Intravenous and inhalational agents: cholinesterase inhibition and suxamethonium: practice question

A Anaesthesia question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Anaesthesia · Intravenous and inhalational agents: cholinesterase inhibition and suxamethonium

Sample item

A 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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Questions about this Anaesthesia question

What is the answer to this Anaesthesia question?

The best answer is A, Organophosphates inhibit plasma cholinesterase, so suxamethonium is not hydrolysed. Suxamethonium is broken down by plasma cholinesterase.

Why is "Organophosphates deplete receptors, so block is permanent" not the answer?

The block is prolonged but not permanent.

Why is "Atropine blocks the nicotinic receptor and prolongs the block" not the answer?

Atropine blocks muscarinic, not nicotinic, receptors.

Why is "Pralidoxime potentiates depolarising block directly" not the answer?

Pralidoxime reactivates cholinesterase and does not potentiate the block.

What concept does this question test?

It tests Intravenous and inhalational agents: cholinesterase inhibition and suxamethonium in Anaesthesia. 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.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Intravenous and inhalational agents: cholinesterase inhibition and suxamethonium?

Make a table of each agent, its key advantage and its main side effect. Then use the flashcards and the other Anaesthesia questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.