Skip to main content
Botany 3% exam weight

Cell Injury

Part of the INI CET (AIIMS PG) study roadmap. Botany topic pathol-003 of Botany.

→ See in Roadmap Build 1-Month Plan

Cell Injury and Adaptation is a foundational pathology topic for INI CET (AIIMS PG).

Key Definitions:

  • Cell injury: Any structural or functional alteration in a cell caused by stress
  • Adaptation: Reversible changes allowing cells to cope with stress
  • Atrophy: Decrease in cell size — from disuse, loss of trophic signals, or aging
  • Hypertrophy: Increase in cell size — from increased workload (e.g., cardiac muscle in hypertension)
  • Hyperplasia: Increase in cell number — from hormonal stimulation (e.g., endometrial hyperplasia)
  • Metaplasia: Replacement of one mature cell type with another — e.g., squamous metaplasia in smoker’s airway

Causes of Cell Injury:

  1. Hypoxia (most common cause) — reduced oxygen delivery
  2. Physical agents — trauma, burns, radiation
  3. Chemical agents — drugs, toxins, poisons
  4. Biological agents — bacteria, viruses, parasites
  5. Nutritional imbalances — protein-calorie deficiency, vitamin deficiencies
  6. Genetic defects — inborn errors of metabolism, chromosomal abnormalities
  7. Immunologic reactions — autoimmune diseases, allergic reactions

Reversible vs Irreversible Injury:

  • Reversible: Cell swelling, fatty change, cellular blebbing — can return to normal
  • Irreversible: Mitochondrial dysfunction, calcium influx, nuclear changes (pyknosis, karyolysis, karyorrhexis) — leads to cell death

⚡ Exam Tip for INI CET (AIIMS PG): Remember: Hypoxia is the most common cause of cell injury. The sequence is: Adapt → Injure (reversible) → Die (irreversible).

Types of Cell Death:

  • Necrosis: Uncontrolled cell death — requires plasma membrane disruption
    • Coagulative necrosis (ischemic organs — heart, kidney)
    • Liquefactive necrosis (brain abscess)
    • Caseous necrosis (tuberculosis)
    • Fat necrosis (pancreatitis — saponification)
    • Fibrinoid necrosis (malignant hypertension, vasculitis)
  • Apoptosis: Programmed cell death — requires ATP; does not cause inflammation
    • Physiological: Embryogenesis, hormonal involution, immune regulation
    • Pathological: DNA damage, viral infections, hormone withdrawal

Key Difference: Necrosis = swelling + inflammation + membrane rupture. Apoptosis = shrinkage + nuclear fragmentation + no inflammation.