Endocrine drugs: desmopressin and hyponatraemia: practice question

A Pharmacology 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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Pharmacology · Endocrine drugs: desmopressin and hyponatraemia

Sample item

A 9-year-old on intranasal desmopressin for nocturnal enuresis drinks a lot of fluid at bedtime and develops headache, vomiting and a seizure. Serum sodium is 120 mmol/L. What is the mechanism?

AIncreased sodium excretion through aldosterone antagonismBOsmotic diuresis with excess urinary sodium lossCDirect central neurotoxicity of the desmopressin moleculeDV2-mediated water retention causing hyponatraemia

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

The answer and the reasoning

D. V2-mediated water retention causing hyponatraemia

Desmopressin stimulates V2 receptors, so aquaporin-2 channels insert in the collecting duct and water is retained. Heavy fluid intake then causes dilutional hyponatraemia and cerebral oedema, so fluids are restricted around the dose.

Option by option

A. Increased sodium excretion through aldosterone antagonism
Desmopressin has no aldosterone antagonist action.
B. Osmotic diuresis with excess urinary sodium loss
Desmopressin reduces urine volume and does not cause osmotic diuresis.
C. Direct central neurotoxicity of the desmopressin molecule
The seizure is secondary to low sodium and brain swelling rather than direct toxicity.
D. V2-mediated water retention causing hyponatraemia (correct)
Correct. V2 stimulation retains water, and extra fluid dilutes the sodium.

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.

Questions about this Pharmacology question

What is the answer to this Pharmacology question?

The best answer is D, V2-mediated water retention causing hyponatraemia. Desmopressin stimulates V2 receptors, so aquaporin-2 channels insert in the collecting duct and water is retained.

Why is "Increased sodium excretion through aldosterone antagonism" not the answer?

Desmopressin has no aldosterone antagonist action.

Why is "Osmotic diuresis with excess urinary sodium loss" not the answer?

Desmopressin reduces urine volume and does not cause osmotic diuresis.

Why is "Direct central neurotoxicity of the desmopressin molecule" not the answer?

The seizure is secondary to low sodium and brain swelling rather than direct toxicity.

What concept does this question test?

It tests Endocrine drugs: desmopressin and hyponatraemia in Pharmacology. Heavy fluid intake then causes dilutional hyponatraemia and cerebral oedema, so fluids are restricted around the dose.

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 Endocrine drugs: desmopressin and hyponatraemia?

Learn drugs as classes, then the exception in each class that an examiner would pick. Then use the flashcards and the other Pharmacology 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.