A 50-year-old man with chronic alcohol abuse is found dead at home. Autopsy reveals a yellow, enlarged, greasy liver weighing 2,400 g. Histology shows large vacuoles displacing hepatocyte nuclei to the periphery. This pattern of hepatic steatosis is predominantly:
- A Microvesicular steatosis, caused by impaired mitochondrial β-oxidation of fatty acids
- B Glycogen accumulation (glycogenosis), caused by alcohol inhibiting glycogenolysis
- C Amyloid deposition with Congo red positivity
- D Macrovesicular steatosis, caused by excess triglyceride accumulation from impaired VLDL export and increased lipogenesis ✓
Explanation
Alcoholic macrovesicular steatosis results from multiple metabolic effects of ethanol: increased NADH/NAD+ ratio shifts metabolism toward lipogenesis and inhibits beta-oxidation; acetaldehyde impairs tubulin polymerization, blocking VLDL secretion from hepatocytes; increased peripheral lipolysis delivers excess fatty acids to the liver. The result is accumulation of large triglyceride vacuoles (macrovesicular steatosis) that displace hepatocyte nuclei to the periphery. Microvesicular steatosis with small fat droplets leaving the nucleus central is seen in mitochondrial disorders (e.g., acute fatty liver of pregnancy, Reye syndrome, valproate toxicity) and is more severe metabolically.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.