Cell injury

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Cell Injury: High-Yield Pathology Essentials

1. Reversible vs. Irreversible Injury

Feature Reversible Irreversible (Necrosis/Apoptosis)
Mitochondria Swelling Large amorphous densities
Cell Membrane Blebbing Rupture (Necrosis)
Nucleus Clumping of chromatin Pyknosis, Karyorrhexis, Karyolysis

2. Mechanisms of Cell Injury

  • ATP Depletion: The most common cause of cell injury (hypoxia/ischemia). Leads to failure of Na^+/K^+ pump → cell swelling.
  • Mitochondrial Damage: Loss of membrane potential → failure of oxidative phosphorylation → Cytochrome C release → Apoptosis.
  • Calcium Influx: Activates intracellular enzymes (proteases, endonucleases, phospholipases) that damage cell structures.
  • Free Radical Injury: O_2-derived radicals (ROS). Handled by enzymes: Superoxide dismutase, Glutathione peroxidase, Catalase.

3. Patterns of Necrosis

  • Coagulative: Infarcts in solid organs (except the brain). Architecture preserved.
  • Liquefactive: Brain infarcts; bacterial/fungal infections. Digestion of dead cells.
  • Caseous: TB. “Cheese-like” appearance; combination of coagulative and liquefactive.
  • Fat Necrosis: Acute pancreatitis (saponification).
  • Fibrinoid: Immune-mediated vasculitis (antigen-antibody complex deposition).

4. High-Yield Exam Pearls

  • Point of No Return: Irreversibility is marked by severe mitochondrial damage and profound membrane damage.
  • Apoptosis vs. Necrosis: Apoptosis = cell shrinkage, no inflammation, ATP-dependent. Necrosis = cell swelling, inflammation, enzyme-mediated digestion.
  • Free Radicals: Know the Fenton reaction (Fe^{2+} + H_2O_2 \rightarrow Fe^{3+} + OH^\bullet + OH^-) as a common source of hydroxyl radicals.