GI physiology: unconjugated hyperbilirubinaemia: 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 · GI physiology: unconjugated hyperbilirubinaemia

Sample item

A 20-year-old man has mild jaundice during a fast and an episode of gastroenteritis. Bilirubin is 34 micromol/L, mainly unconjugated, with normal liver enzymes, haemoglobin and reticulocytes, and no bilirubin in urine. What is the underlying defect?

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

The answer and the reasoning

B. Reduced activity of UDP-glucuronosyltransferase 1A1

Gilbert syndrome is a common benign condition caused by reduced expression of UGT1A1, so conjugation of bilirubin is about 30% of normal. Fasting, illness and stress raise unconjugated bilirubin mildly, and unconjugated bilirubin is bound to albumin and so does not appear in urine (acholuric jaundice). No treatment is needed.

Option by option

  • A. Increased red cell destruction in the spleen

    Haemolysis is excluded by the normal haemoglobin and reticulocyte count.

  • B. Reduced activity of UDP-glucuronosyltransferase 1A1 (correct)

    Reduced UGT1A1 activity causes mild unconjugated hyperbilirubinaemia that rises on fasting.

  • C. Absent hepatic uptake of conjugated bilirubin because of OATP failure

    Failure of hepatic uptake of conjugated bilirubin is not the problem, since the bilirubin is unconjugated.

  • D. Defective canalicular excretion of conjugated bilirubin by MRP2

    MRP2 defect is the cause of Dubin-Johnson syndrome, with conjugated hyperbilirubinaemia and bilirubinuria.

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, Reduced activity of UDP-glucuronosyltransferase 1A1. Gilbert syndrome is a common benign condition caused by reduced expression of UGT1A1, so conjugation of bilirubin is about 30% of normal.

Why is "Increased red cell destruction in the spleen" not the answer?

Haemolysis is excluded by the normal haemoglobin and reticulocyte count.

Why is "Absent hepatic uptake of conjugated bilirubin because of OATP failure" not the answer?

Failure of hepatic uptake of conjugated bilirubin is not the problem, since the bilirubin is unconjugated.

Why is "Defective canalicular excretion of conjugated bilirubin by MRP2" not the answer?

MRP2 defect is the cause of Dubin-Johnson syndrome, with conjugated hyperbilirubinaemia and bilirubinuria.

What concept does this question test?

It tests GI physiology: unconjugated hyperbilirubinaemia in Physiology. Fasting, illness and stress raise unconjugated bilirubin mildly, and unconjugated bilirubin is bound to albumin and so does not appear in urine (acholuric jaundice). No treatment is needed.

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 GI physiology: unconjugated hyperbilirubinaemia?

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.