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Pathology ` PATHOLOGY—CeLLuLAr InjurY Pathology ` PATHOLOGY—CeLLuLAr InjurY SECtIoN II 209
Necrosis Exogenous injury plasma membrane damage cell undergoes enzymatic degradation and protein
denaturation, intracellular components leak local inflammatory reaction (unlike apoptosis).
TYPe Seen In Due TO HISTOLOGY
Coagulative Ischemia/infarcts in Ischemia or infarction; Preserved cellular architecture (cell
most tissues (except injury denatures outlines seen), but nuclei disappear;
brain) enzymes proteolysis cytoplasmic binding of eosin stain
blocked ( eosinophilia; red/pink color) A
Liquefactive Bacterial abscesses, Neutrophils release Early: cellular debris and macrophages
brain infarcts lysosomal enzymes that Late: cystic spaces and cavitation (brain)
digest the tissue B Neutrophils and cell debris seen with
bacterial infection
Caseous TB, systemic fungi Macrophages wall off the Fragmented cells and debris surrounded
(eg, Histoplasma infecting microorganism by lymphocytes and macrophages
capsulatum), Nocardia granular debris C (granuloma)
Fat Enzymatic: acute Damaged pancreatic Outlines of dead fat cells without
pancreatitis cells release lipase, peripheral nuclei; saponification of fat
2+
(saponification of which breaks down (combined with Ca ) appears dark blue
peripancreatic fat) triglycerides; liberated on H&E stain D
Nonenzymatic: fatty acids bind calcium
traumatic (eg, injury to saponification (chalky-
breast tissue) white appearance)
Fibrinoid Immune vascular Immune complex Vessel walls are thick and pink E
reactions (eg, PAN) deposition (type III
Nonimmune hypersensitivity reaction)
vascular reactions and/or plasma protein
(eg, hypertensive (eg, fibrin) leakage from
emergency, damaged vessel
preeclampsia)
Gangrenous Distal extremity and Dry: ischemia F Coagulative
GI tract, after chronic Wet: superinfection Liquefactive superimposed on coagulative
ischemia
A B C
D E F
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