MLT GlobeChemistry: Liver function & bilirubin – page 4
84 Chemistry MCQs on Liver function & bilirubin with answers and explanations.
A pregnant woman at 32 weeks has severe itching of the palms and soles without a rash; ALT is mildly raised. Which test best supports the diagnosis?
Intrahepatic cholestasis of pregnancy is diagnosed by raised serum bile acids (typically 10 µmol/L or more); high values increase fetal risk. Itching may appear before other liver tests change.
A young woman has raised aminotransferases, high serum IgG, positive anti-smooth muscle antibodies and negative viral hepatitis markers. The most likely diagnosis is:
Type 1 autoimmune hepatitis shows a hepatitic enzyme pattern with raised IgG and ANA and/or anti-smooth muscle antibodies. Primary biliary cholangitis gives a cholestatic pattern with antimitochondrial antibodies.
A man with ulcerative colitis has raised ALP and GGT with mildly raised ALT. Cholangiography shows multiple strictures giving a 'beaded' bile duct appearance. The most likely diagnosis is:
Primary sclerosing cholangitis causes fibrosing strictures of intra- and extrahepatic ducts and is strongly linked with inflammatory bowel disease, especially ulcerative colitis.
A transcutaneous bilirubin reading in a jaundiced newborn is close to the phototherapy threshold. What is the correct next step?
Transcutaneous meters are screening tools and are less accurate at high levels, in dark skin and during phototherapy. Treatment decisions near thresholds should use total serum bilirubin.
About 80% of the bilirubin produced each day comes from:
An adult produces about 250–350 mg (4–6 mmol) bilirubin daily, mostly from senescent red cells destroyed by macrophages. The rest comes from ineffective erythropoiesis and other heme proteins.
Calculate the APRI score: AST 80 U/L (upper limit 40 U/L), platelets 100 × 10⁹/L. [APRI = (AST ÷ AST ULN) ÷ platelets (10⁹/L) × 100]
APRI = (80 ÷ 40) ÷ 100 × 100 = 2.0. In chronic viral hepatitis, an APRI above 2.0 suggests cirrhosis (WHO).
The original MELD score, used to prioritize liver transplantation, is calculated from:
MELD uses serum bilirubin, INR and creatinine; later versions add sodium (MELD-Na) and albumin and sex (MELD 3.0). Albumin and ascites are parts of the Child–Pugh score.
A patient with fulminant liver failure becomes hypoglycemic. The main cause is:
The liver maintains fasting glucose through glycogenolysis and gluconeogenesis. Massive hepatocyte loss removes both; reduced hepatic insulin clearance adds to the problem. Glucose must be checked often.
Acute liver failure is defined as severe liver injury with an INR of 1.5 or more plus which finding, in a patient without pre-existing cirrhosis and with illness under 26 weeks?
Acute liver failure requires coagulopathy (INR ≥1.5) with any degree of encephalopathy. Very high ALT alone indicates severe injury but not liver failure.
Serum albumin is 2.8 g/dL (28 g/L) and ascitic fluid albumin is 1.2 g/dL (12 g/L), collected the same day. What is the serum–ascites albumin gradient (SAAG) and its meaning?
SAAG = 2.8 − 1.2 = 1.6 g/dL. A gradient of 1.1 g/dL (11 g/L) or more indicates portal hypertension, as in cirrhosis; a lower gradient suggests peritoneal causes.
A patient with epilepsy on valproate becomes drowsy and confused. Plasma ammonia is high while aminotransferases, bilirubin and INR are normal. The most likely cause is:
Valproate can inhibit the urea cycle (via reduced N-acetylglutamate) and cause hyperammonemic encephalopathy without liver damage. Normal INR and enzymes argue against liver failure.
A jaundiced patient has total bilirubin 4.0 mg/dL (68 µmol/L) and direct bilirubin 3.2 mg/dL (55 µmol/L). The hyperbilirubinemia is mainly:
Direct (conjugated) bilirubin makes up 80% of the total, so this is a conjugated hyperbilirubinemia, which points to hepatic or post-hepatic (obstructive) causes rather than hemolysis.
A man with long-term heavy alcohol use has low serum albumin and a prolonged prothrombin time that does not correct with vitamin K. This best reflects:
Low albumin and a PT not corrected by vitamin K indicate that the liver cannot make proteins and clotting factors, as in cirrhosis. In obstruction, PT usually corrects with vitamin K.
An adult has a raised alkaline phosphatase. Which additional result best supports a liver (rather than bone) source?
GGT rises in hepatobiliary disease but not in bone disease. A raised ALP with raised GGT therefore suggests a hepatobiliary source; ALP with normal GGT favours bone.
After surgical relief of a bile duct obstruction, a patient's serum direct bilirubin stays raised for weeks despite normal bile flow. The best explanation is:
Delta bilirubin is conjugated bilirubin covalently linked to albumin, so it has albumin's long half-life (about 2–3 weeks) and is not excreted in urine. It reacts in the direct bilirubin assay.
Which inherited condition causes mild conjugated hyperbilirubinemia with a normal-looking liver on biopsy (no pigment)?
Rotor syndrome gives benign conjugated hyperbilirubinemia without hepatic pigment. Gilbert and Crigler–Najjar are unconjugated disorders.
Direct spectrophotometric (bilirubinometer) measurement of neonatal bilirubin reads absorbance at 454 nm and 540 nm. The 540 nm reading is used to:
Bilirubin absorbs strongly at 454 nm, but hemoglobin also absorbs there; measuring at 540 nm allows correction for hemoglobin. This method suits neonates, whose serum lacks carotenoids that would interfere.
A 3-day-old boy has lethargy and ammonia above 300 µmol/L (510 µg/dL), low plasma citrulline and high urine orotic acid. The most likely disorder is:
OTC deficiency blocks carbamoyl phosphate use, which spills into pyrimidine synthesis and raises orotic acid; citrulline is low. CPS deficiency also has low citrulline but low or normal orotic acid.
Calculate the FIB-4 index: age 50 years, AST 40 U/L, ALT 25 U/L, platelets 200 × 10⁹/L. [FIB-4 = (age × AST) ÷ (platelets × √ALT)]
(50 × 40) ÷ (200 × √25) = 2000 ÷ (200 × 5) = 2000 ÷ 1000 = 2.0. Forgetting the square root of ALT gives 0.4, not 2.0.
A markedly icteric sample (total bilirubin 20 mg/dL, 342 µmol/L) is tested for cholesterol with a peroxidase (Trinder) end-point method. The expected bias is:
Bilirubin reacts with hydrogen peroxide and competes in the peroxidase step, causing negative interference in Trinder-type assays such as cholesterol and enzymatic creatinine.