Muscle physiology: thyrotoxic periodic paralysis: 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 · Muscle physiology: thyrotoxic periodic paralysis

Sample item

A 28-year-old man wakes with sudden flaccid weakness of both legs after a heavy carbohydrate meal the night before. He has tremor, tachycardia and a goitre; serum potassium is 2.4 mmol/L and TSH is suppressed. What best explains the weakness?

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

The answer and the reasoning

B. A shift of potassium into muscle cells that hyperpolarises the membrane and makes fibres inexcitable

Thyroid hormone raises Na+-K+ ATPase activity, and carbohydrate-induced insulin adds to the intracellular shift of potassium. Extracellular potassium falls acutely, the resting potential becomes more negative and muscle fibres cannot reach threshold. Total body potassium is normal, so recovery is prompt once potassium redistributes.

Option by option

  • A. Failure of acetylcholine release from motor nerve terminals

    Presynaptic failure of acetylcholine release is the mechanism of botulism and the Lambert-Eaton syndrome, not this picture.

  • B. A shift of potassium into muscle cells that hyperpolarises the membrane and makes fibres inexcitable (correct)

    Correct. Transcellular potassium shift produces hyperpolarisation and paralysis.

  • C. Total body potassium loss from renal wasting

    Urinary potassium is typically low in this condition, so the problem is redistribution, not true depletion.

  • D. Depolarisation block from raised extracellular potassium

    Hyperkalaemia would cause depolarisation block, but potassium here is low.

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 B, A shift of potassium into muscle cells that hyperpolarises the membrane and makes fibres inexcitable. Thyroid hormone raises Na+-K+ ATPase activity, and carbohydrate-induced insulin adds to the intracellular shift of potassium.

Why is "Failure of acetylcholine release from motor nerve terminals" not the answer?

Presynaptic failure of acetylcholine release is the mechanism of botulism and the Lambert-Eaton syndrome, not this picture.

Why is "Total body potassium loss from renal wasting" not the answer?

Urinary potassium is typically low in this condition, so the problem is redistribution, not true depletion.

Why is "Depolarisation block from raised extracellular potassium" not the answer?

Hyperkalaemia would cause depolarisation block, but potassium here is low.

What concept does this question test?

It tests Muscle physiology: thyrotoxic periodic paralysis in Physiology. Extracellular potassium falls acutely, the resting potential becomes more negative and muscle fibres cannot reach threshold. Total body potassium is normal, so recovery is prompt once potassium redistributes.

How hard is this question?

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.

How should I study Muscle physiology: thyrotoxic periodic paralysis?

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.