Neuromuscular junction: myasthenia gravis: 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.

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Physiology · Neuromuscular junction: myasthenia gravis

Sample item

A 26-year-old woman has ptosis and diplopia that worsen towards the evening. Repetitive nerve stimulation at 3 Hz shows a progressive fall in the compound muscle action potential. What explains this decrement?

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

The answer and the reasoning

C. Fewer postsynaptic receptors, so the normal fall in acetylcholine release leaves some end-plate potentials below threshold

Antibodies to postsynaptic nicotinic receptors reduce the number of receptors and the safety margin of transmission. With repeated stimulation the quantity of acetylcholine released per impulse falls normally, so the end-plate potential in more and more fibres fails to reach threshold, giving a decremental response. Anticholinesterase drugs such as pyridostigmine prolong transmitter action and improve strength.

Option by option

  • A. A presynaptic calcium channel defect that is overcome by repeated stimulation

    A presynaptic calcium channel defect characterises Lambert-Eaton syndrome, which shows an increment after rapid stimulation.

  • B. Excess acetylcholinesterase activity that destroys the transmitter before it can bind

    Excess acetylcholinesterase is not the disorder; blocking the enzyme improves myasthenia.

  • C. Fewer postsynaptic receptors, so the normal fall in acetylcholine release leaves some end-plate potentials below threshold (correct)

    A reduced receptor population removes the safety factor, so the normal fall in release causes decrement.

  • D. Destruction of the muscle fibres so that fewer fibres can contract

    Muscle fibres are structurally intact in myasthenia; the defect is at the end plate.

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 Physiology question

What is the answer to this Physiology question?

The best answer is C, Fewer postsynaptic receptors, so the normal fall in acetylcholine release leaves some end-plate potentials below threshold. Antibodies to postsynaptic nicotinic receptors reduce the number of receptors and the safety margin of transmission.

Why is "A presynaptic calcium channel defect that is overcome by repeated sti…" not the answer?

A presynaptic calcium channel defect characterises Lambert-Eaton syndrome, which shows an increment after rapid stimulation.

Why is "Excess acetylcholinesterase activity that destroys the transmitter be…" not the answer?

Excess acetylcholinesterase is not the disorder; blocking the enzyme improves myasthenia.

Why is "Destruction of the muscle fibres so that fewer fibres can contract" not the answer?

Muscle fibres are structurally intact in myasthenia; the defect is at the end plate.

What concept does this question test?

It tests Neuromuscular junction: myasthenia gravis in Physiology. With repeated stimulation the quantity of acetylcholine released per impulse falls normally, so the end-plate potential in more and more fibres fails to reach threshold, giving a decremental response. Anticholinesterase drugs such as pyridostigmine prolong transmitter action and improve strength.

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 junction: myasthenia gravis?

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.