D. Carbamates act on muscarinic receptors directly
Carbamates inhibit cholinesterase rather than directly activating receptors.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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