Neuromuscular junction: Lambert-Eaton syndrome: 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 junction: Lambert-Eaton syndrome

Sample item

A 62-year-old smoker has proximal leg weakness that briefly improves after repeated effort, dry mouth and absent knee jerks. Electrophysiology shows an incremental response to high-frequency stimulation. Which drug is the most effective symptomatic treatment, and how does it act?

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

The answer and the reasoning

B. Amifampridine, by blocking presynaptic potassium channels to increase acetylcholine release

This is the Lambert-Eaton syndrome, caused by antibodies against presynaptic voltage-gated calcium channels, often in small cell lung cancer. 3,4-Diaminopyridine (amifampridine) blocks voltage-gated potassium channels, prolongs depolarisation, enhances calcium entry and increases acetylcholine release. Anticholinesterases are less effective and are used only as adjuncts.

Option by option

  • A. Edrophonium, by directly stimulating nicotinic receptors

    Edrophonium inhibits acetylcholinesterase and is a diagnostic aid in myasthenia gravis; it is not a direct receptor agonist.

  • B. Amifampridine, by blocking presynaptic potassium channels to increase acetylcholine release (correct)

    Potassium channel blockade prolongs terminal depolarisation and boosts quantal acetylcholine release.

  • C. Dantrolene, by blocking the ryanodine receptor

    Dantrolene lowers muscle calcium release and would worsen weakness.

  • D. Neostigmine, by blocking calcium channels

    Neostigmine inhibits acetylcholinesterase rather than blocking calcium channels, and is only a weak adjunct here.

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, Amifampridine, by blocking presynaptic potassium channels to increase acetylcholine release. This is the Lambert-Eaton syndrome, caused by antibodies against presynaptic voltage-gated calcium channels, often in small cell lung cancer.

Why is "Edrophonium, by directly stimulating nicotinic receptors" not the answer?

Edrophonium inhibits acetylcholinesterase and is a diagnostic aid in myasthenia gravis; it is not a direct receptor agonist.

Why is "Dantrolene, by blocking the ryanodine receptor" not the answer?

Dantrolene lowers muscle calcium release and would worsen weakness.

Why is "Neostigmine, by blocking calcium channels" not the answer?

Neostigmine inhibits acetylcholinesterase rather than blocking calcium channels, and is only a weak adjunct here.

What concept does this question test?

It tests Neuromuscular junction: Lambert-Eaton syndrome in Pharmacology. 3,4-Diaminopyridine (amifampridine) blocks voltage-gated potassium channels, prolongs depolarisation, enhances calcium entry and increases acetylcholine release. Anticholinesterases are less effective and are used only as adjuncts.

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 junction: Lambert-Eaton syndrome?

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.