U01.04.004 Necrosis

Learning Objective

By the end of this lesson, the learner will be able to identify different types of necrosis, describe their mechanisms, recognize clinical causes, and correlate them with characteristic microscopic and gross features.


Necrosis

Necrosis is a pathologic cell death due to external injury, causing:

  • Plasma membrane disruption
  • Leakage of intracellular contents
  • Enzymatic digestion and denaturation
  • Local inflammatory reaction (unlike apoptosis)

Necrosis triggers neutrophils and macrophages due to released intracellular molecules acting as DAMPs (damage-associated molecular patterns).


Types of Necrosis


1. Coagulative Necrosis

Seen In

  • Most ischemic/infarcted tissues
  • Exception: brain

Mechanism

  • Injury → protein denaturation → enzymes are also denatured → proteolysis is inhibited

Histologic Appearance

  • Preserved cell outlines & architecture
  • Loss of nuclei
  • Increased eosinophilia (bright pink cytoplasm)

Typical Example

  • Myocardial infarction
  • Renal infarction

2. Liquefactive Necrosis

Seen In

  • Bacterial infections (abscesses)
  • CNS infarcts

Mechanism

  • Neutrophils release lysosomal enzymes → digestion and liquefaction of tissue

Histology

  • Early: necrotic debris + neutrophils
  • Later: cystic spaces, cavitation, microglial phagocytosis in CNS

Examples

  • Brain infarction
  • Lung abscess
  • Liver abscess

3. Caseous Necrosis

Seen In

  • Tuberculosis
  • Systemic fungal infections
    (e.g., Histoplasma capsulatum)
  • Nocardia infections

Mechanism

  • Macrophages wall off organisms → granuloma formation

Histology

  • Fragmented, granular cells
  • Surrounded by macrophages, epithelioid histiocytes, and lymphocytes
  • “Cheesy” gross appearance

Gross Finding

  • Soft, crumbly, white-yellow necrosis

4. Fat Necrosis

Two forms:

A. Enzymatic Fat Necrosis

Seen in:

  • Acute pancreatitis
    → pancreatic lipase escapes into the peripancreatic fat

Mechanism

  • Triglycerides → free fatty acids
    Free fatty acids + Ca²⁺ → saponification (soap formation)

Histology

  • Chalky-white deposits
  • Blue saponification deposits on H&E

B. Traumatic Fat Necrosis

Seen with:

  • Breast trauma

Produces:

  • Rupture of fat cells
  • Inflammatory reaction

5. Fibrinoid Necrosis

Seen In

  • Immune-mediated vasculitis
    e.g., Polyarteritis nodosa
  • Severe hypertension
  • Preeclampsia
  • Malignant hypertension

Mechanism

  • Immune complexes + fibrin leak → vessel wall degeneration

Histology

  • Eosinophilic, protein-rich material in the vessel wall (“fibrin-like”)

6. Gangrenous Necrosis

Occurs in the distal extremities or bowel after chronic ischemia.

Two Subtypes


A. Dry Gangrene

  • Due to ischemia alone
  • Coagulative necrosis pattern
  • Dry, shrunken, black tissue

B. Wet Gangrene

  • When an infection superimposes
  • Liquefactive necrosis over coagulative
  • Swollen, foul-smelling, fluid-filled tissue

Activity


Summary Table of Necrosis Types

Type Typical Cause Key Feature Appearance
Coagulative Ischemia (except brain) Proteins denature → architecture preserved Red/pink eosinophilic cells without nuclei
Liquefactive Bacterial abscess, CNS infarct Enzyme digestion of tissue Cystic cavity, pus
Caseous TB, fungi Granuloma formation Soft “cheesy” debris
Fat Pancreatitis, trauma Saponification Chalky deposits
Fibrinoid Vasculitides, HTN disorders Immune complex deposition Pink fibrin-like material in vessel walls
Gangrenous Chronic ischemia (limbs, GI) Dry = coagulative; Wet = infectious liquefactive Black, necrotic tissue

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