Nerve physiology: toxins and channels: 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.

Try it

Physiology · Nerve physiology: toxins and channels

Sample item

A 35-year-old man develops perioral numbness, vomiting and progressive paralysis within an hour of eating pufferfish. He remains conscious. Which molecular action is responsible?

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

The answer and the reasoning

A. Blockade of voltage-gated sodium channels from the outer mouth of the pore

Tetrodotoxin binds the extracellular opening of the sodium channel pore and prevents the action potential upstroke in nerve and muscle. Sensory loss, paralysis and respiratory failure result while consciousness is preserved. Treatment is supportive with ventilation until the toxin is cleared.

Option by option

  • A. Blockade of voltage-gated sodium channels from the outer mouth of the pore (correct)

    Tetrodotoxin blocks the sodium channel pore, abolishing action potentials in axons.

  • B. Prevention of calcium re-uptake into the sarcoplasmic reticulum

    Impaired calcium re-uptake would cause sustained contraction or cramp, not flaccid paralysis.

  • C. Opening of voltage-gated potassium channels in motor axons

    Opening of potassium channels is not the toxin's action and would cause hyperpolarisation rather than a pore block.

  • D. Inhibition of acetylcholinesterase at the neuromuscular junction

    Acetylcholinesterase inhibition causes depolarising block with muscle fasciculation, as in organophosphate poisoning.

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.

More Physiology questions

Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is A, Blockade of voltage-gated sodium channels from the outer mouth of the pore. Tetrodotoxin binds the extracellular opening of the sodium channel pore and prevents the action potential upstroke in nerve and muscle.

Why is "Prevention of calcium re-uptake into the sarcoplasmic reticulum" not the answer?

Impaired calcium re-uptake would cause sustained contraction or cramp, not flaccid paralysis.

Why is "Opening of voltage-gated potassium channels in motor axons" not the answer?

Opening of potassium channels is not the toxin's action and would cause hyperpolarisation rather than a pore block.

Why is "Inhibition of acetylcholinesterase at the neuromuscular junction" not the answer?

Acetylcholinesterase inhibition causes depolarising block with muscle fasciculation, as in organophosphate poisoning.

What concept does this question test?

It tests Nerve physiology: toxins and channels in Physiology. Sensory loss, paralysis and respiratory failure result while consciousness is preserved. Treatment is supportive with ventilation until the toxin is cleared.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. 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 Nerve physiology: toxins and channels?

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.