Gastrointestinal: hepatic encephalopathy and ammonia: 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 · Gastrointestinal: hepatic encephalopathy and ammonia

Sample item

A 55-year-old man with cirrhosis becomes confused after an upper gastrointestinal bleed, and his arterial ammonia is raised. Which physiological failure mainly explains the hyperammonaemia?

AImpaired intestinal bacterial production of ammoniaBIncreased urea synthesis by the failing liverCReduced hepatic conversion of ammonia to urea, with portosystemic shunting of gut-derived ammoniaDIncreased renal excretion of ammonium

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

The answer and the reasoning

C. Reduced hepatic conversion of ammonia to urea, with portosystemic shunting of gut-derived ammonia

Colonic bacteria and intestinal glutaminase produce ammonia, which is normally removed by the liver through the urea cycle on its first pass. In cirrhosis, reduced hepatocyte mass and shunting of portal blood around the liver allow ammonia into the systemic circulation, and a gastrointestinal bleed adds a protein load.

Option by option

A. Impaired intestinal bacterial production of ammonia
Gut ammonia production is intact, and is increased by a blood protein load.
B. Increased urea synthesis by the failing liver
Urea synthesis falls, not rises, in a failing liver.
C. Reduced hepatic conversion of ammonia to urea, with portosystemic shunting of gut-derived ammonia (correct)
Correct. The cirrhotic liver clears too little ammonia as urea, and shunting bypasses it.
D. Increased renal excretion of ammonium
Renal ammonium excretion cannot compensate for the hepatic failure and does not explain the rise.

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.

Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is C, Reduced hepatic conversion of ammonia to urea, with portosystemic shunting of gut-derived ammonia. Colonic bacteria and intestinal glutaminase produce ammonia, which is normally removed by the liver through the urea cycle on its first pass.

Why is "Impaired intestinal bacterial production of ammonia" not the answer?

Gut ammonia production is intact, and is increased by a blood protein load.

Why is "Increased urea synthesis by the failing liver" not the answer?

Urea synthesis falls, not rises, in a failing liver.

Why is "Increased renal excretion of ammonium" not the answer?

Renal ammonium excretion cannot compensate for the hepatic failure and does not explain the rise.

What concept does this question test?

It tests Gastrointestinal: hepatic encephalopathy and ammonia in Physiology. In cirrhosis, reduced hepatocyte mass and shunting of portal blood around the liver allow ammonia into the systemic circulation, and a gastrointestinal bleed adds a protein load.

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 Gastrointestinal: hepatic encephalopathy and ammonia?

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.