1.4 - Patterns of Tissue Necrosis

Once enough neighboring cells die, we can recognize patterns of tissue necrosis. The pattern often provides a clue to the underlying causes. cell necrosis -> tissue necrosis -> organ dysfunction

coagulative necrosis

• texture — firm

• result of — cell death with architecture preservation

  • can recognize outlines of where cells used to be microscopically, but nuclei are gone

  • ischemia denatures structural proteins and digestive enzymes, so architecture remains

• clinical scenarios — infarcted organs

  • EXCEPTION — CNS (brain)

liquefactive necrosis

• texture — liquid

• result of — digestion of dead cells to a liquid

• clinical scenarios —

  • ischemic necrosis of CNS

  • infections (pus) → bacterial/fungal infections recruit white blood cells that digest tissue to form pus

caseous necrosis

• texture — cheese-like

• result of — granulomatous inflammation without architecture preservation

• clinical scenario — tuberculosis, deep fungal infections

fat necrosis

• texture — chalky

• result of — enzymatic digestion of fats with saponification

  • released fatty acids bind calcium to form calcium soaps

• clinical scenario — acute pancreatitis

  • damaged pancreas releases lipase that digests nearby fats and cause saponification

gangrenous necrosis

• texture — no distinctive pattern histologically

  • clinical term that refers to ischemic necrosis of a lower limb

  • multiple layers of coagulative necrosis

• wet gangrene — purulent/liquified material

  • coagulative necrosis + bacterial infection → enzymatic liquefaction → wet gangrene

  • clinical scenario — diabetic patient with peripheral arterial disease

fibrinoid necrosis

• texture — no gross appearance; purely microscopic

• result of — antigen-antibody complexes deposited in arterial walls

  • pink fibrin-like material leaks out of vessels

• clinical scenario — immunologically mediated diseases

  • polyarteritis nodosa

tissue-specific markers of necrosis

cell membrane breaks → intracellular proteins leak → proteins enter blood → serum test detects them (diagnostic or quantitative)

• example — cardiac troponin I or troponin T released following myocardial infarction

  • highly cardiac-specific and rises within 1-3 hours after myocardial injury

  • central to diagnosing MI and interpreted using serial changes over time