Renal and acid–base: alkalosis and hypokalaemia in primary aldosteronism: 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 · Renal and acid–base: alkalosis and hypokalaemia in primary aldosteronism

Sample item

A woman with an aldosterone-secreting adenoma has hypertension, hypokalaemia and a mild metabolic alkalosis. Which tubular mechanism accounts for the potassium and hydrogen ion loss?

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

The answer and the reasoning

D. Greater ENaC sodium uptake makes the lumen negative and drives K+ and H+ secretion

Aldosterone increases the number of open ENaC channels and Na+/K+ ATPase pumps in principal cells. The resulting lumen-negative potential favours K+ secretion by principal cells and H+ secretion by intercalated cells. Aldosterone also directly stimulates H+-ATPase.

Option by option

  • A. Impaired aquaporin insertion in the collecting duct

    Aquaporin defects affect water, not potassium and hydrogen ion secretion.

  • B. Reduced Na+ reabsorption in the proximal tubule

    Aldosterone acts distally and not in the proximal tubule.

  • C. Blockade of the thiazide-sensitive cotransporter

    That would mimic Gitelman syndrome, with normal or low blood pressure.

  • D. Greater ENaC sodium uptake makes the lumen negative and drives K+ and H+ secretion (correct)

    Correct. Increased sodium entry makes the lumen negative and promotes K+ and H+ secretion.

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 D, Greater ENaC sodium uptake makes the lumen negative and drives K+ and H+ secretion. Aldosterone increases the number of open ENaC channels and Na+/K+ ATPase pumps in principal cells.

Why is "Impaired aquaporin insertion in the collecting duct" not the answer?

Aquaporin defects affect water, not potassium and hydrogen ion secretion.

Why is "Reduced Na+ reabsorption in the proximal tubule" not the answer?

Aldosterone acts distally and not in the proximal tubule.

Why is "Blockade of the thiazide-sensitive cotransporter" not the answer?

That would mimic Gitelman syndrome, with normal or low blood pressure.

What concept does this question test?

It tests Renal and acid–base: alkalosis and hypokalaemia in primary aldosteronism in Physiology. The resulting lumen-negative potential favours K+ secretion by principal cells and H+ secretion by intercalated cells. Aldosterone also directly stimulates H+-ATPase.

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 Renal and acid–base: alkalosis and hypokalaemia in primary aldosteronism?

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.