Necrosis

Necrosis is cell death resulting from irreversible injury — ischemia (loss of blood supply), infection, toxins, or physical trauma. Injured cells swell, their membranes rupture, and their contents spill into the surrounding tissue, provoking an inflammatory response. This distinguishes necrosis from apoptosis, the orderly, energy-dependent form of programmed cell death in which cells shrink and are cleared without inflammation.

Under the microscope, necrotic cells show characteristic nuclear changes: pyknosis (nuclear shrinkage and condensation), karyorrhexis (fragmentation), and karyolysis (dissolution). Pathologists also classify necrosis by its gross and microscopic pattern, and each pattern points to a cause and location.

The major patterns are: coagulative necrosis, in which tissue architecture is preserved for days — typical of infarcts in the heart, kidney, and other solid organs; liquefactive necrosis, in which enzymes digest tissue into fluid — seen in brain infarcts and abscesses; caseous necrosis, the cheese-like pattern of tuberculosis granulomas; fat necrosis, seen in acute pancreatitis when lipases split fat into fatty acids that saponify with calcium; fibrinoid necrosis of vessel walls in vasculitis and malignant hypertension; and gangrenous necrosis of ischemic limbs, which is termed wet when infection is superimposed.

The USMLE Step 1 exam tests necrosis in general pathology — matching each pattern to its classic setting and recognizing the microscopic changes. The NPTE and NPTE-PTA address necrotic tissue in the integumentary system, where recognizing nonviable tissue in wounds guides physical therapy wound management.