Neuromuscular blockers: succinylcholine hyperkalaemia: practice question

A Pharmacology 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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Pharmacology · Neuromuscular blockers: succinylcholine hyperkalaemia

Sample item

A man with 40% burns sustained 12 days ago is anaesthetised for debridement and given succinylcholine. Within minutes he develops peaked T waves and ventricular arrhythmia. What is the mechanism?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

B. Upregulated extrajunctional acetylcholine receptors causing massive potassium efflux

After burns, denervation, or prolonged immobilisation, muscle expresses extrajunctional nicotinic receptors across its surface. Succinylcholine depolarises all of them and a large potassium load leaves the cells, causing life-threatening hyperkalaemia. The risk is highest from about the first week to months after injury.

Option by option

  • A. Histamine release causing vasodilatation

    Histamine release causes hypotension and flushing, not a hyperkalaemic arrhythmia.

  • B. Upregulated extrajunctional acetylcholine receptors causing massive potassium efflux (correct)

    Correct. Widespread depolarisation of upregulated receptors releases potassium into the plasma.

  • C. Blockade of muscarinic receptors in the sinus node

    Succinylcholine is a nicotinic agonist and does not block muscarinic receptors.

  • D. Inhibition of plasma cholinesterase by the burn injury

    Reduced cholinesterase would prolong block, not produce peaked T waves.

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 Pharmacology question

What is the answer to this Pharmacology question?

The best answer is B, Upregulated extrajunctional acetylcholine receptors causing massive potassium efflux. After burns, denervation, or prolonged immobilisation, muscle expresses extrajunctional nicotinic receptors across its surface.

Why is "Histamine release causing vasodilatation" not the answer?

Histamine release causes hypotension and flushing, not a hyperkalaemic arrhythmia.

Why is "Blockade of muscarinic receptors in the sinus node" not the answer?

Succinylcholine is a nicotinic agonist and does not block muscarinic receptors.

Why is "Inhibition of plasma cholinesterase by the burn injury" not the answer?

Reduced cholinesterase would prolong block, not produce peaked T waves.

What concept does this question test?

It tests Neuromuscular blockers: succinylcholine hyperkalaemia in Pharmacology. Succinylcholine depolarises all of them and a large potassium load leaves the cells, causing life-threatening hyperkalaemia. The risk is highest from about the first week to months after injury.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. 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 Neuromuscular blockers: succinylcholine hyperkalaemia?

Learn drugs as classes, then the exception in each class that an examiner would pick. Then use the flashcards and the other Pharmacology 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.