Fat, caseous and fibrinoid necrosis and its organ manifestation

1. Fat Necrosis (脂肪壊死)

• Necrosis where digestive enzymes (lipase) act on fat.
• Associated with acute pancreatitis and bile-duct obstruction (activates pancreatic enzymes).

Pathogenesis

1. Release of activated pancreatic enzymes.
2. Lipase digests membranes → frees fatty acids from triglycerides.
3. Free fatty acids + Ca²⁺ → chalky white “soap” deposits = saponification (a form of dystrophic calcification — normal serum Ca²⁺/PO₄).
4. Common-bile-duct stone → bile refluxes → enzyme activation → pancreatic autodigestion.
5. Alcohol promotes it (↑enzyme production + acinar obstruction → leakage).

Morphology & Clinical

• Lipase necrosis of fat, proteolytic destruction of pancreatic parenchyma, vessel destruction → haemorrhage.
• Clinical: acute abdominal pain, ↑amylase/lipase; systemic enzyme release → DIC, ARDS.

2. Caseous Necrosis (乾酪壊死)

• Combination of coagulative + liquefactive; classically tuberculosis (M. tuberculosis), also some fungi.
• Cell outlines lost (like liquefactive) but protein coagulation present → yellow-white, cheese-like.
• Surrounded by inflammatory cells → caseating granuloma:
  • T-cells, macrophages, epithelioid cells, Langhans giant cells (fused epithelioid cells; nuclei in peripheral horseshoe pattern).
• Mainly lung (hilar lymph nodes); also kidney, pancreas.

3. Fibrinoid Necrosis (線維素様壊死)

• “Fibrin-like”; from vascular damage (often autoimmune) + exudation of plasma proteins (fibrin).
• Endothelial lysis → leaky vessels → antigen–antibody complexes + fibrin deposit in vessel wall.
• Amorphous, bright-pink (acidophilic) appearance on H&E.
• Settings: malignant hypertension, vasculitis (e.g. polyarteritis nodosa), pre-eclampsia (placental vessels).

💡 High-yield: Fat necrosis → pancreatitis (saponification, chalky white). Caseous necrosis → TB (caseating granuloma, Langhans giant cells). Fibrinoid necrosis → immune-mediated vascular damage (bright pink vessel walls).