General physiology: neuromuscular transmission defect: practice question

A Physiology 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.

Try it

Physiology · General physiology: neuromuscular transmission defect

Sample item

A 62-year-old smoker has proximal leg weakness, dry mouth and absent tendon reflexes. Strength improves briefly after sustained effort, and high-frequency repetitive nerve stimulation increases the muscle action potential amplitude. What is the underlying defect?

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

The answer and the reasoning

A. Autoantibodies against presynaptic voltage-gated calcium channels reduce acetylcholine release

Lambert-Eaton syndrome is a presynaptic disorder, often paraneoplastic with small cell lung cancer, in which antibodies to P/Q-type calcium channels lower quantal release of acetylcholine. Repeated stimulation builds up residual presynaptic calcium, so release and strength increase, whereas in myasthenia gravis they decline.

Option by option

  • A. Autoantibodies against presynaptic voltage-gated calcium channels reduce acetylcholine release (correct)

    Reduced presynaptic calcium entry explains weakness that facilitates with repeated stimulation.

  • B. Autoantibodies against postsynaptic nicotinic receptors reduce the end-plate response

    Postsynaptic receptor antibodies cause myasthenia gravis, with fatigable weakness and a decremental response.

  • C. Loss of dystrophin weakens the muscle fibre membrane

    Dystrophin loss causes muscular dystrophy, and does not produce a facilitation response or autonomic dryness.

  • D. Organophosphate inhibition of acetylcholinesterase causes persistent depolarisation

    Organophosphates cause cholinergic excess with fasciculations, miosis and secretions, not the facilitation pattern.

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.

More Physiology questions

Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is A, Autoantibodies against presynaptic voltage-gated calcium channels reduce acetylcholine release. Lambert-Eaton syndrome is a presynaptic disorder, often paraneoplastic with small cell lung cancer, in which antibodies to P/Q-type calcium channels lower quantal release of acetylcholine.

Why is "Autoantibodies against postsynaptic nicotinic receptors reduce the en…" not the answer?

Postsynaptic receptor antibodies cause myasthenia gravis, with fatigable weakness and a decremental response.

Why is "Loss of dystrophin weakens the muscle fibre membrane" not the answer?

Dystrophin loss causes muscular dystrophy, and does not produce a facilitation response or autonomic dryness.

Why is "Organophosphate inhibition of acetylcholinesterase causes persistent…" not the answer?

Organophosphates cause cholinergic excess with fasciculations, miosis and secretions, not the facilitation pattern.

What concept does this question test?

It tests General physiology: neuromuscular transmission defect in Physiology. Repeated stimulation builds up residual presynaptic calcium, so release and strength increase, whereas in myasthenia gravis they decline.

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 General physiology: neuromuscular transmission defect?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology 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.