Cell injury and adaptation: Dubin-Johnson pigment: practice question

A Pathology 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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Pathology · Cell injury and adaptation: Dubin-Johnson pigment

Sample item

A 20-year-old man has mild fluctuating jaundice. Liver enzymes are normal, the bilirubin is predominantly conjugated, and at laparoscopy the liver is uniformly black. Which defect explains the jaundice?

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

The answer and the reasoning

D. Defective canalicular export of conjugated bilirubin

Dubin-Johnson syndrome results from loss of the canalicular transporter MRP2, so conjugated bilirubin cannot be secreted into bile and regurgitates into plasma. Dark pigment accumulates in hepatocyte lysosomes and blackens the liver, while the histology is otherwise normal. The condition is benign and needs no treatment.

Option by option

  • A. Failure of ATP7B-mediated copper excretion into the bile

    Copper excretion failure is Wilson disease, which does not blacken the liver.

  • B. Complete absence of bilirubin UDP-glucuronosyltransferase activity

    Absent glucuronyl transferase gives unconjugated hyperbilirubinaemia, as in Crigler-Najjar type I.

  • C. Impaired hepatocyte uptake of unconjugated bilirubin from plasma

    Reduced uptake gives unconjugated hyperbilirubinaemia and is part of Gilbert syndrome.

  • D. Defective canalicular export of conjugated bilirubin (correct)

    Correct. A transporter defect traps conjugated bilirubin and produces the black pigment.

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 Pathology question

What is the answer to this Pathology question?

The best answer is D, Defective canalicular export of conjugated bilirubin. Dubin-Johnson syndrome results from loss of the canalicular transporter MRP2, so conjugated bilirubin cannot be secreted into bile and regurgitates into plasma.

Why is "Failure of ATP7B-mediated copper excretion into the bile" not the answer?

Copper excretion failure is Wilson disease, which does not blacken the liver.

Why is "Complete absence of bilirubin UDP-glucuronosyltransferase activity" not the answer?

Absent glucuronyl transferase gives unconjugated hyperbilirubinaemia, as in Crigler-Najjar type I.

Why is "Impaired hepatocyte uptake of unconjugated bilirubin from plasma" not the answer?

Reduced uptake gives unconjugated hyperbilirubinaemia and is part of Gilbert syndrome.

What concept does this question test?

It tests Cell injury and adaptation: Dubin-Johnson pigment in Pathology. Dark pigment accumulates in hepatocyte lysosomes and blackens the liver, while the histology is otherwise normal. The condition is benign and needs no treatment.

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 Cell injury and adaptation: Dubin-Johnson pigment?

Learn each disease as a bundle: cause, key histology, markers, and the clinical hallmark. Then use the flashcards and the other Pathology 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.