In a patient with severe hypokalemia, the resting membrane potential of large motor neurons shifts from -70 mV to approximately -80 mV. What is the expected effect on neuronal excitability and the clinical correlate?

• A Membrane moves closer to threshold, causing spontaneous fasciculations and cramps
• B Threshold itself falls below the resting potential, producing continuous discharge
• C Resting potential approaches the sodium equilibrium potential, abolishing excitability entirely
• D Membrane moves further from threshold, decreasing excitability and contributing to weakness ✓

Explanation

With low extracellular potassium, the potassium concentration gradient steepens and the resting membrane potential moves closer to the potassium equilibrium potential, becoming more negative (hyperpolarized). The distance between resting potential and firing threshold widens, so larger inputs are needed to fire the cell: excitability falls, matching the flaccid weakness seen clinically. Option A reverses the direction of the shift and describes states such as early hyperkalemia, where partial depolarization raises excitability before inactivation supervenes.

Reference: Ganong's Review of Medical Physiology, 26th ed.

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