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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.

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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.

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Nerve physiology: resting… MCQ (B7-PHYS3-1)

Q: What is the answer to this Physiology question?

The best answer is C, Persistent partial depolarisation that inactivates voltage-gated sodium channels. Raising extracellular potassium makes the potassium equilibrium potential less negative, so the resting potential moves toward threshold.

Q: What concept does this question test?

It tests Nerve physiology: resting potential in Physiology. A small rise causes transient hyperexcitability, but a sustained depolarisation keeps the inactivation gates of sodium channels closed. The membrane then cannot generate action potentials, producing weakness and conduction block.

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Physiology · Nerve physiology: resting potential

Sample item

A 55-year-old man with advanced kidney disease has a serum potassium of 7.8 mmol/L and generalised muscle weakness. Which change in his excitable membranes best explains the weakness?

AHyperpolarisation of the resting membrane that moves it further from thresholdBIncreased sodium permeability at rest that raises the action potential amplitudeCPersistent partial depolarisation that inactivates voltage-gated sodium channelsDFailure of calcium release from the sarcoplasmic reticulum despite a normal action potential

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The answer and the reasoning

C. Persistent partial depolarisation that inactivates voltage-gated sodium channels

Raising extracellular potassium makes the potassium equilibrium potential less negative, so the resting potential moves toward threshold. A small rise causes transient hyperexcitability, but a sustained depolarisation keeps the inactivation gates of sodium channels closed. The membrane then cannot generate action potentials, producing weakness and conduction block.

Option by option

A. Hyperpolarisation of the resting membrane that moves it further from threshold
Hyperkalaemia depolarises the membrane; hyperpolarisation is the effect of hypokalaemia.
B. Increased sodium permeability at rest that raises the action potential amplitude
Resting sodium permeability does not rise, and inactivated channels lower rather than raise the spike amplitude.
C. Persistent partial depolarisation that inactivates voltage-gated sodium channels (correct)
Sustained depolarisation inactivates sodium channels, so fewer fibres can fire.
D. Failure of calcium release from the sarcoplasmic reticulum despite a normal action potential
Excitation-contraction coupling fails here because no action potential is generated, not because of a primary defect of calcium release.

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.

Nerve physiology: resting potential: practice question

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The answer and the reasoning

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