Necrosis = Cell death in living tissue, typically accompanied by an inflammatory response. It represents irreversible cell injury and shows distinct morphologic patterns depending on the cause and tissue type.
Overview Table
| Type of Necrosis | Cause / Mechanism | Microscopic / Gross Features | Common Sites |
|---|---|---|---|
| Coagulative | Ischemia → Denaturation of structural & enzymatic proteins | – Preserved cell shape, lost nuclei – Firm texture |
Heart, liver, kidney (❌ not brain) |
| Liquefactive | Hydrolytic enzymes from neutrophils or lysosomes | – Complete tissue digestion – Liquefied tissue |
Brain infarcts, abscesses, pancreas |
| Caseous | Combination of coagulative + liquefactive necrosis (due to TB or fungi) | – Soft, friable, “cheese-like” appearance | Granulomatous inflammation (e.g., TB) |
| Fat | Lipases act on adipocytes → fatty acid + Ca²⁺ → saponification | – Chalky white deposits (calcium soaps) | Pancreas, fat around organs |
| Fibrinoid | Immune-mediated vascular damage (type II/III hypersensitivity) | – Eosinophilic, fibrin-like appearance in vessel walls | Arteries in autoimmune disease, vasculitis, and hypertension. |
| Gangrenous | Loss of blood supply (ischemia) → coagulative necrosis ± infection | – Dry gangrene: coagulative necrosis – Wet gangrene: liquefactive necrosis with infection |
Lower limbs, GI tract, gallbladder, testes |
- Coagulative Necrosis
- Cause:
- Ischemia or infarction → denaturation of cytoplasmic proteins → structural preservation but functional loss.
- Histology:
- Outlines of dead cells remain (ghost cells)
- Loss of nuclei but preserved architecture
- Common Sites:
- Heart,
- Kidney,
- Liver (Not brain)
- Cause:
- Liquefactive Necrosis
- Cause:
- Hydrolytic enzyme digestion of dead cells by neutrophils or lysosomes
- Features:
- Tissue becomes soft and liquid
- Seen in
- Brain infarction,
- Abscesses, and
- Pancreatitis
- 🩺 Note: Liquefaction by leukocyte enzymes → suppuration; the resulting fluid = pus or purulent material
- Cause:
- Caseous Necrosis
- Cause:
- Mycobacterium tuberculosis or fungal infection
- Combination of coagulative + liquefactive necrosis
- Gross Appearance:
- Soft, crumbly, “cheese-like” (caseous) material
- Histology:
- Granulomatous inflammation with central necrosis
- Cause:
- Fat Necrosis
- Cause:
- Lipase activity on triglycerides → fatty acids → binds calcium → saponification
- Gross Appearance:
- Chalky white areas in fat tissue
- Common Sites:
- Acute pancreatitis,
- Trauma to adipose tissue
- Bridge to Biochemistry: Fat cell damage → triglyceride breakdown → free fatty acids + calcium → calcium soaps (chalky white on gross exam)
- Cause:
- Fibrinoid Necrosis
- Cause:
- Immune complex deposition (type II or III hypersensitivity) or hypertension damages vessel walls.
- Histology:
- Eosinophilic (pink), homogeneous material resembling fibrin within vessel walls.
- Common Sites:
- Arterioles in autoimmune disease
- Severe hypertension
- Cause:
- Gangrenous Necrosis
- Definition:
- Clinical term describing necrosis of large tissue areas due to ischemia, often involving limbs or organs
- Types:
- Dry Gangrene: Coagulative necrosis (ischemic, non-infective)
- Wet Gangrene: Superimposed infection → liquefactive necrosis
- Sites:
- Lower limbs,
- Gallbladder,
- GI tract,
- Testes
- Definition:

Key Points to Remember
- Necrosis = Cell death + inflammation
- Coagulative → Ischemia
- Liquefactive → Enzyme digestion
- Caseous → TB / fungi
- Fat → Pancreatitis
- Fibrinoid → Immune injury
- Gangrenous → Ischemia ± infection
Learning Objective
By the end of this topic, the student should be able to:
- Differentiate between major morphologic types of necrosis.
- Correlate each type with its underlying cause and tissue distribution.
- Identify necrotic patterns in histologic or clinical contexts (e.g., infarction, abscess, pancreatitis, TB).









You must be logged in to post a comment.