Types of fatty degeneration and its organ manifestation

1. Definition

• Fatty degeneration / steatosis (脂肪変性) = abnormal build-up and retention of triglycerides in cells, reflecting impaired synthesis/elimination of fat.
• Affects cells of fat metabolism: hepatocytes, myocardium, kidney.

2. Microscopy & Detection

• Fat vacuoles in cytoplasm push the nucleus to the periphery.
• Morphology: diffuse (toxic effect) vs spotty (hypoxic effect).
• Stains: Oil-red O, Sudan black.

3. Mechanism of Fat Accumulation

Normal flow: fatty acids → esterified to TAG → + apoprotein → lipoproteins exported. Disruption causes accumulation:

• Toxins (alcohol): ↓NAD → ↓fatty-acid oxidation.
• Hypoxia/anoxia: ↓fatty-acid oxidation.
• Protein malnutrition: ↓apoprotein → ↓lipoprotein export → ↑TAG.
• Diabetes/obesity: excess dietary fat / FA delivery.

4. Organ Manifestations

Hepatic steatosis (fatty liver)

• Alcoholic liver disease: ↓fat catabolism + ↓lipoprotein synthesis; sequence steatosis → hepatitis → cirrhosis.
• NAFLD: type 2 DM / obesity; insulin resistance → impaired FA oxidation, ↑FA uptake, ↓VLDL. Fat alone = NAFLD; fat + inflammation/damage = NASH.
• Morphology: enlarged (4–6 kg), soft, yellow liver, tense capsule (reversible) → fibrosis around central veins → cirrhosis (shrunken, fibrotic).

Nutmeg liver (hepar moschatum)

• Right-sided heart failure → venous congestion/stasis → centrilobular hepatocytes deoxygenated + fatty; periportal (better-oxygenated) cells spared → nutmeg pattern.

Tiger heart (degeneratio adiposa insularis)

• Yellow-brown subendocardial stripes of fat; from prolonged hypoxia (anemia, lung disease); usually reversible.

Diffuse myocardial fatty change

• Toxic causes: diphtheria toxin, chemotherapy (adriamycin).

💡 High-yield: Macrovesicular fat (single large vacuole, peripheral nucleus) = alcohol/NAFLD; microvesicular fat = severe mitochondrial dysfunction (Reye, acute fatty liver of pregnancy). Nutmeg liver = right heart failure congestion; tiger heart = chronic hypoxia.