Hepatic pathology: ascites in cirrhosis: 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 · Hepatic pathology: ascites in cirrhosis

Sample item

A 52-year-old man with alcoholic cirrhosis has tense ascites, splenomegaly and oesophageal varices. Which combination best explains the accumulation of ascitic fluid?

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

The answer and the reasoning

B. Sinusoidal portal hypertension with hypoalbuminaemia and sodium retention from splanchnic vasodilatation

Distortion of the sinusoids by fibrosis and regenerative nodules raises portal pressure and filtration of fluid from the splanchnic bed. Reduced albumin synthesis lowers oncotic pressure, and splanchnic vasodilatation lowers effective arterial volume, activating the renin-angiotensin-aldosterone system and causing sodium and water retention. Lymph from the liver also exceeds the capacity of the lymphatics.

Option by option

  • A. Raised hepatic albumin synthesis drawing fluid into the peritoneum

    Albumin synthesis falls in cirrhosis and does not rise.

  • B. Sinusoidal portal hypertension with hypoalbuminaemia and sodium retention from splanchnic vasodilatation (correct)

    Correct. Portal hypertension, low oncotic pressure and neurohormonal sodium retention act together.

  • C. Primary renal sodium wasting with secondary peritoneal leakage

    The kidney retains sodium avidly in cirrhosis and does not waste it.

  • D. Obstruction of the thoracic duct by regenerative nodules

    The thoracic duct is not obstructed in cirrhosis.

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 B, Sinusoidal portal hypertension with hypoalbuminaemia and sodium retention from splanchnic vasodilatation. Distortion of the sinusoids by fibrosis and regenerative nodules raises portal pressure and filtration of fluid from the splanchnic bed.

Why is "Raised hepatic albumin synthesis drawing fluid into the peritoneum" not the answer?

Albumin synthesis falls in cirrhosis and does not rise.

Why is "Primary renal sodium wasting with secondary peritoneal leakage" not the answer?

The kidney retains sodium avidly in cirrhosis and does not waste it.

Why is "Obstruction of the thoracic duct by regenerative nodules" not the answer?

The thoracic duct is not obstructed in cirrhosis.

What concept does this question test?

It tests Hepatic pathology: ascites in cirrhosis in Pathology. Reduced albumin synthesis lowers oncotic pressure, and splanchnic vasodilatation lowers effective arterial volume, activating the renin-angiotensin-aldosterone system and causing sodium and water retention. Lymph from the liver also exceeds the capacity of the lymphatics.

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 Hepatic pathology: ascites in cirrhosis?

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.