Nerve physiology: calcium and excitability: 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 · Nerve physiology: calcium and excitability

Sample item

A 40-year-old woman develops perioral tingling and carpopedal spasm the day after total thyroidectomy. Her serum calcium is 1.6 mmol/L. Why has her nerve excitability increased?

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

The answer and the reasoning

D. Less calcium screens membrane surface charge, so sodium channels open at a smaller depolarisation

Extracellular calcium binds to the outer membrane and raises the local positive surface potential, which stabilises the voltage sensors of sodium channels. In hypocalcaemia the threshold effectively moves closer to the resting potential, so axons discharge spontaneously, causing tetany, paraesthesia and positive Chvostek and Trousseau signs. The resting potential itself is little changed.

Option by option

  • A. Potassium channels are blocked, which raises the resting potential above threshold

    Potassium channel blockade is not the mechanism, and the resting potential does not rise above threshold.

  • B. Sodium channels are inactivated, so axons fire spontaneously

    Inactivation of sodium channels is the result of sustained depolarisation, as in hyperkalaemia, and causes weakness.

  • C. Acetylcholine release is reduced, causing denervation hypersensitivity

    Reduced acetylcholine release would cause weakness, whereas hypocalcaemia causes spontaneous firing of axons.

  • D. Less calcium screens membrane surface charge, so sodium channels open at a smaller depolarisation (correct)

    Reduced calcium screening lowers the threshold for sodium channel opening.

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 D, Less calcium screens membrane surface charge, so sodium channels open at a smaller depolarisation. Extracellular calcium binds to the outer membrane and raises the local positive surface potential, which stabilises the voltage sensors of sodium channels.

Why is "Potassium channels are blocked, which raises the resting potential ab…" not the answer?

Potassium channel blockade is not the mechanism, and the resting potential does not rise above threshold.

Why is "Sodium channels are inactivated, so axons fire spontaneously" not the answer?

Inactivation of sodium channels is the result of sustained depolarisation, as in hyperkalaemia, and causes weakness.

Why is "Acetylcholine release is reduced, causing denervation hypersensitivity" not the answer?

Reduced acetylcholine release would cause weakness, whereas hypocalcaemia causes spontaneous firing of axons.

What concept does this question test?

It tests Nerve physiology: calcium and excitability in Physiology. In hypocalcaemia the threshold effectively moves closer to the resting potential, so axons discharge spontaneously, causing tetany, paraesthesia and positive Chvostek and Trousseau signs. The resting potential itself is little changed.

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 Nerve physiology: calcium and excitability?

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.