Pathology · Cell Injury, Death and Adaptations (Apoptosis, Necrosis, Free Radicals)

A 45-year-old man with chronic alcohol use presents with hepatomegaly. Liver biopsy shows large fat vacuoles displacing the nucleus to the periphery. In alcoholic fatty liver, which mechanism is most directly responsible for triglyceride accumulation in hepatocytes?

  • A Increased lipolysis in peripheral adipose tissue
  • B Decreased synthesis of apolipoproteins due to rough ER damage
  • C Impaired mitochondrial beta-oxidation of fatty acids
  • D Defective conjugation of lipids with transport proteins
Correct answer: C. Impaired mitochondrial beta-oxidation of fatty acids

Explanation

In alcoholic steatosis, ethanol metabolism increases NADH/NAD+ ratio, which impairs mitochondrial beta-oxidation of fatty acids, causing lipid accumulation. While alcohol also increases lipolysis and fatty acid synthesis, impaired beta-oxidation is the predominant mechanism. Apolipoprotein synthesis defect is characteristic of carbon tetrachloride toxicity, not alcohol.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.

Sponsored

Want to test yourself?

Create a free account for timed mock tests, mistake tracking, and FSRS spaced-repetition revision across 43,000+ MCQs.

Start free → Log in

More Cell Injury, Death and Adaptations (Apoptosis, Necrosis, Free Radicals) MCQs

See all Cell Injury, Death and Adaptations (Apoptosis, Necrosis, Free Radicals) MCQs →