A patient has the following results: LDH 550 U/L; AST 90 U/L; ALT 120 U/L; ALP 400 U/L; AMM 60 umol/L; GGT 92 U/L; CHE 1000 U/L; UREA 2.0 mmol/L; CREA 105 umol/L; sOSMO 200 Osm/kg; Urinalysis: BIL 2+; UROBIL 4 Ehrlich unit; BILIRUBIN: PRESENT; TYROSINE: PRESENT; LEUCINE: PRESENT. What is the suspected diagnosis?

Prepare for the CAMLPR Chemistry Test. Enhance your understanding with interactive quizzes, flashcards, and detailed explanations. Boost your confidence and readiness for exam success!

Multiple Choice

A patient has the following results: LDH 550 U/L; AST 90 U/L; ALT 120 U/L; ALP 400 U/L; AMM 60 umol/L; GGT 92 U/L; CHE 1000 U/L; UREA 2.0 mmol/L; CREA 105 umol/L; sOSMO 200 Osm/kg; Urinalysis: BIL 2+; UROBIL 4 Ehrlich unit; BILIRUBIN: PRESENT; TYROSINE: PRESENT; LEUCINE: PRESENT. What is the suspected diagnosis?

Pattern being tested is how liver failure disrupts metabolism. When the liver isn’t functioning well, detoxifying ammonia to urea is impaired and aromatic amino acids build up, which can show up as amino acids (like tyrosine and leucine) in the urine. Here, ammonia is elevated and urea is low, indicating a compromised urea cycle and reduced ammonia clearance. That signal is a hallmark of chronic liver dysfunction rather than a simple, isolated injury. The liver enzymes are modestly raised, and bilirubin with bilirubin-related urine findings point to some cholestasis, which can accompany cirrhosis. In chronic liver disease, you often see a blend of hepatocellular injury and cholestasis, not the extreme spike of transaminases typical of acute hepatitis. Hepatic steatosis usually presents with milder or more isolated lipid-related changes and not the pronounced disturbances in ammonia handling and aromatic amino acid metabolism. Cholestatic disease alone would emphasize cholestasis markers more than the metabolic derangements seen here. Together, the combination of hyperammonemia with low urea, aromatic aminoaciduria, and mixed hepatocellular/cholestatic abnormalities fits chronic liver disease with hepatic failure, i.e., cirrhosis.

Pattern being tested is how liver failure disrupts metabolism. When the liver isn’t functioning well, detoxifying ammonia to urea is impaired and aromatic amino acids build up, which can show up as amino acids (like tyrosine and leucine) in the urine. Here, ammonia is elevated and urea is low, indicating a compromised urea cycle and reduced ammonia clearance. That signal is a hallmark of chronic liver dysfunction rather than a simple, isolated injury.

The liver enzymes are modestly raised, and bilirubin with bilirubin-related urine findings point to some cholestasis, which can accompany cirrhosis. In chronic liver disease, you often see a blend of hepatocellular injury and cholestasis, not the extreme spike of transaminases typical of acute hepatitis. Hepatic steatosis usually presents with milder or more isolated lipid-related changes and not the pronounced disturbances in ammonia handling and aromatic amino acid metabolism. Cholestatic disease alone would emphasize cholestasis markers more than the metabolic derangements seen here.

Together, the combination of hyperammonemia with low urea, aromatic aminoaciduria, and mixed hepatocellular/cholestatic abnormalities fits chronic liver disease with hepatic failure, i.e., cirrhosis.

More practice questions