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Physiology · General physiology: excitability and potassium
Sample itemA 60-year-old man with renal failure has serum potassium of 7.2 mmol/L and generalised muscle weakness. Which mechanism explains the weakness?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. The resting potential becomes less negative, so Na+ channels inactivate and excitability falls
Raising extracellular K+ reduces the K+ gradient and shifts the K+ equilibrium potential and resting potential toward zero. Sustained partial depolarisation inactivates voltage-gated Na+ channels, so action potentials cannot be generated normally and flaccid weakness results; cardiac conduction is similarly affected.
Option by option
A. The resting potential becomes less negative, so Na+ channels inactivate and excitability falls (correct)
Persistent depolarisation inactivates Na+ channels, leaving the cell less excitable.
B. Extracellular K+ blocks acetylcholine release from the motor nerve terminal
Hyperkalaemia does not impair acetylcholine release; it acts on the excitable membrane itself.
C. Extracellular K+ directly inhibits Ca2+ release from the sarcoplasmic reticulum
Potassium has no direct effect on sarcoplasmic reticulum Ca2+ release.
D. The K+ equilibrium potential becomes more negative, so the membrane hyperpolarises and cannot reach threshold
Hyperpolarisation is the effect of hypokalaemia, which also causes weakness through a different route.
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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