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Physiology · Nerve physiology: calcium and excitability
Sample itemA 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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