M08.02.003 Cell death with an Inflammatory response

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

  1. Coagulative Necrosis
    1. Cause:
      • Ischemia or infarction → denaturation of cytoplasmic proteins → structural preservation but functional loss.
    2. Histology:
      • Outlines of dead cells remain (ghost cells)
      • Loss of nuclei but preserved architecture
    3. Common Sites:
      • Heart,
      • Kidney,
      • Liver (Not brain)
  2. Liquefactive Necrosis
    1. Cause:
      • Hydrolytic enzyme digestion of dead cells by neutrophils or lysosomes
    2. Features:
      • Tissue becomes soft and liquid
    3. Seen in
      • Brain infarction,
      • Abscesses, and
      • Pancreatitis
      • 🩺 Note: Liquefaction by leukocyte enzymes → suppuration; the resulting fluid = pus or purulent material
  3. Caseous Necrosis
    1. Cause:
      • Mycobacterium tuberculosis or fungal infection
      • Combination of coagulative + liquefactive necrosis
    2. Gross Appearance:
      • Soft, crumbly, “cheese-like” (caseous) material
    3. Histology:
      • Granulomatous inflammation with central necrosis
  4. Fat Necrosis
    1. Cause:
      • Lipase activity on triglycerides → fatty acids → binds calcium → saponification
    2. Gross Appearance:
      • Chalky white areas in fat tissue
    3. 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)
  5. Fibrinoid Necrosis
    1. Cause:
      • Immune complex deposition (type II or III hypersensitivity) or hypertension damages vessel walls.
    2. Histology:
      • Eosinophilic (pink), homogeneous material resembling fibrin within vessel walls.
    3. Common Sites:
      • Arterioles in autoimmune disease
      • Severe hypertension
  6. Gangrenous Necrosis
    1. Definition:
      • Clinical term describing necrosis of large tissue areas due to ischemia, often involving limbs or organs
    2. Types:
      • Dry Gangrene: Coagulative necrosis (ischemic, non-infective)
      • Wet Gangrene: Superimposed infection → liquefactive necrosis
    3. Sites:
      • Lower limbs,
      • Gallbladder,
      • GI tract,
      • Testes


Key Points to Remember

  1. Necrosis = Cell death + inflammation
  2. Coagulative → Ischemia
  3. Liquefactive → Enzyme digestion
  4. Caseous → TB / fungi
  5. Fat → Pancreatitis
  6. Fibrinoid → Immune injury
  7. Gangrenous → Ischemia ± infection

Learning Objective

By the end of this topic, the student should be able to:

  1. Differentiate between major morphologic types of necrosis.
  2. Correlate each type with its underlying cause and tissue distribution.
  3. Identify necrotic patterns in histologic or clinical contexts (e.g., infarction, abscess, pancreatitis, TB).

Activity:


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