A chronic alcoholic develops hepatomegaly. Liver biopsy shows large lipid vacuoles displacing the nucleus peripherally in centrilobular hepatocytes. The primary mechanism of hepatic steatosis in this patient is:
- A Increased peripheral lipolysis exceeding hepatic fatty acid oxidation and VLDL export ✓
- B Impaired lysosomal degradation of VLDL particles
- C Defective apolipoprotein B-100 synthesis alone
- D Block in conjugation of bilirubin in hepatocytes
Explanation
In alcoholic fatty liver, ethanol metabolism shifts the hepatic NADH/NAD+ ratio, increasing fatty acid synthesis while impairing fatty acid oxidation, and excess adipose tissue lipolysis delivers free fatty acids to the liver. The net effect is triglyceride accumulation exceeding VLDL assembly and export. Option C alone describes abetalipoproteinemia, which is not the mechanism in alcoholic steatosis. Option D is unrelated to steatosis.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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