Endocrinology: secondary hyperaldosteronism: 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 · Endocrinology: secondary hyperaldosteronism

Sample item

A patient with decompensated cirrhosis and ascites has hypokalaemia, high aldosterone and high plasma renin activity. Why does this differ from primary aldosteronism, in which renin is suppressed?

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

The answer and the reasoning

B. Low effective arterial volume activates the renin-angiotensin system, driving aldosterone secretion

In cirrhosis, splanchnic vasodilation lowers effective arterial volume, so the juxtaglomerular cells secrete renin and angiotensin II stimulates aldosterone. This is secondary hyperaldosteronism with high renin. In primary disease, autonomous aldosterone expands volume and suppresses renin.

Option by option

  • A. Cortisol saturates the receptor and suppresses the renin-secreting cells

    Cortisol does not suppress renin in this way, and cortisol excess is not the problem here.

  • B. Low effective arterial volume activates the renin-angiotensin system, driving aldosterone secretion (correct)

    Correct. Low effective circulating volume drives renin and therefore aldosterone, so renin is high.

  • C. Raised atrial natriuretic peptide stimulates renin release

    Atrial natriuretic peptide inhibits renin release rather than stimulating it.

  • D. A tumour of the zona glomerulosa secretes aldosterone autonomously

    Autonomous aldosterone from a tumour would suppress renin, which is the primary pattern.

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, Low effective arterial volume activates the renin-angiotensin system, driving aldosterone secretion. In cirrhosis, splanchnic vasodilation lowers effective arterial volume, so the juxtaglomerular cells secrete renin and angiotensin II stimulates aldosterone.

Why is "Cortisol saturates the receptor and suppresses the renin-secreting ce…" not the answer?

Cortisol does not suppress renin in this way, and cortisol excess is not the problem here.

Why is "Raised atrial natriuretic peptide stimulates renin release" not the answer?

Atrial natriuretic peptide inhibits renin release rather than stimulating it.

Why is "A tumour of the zona glomerulosa secretes aldosterone autonomously" not the answer?

Autonomous aldosterone from a tumour would suppress renin, which is the primary pattern.

What concept does this question test?

It tests Endocrinology: secondary hyperaldosteronism in Physiology. This is secondary hyperaldosteronism with high renin. In primary disease, autonomous aldosterone expands volume and suppresses renin.

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 Endocrinology: secondary hyperaldosteronism?

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.