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Anaesthesia · Intravenous and inhalational agents: cholinesterase inhibition and suxamethonium
Sample itemA farmer with organophosphate poisoning has been stabilised with atropine and pralidoxime and needs surgery. After suxamethonium for intubation, he remains apnoeic for more than two hours. Why?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Organophosphates inhibit plasma cholinesterase, so suxamethonium is not hydrolysed
Suxamethonium is broken down by plasma cholinesterase. Organophosphate poisoning depresses this enzyme, so the block is greatly prolonged and ventilation must be continued until recovery. Other drugs hydrolysed by esterases, such as mivacurium, behave similarly.
Option by option
A. Organophosphates inhibit plasma cholinesterase, so suxamethonium is not hydrolysed (correct)
Correct. Reduced plasma cholinesterase prolongs suxamethonium.
B. Organophosphates deplete receptors, so block is permanent
The block is prolonged but not permanent.
C. Atropine blocks the nicotinic receptor and prolongs the block
Atropine blocks muscarinic, not nicotinic, receptors.
D. Pralidoxime potentiates depolarising block directly
Pralidoxime reactivates cholinesterase and does not potentiate the block.
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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