A pathologist notes 'coagulative necrosis' in infarcted kidney tissue. The cell outlines are preserved for days despite cell death. This is explained by which mechanism that is ABSENT in the CNS (explaining why brain infarcts show liquefactive necrosis)?

• A Abundance of myelin in renal tubular cells
• B Protein denaturation by hypoxia that also inhibits hydrolytic lysosomal enzymes ✓
• C Higher collagen content in kidney stroma
• D Greater resistance of renal cells to ischemia

Explanation

In coagulative necrosis (as in most solid organ infarcts), the same process that denatures structural proteins also denatures hydrolytic lysosomal enzymes, preventing autolysis and preserving the 'ghost' cell outlines. In the brain, the high lipid content and abundance of hydrolytic enzymes in microglial/macrophage-like cells overwhelm protein denaturation, resulting in liquefaction (liquefactive necrosis). The lipid-rich environment does not coagulate well. This explains the organ-specific pattern: solid organs → coagulative; brain → liquefactive; lung TB → caseous (combination of coagulation + lipid content from mycobacteria).

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

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Written and medically reviewed by the StethoPrep medical team.