Neuromuscular blockers: pseudocholinesterase deficiency: 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: pseudocholinesterase deficiency

Sample item

A 28-year-old man remains apnoeic and paralysed for three hours after a standard dose of suxamethonium for a short procedure. His brother had a similar episode. What is the most likely explanation and confirmatory test?

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

The answer and the reasoning

C. Atypical plasma cholinesterase, with a reduced dibucaine number

Suxamethonium is normally hydrolysed within minutes by plasma cholinesterase. Genetic variants with an atypical enzyme cause prolonged apnoea, and a low dibucaine number (reduced inhibition by dibucaine) identifies them. Management is sedation and ventilation until the drug is cleared, or fresh frozen plasma or purified cholinesterase.

Option by option

  • A. Phase II block from overdose, with a fade on train-of-four

    Phase II block follows large or repeated doses, which is not the case after a single standard dose.

  • B. Malignant hyperthermia, with the caffeine-halothane contracture test

    Malignant hyperthermia causes rigidity, hypercarbia and fever, not isolated prolonged paralysis.

  • C. Atypical plasma cholinesterase, with a reduced dibucaine number (correct)

    Correct. Atypical cholinesterase explains familial prolonged block after a normal dose.

  • D. Myasthenia gravis, with anti-acetylcholine receptor antibodies

    Myasthenia would give an exaggerated response to non-depolarising blockers and resistance to suxamethonium.

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 C, Atypical plasma cholinesterase, with a reduced dibucaine number. Suxamethonium is normally hydrolysed within minutes by plasma cholinesterase.

Why is "Phase II block from overdose, with a fade on train-of-four" not the answer?

Phase II block follows large or repeated doses, which is not the case after a single standard dose.

Why is "Malignant hyperthermia, with the caffeine-halothane contracture test" not the answer?

Malignant hyperthermia causes rigidity, hypercarbia and fever, not isolated prolonged paralysis.

Why is "Myasthenia gravis, with anti-acetylcholine receptor antibodies" not the answer?

Myasthenia would give an exaggerated response to non-depolarising blockers and resistance to suxamethonium.

What concept does this question test?

It tests Neuromuscular blockers: pseudocholinesterase deficiency in Pharmacology. Genetic variants with an atypical enzyme cause prolonged apnoea, and a low dibucaine number (reduced inhibition by dibucaine) identifies them. Management is sedation and ventilation until the drug is cleared, or fresh frozen plasma or purified cholinesterase.

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 Neuromuscular blockers: pseudocholinesterase deficiency?

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.