Liquefactive necrosis, rather than coagulative necrosis, characteristically occurs in brain infarcts primarily because:

• A The brain has a high iron content that catalyzes Fenton reactions
• B Neurons lack heat shock proteins protecting against proteolytic digestion
• C Abundant lysosomal enzymes from microglia and recruited leukocytes digest the necrotic tissue ✓
• D Cerebral blood flow during ischemia is never completely stopped, allowing ongoing perfusion of enzymes

Explanation

Brain tissue undergoes liquefactive necrosis because microglial cells (brain macrophages) and recruited neutrophils release abundant hydrolytic enzymes and proteases that rapidly digest the necrotic tissue, converting it to a liquid cystic cavity. Additionally, the brain's high lipid content makes it susceptible to enzymatic digestion. This contrasts with coagulative necrosis where structural proteins are preserved and the architectural 'ghost' outline of cells persists.

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

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Written and medically reviewed by the StethoPrep medical team.