Chemotherapy: co-trimoxazole and hyperkalaemia: 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 · Chemotherapy: co-trimoxazole and hyperkalaemia

Sample item

A 34-year-old man with HIV on high-dose co-trimoxazole for Pneumocystis pneumonia has potassium 6.1 mmol/L with a small rise in creatinine. What explains the hyperkalaemia?

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

The answer and the reasoning

B. Trimethoprim blocks ENaC in the collecting duct, as amiloride does

Trimethoprim is structurally similar to amiloride and blocks the epithelial sodium channel in the distal nephron. This reduces the lumen-negative potential that drives potassium secretion, so potassium is retained, especially at high doses and in renal impairment. It also blocks tubular creatinine secretion, producing a small rise in creatinine without a true fall in GFR.

Option by option

  • A. Trimethoprim inhibits the Na+-K+-2Cl- cotransporter

    Blocking NKCC2 is the action of loop diuretics, which cause potassium loss.

  • B. Trimethoprim blocks ENaC in the collecting duct, as amiloride does (correct)

    Correct. ENaC blockade impairs potassium secretion.

  • C. G6PD-related haemolysis releasing intracellular potassium

    Haemolysis can occur in G6PD deficiency, but it seldom produces this degree of hyperkalaemia.

  • D. Sulfamethoxazole antagonises aldosterone receptors

    Sulfamethoxazole is not a mineralocorticoid antagonist; spironolactone is.

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 Pharmacology question

What is the answer to this Pharmacology question?

The best answer is B, Trimethoprim blocks ENaC in the collecting duct, as amiloride does. Trimethoprim is structurally similar to amiloride and blocks the epithelial sodium channel in the distal nephron.

Why is "Trimethoprim inhibits the Na+-K+-2Cl- cotransporter" not the answer?

Blocking NKCC2 is the action of loop diuretics, which cause potassium loss.

Why is "G6PD-related haemolysis releasing intracellular potassium" not the answer?

Haemolysis can occur in G6PD deficiency, but it seldom produces this degree of hyperkalaemia.

Why is "Sulfamethoxazole antagonises aldosterone receptors" not the answer?

Sulfamethoxazole is not a mineralocorticoid antagonist; spironolactone is.

What concept does this question test?

It tests Chemotherapy: co-trimoxazole and hyperkalaemia in Pharmacology. This reduces the lumen-negative potential that drives potassium secretion, so potassium is retained, especially at high doses and in renal impairment. It also blocks tubular creatinine secretion, producing a small rise in creatinine without a true fall in GFR.

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 Chemotherapy: co-trimoxazole and hyperkalaemia?

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.