Cell Injury Overview and Types

Cell Injury Overview

• Cell injury is the damage to cells, resulting in various morphological alterations.
• Injury can be reversible or irreversible.
• Reversible injury leads to degeneration, while irreversible injury results in necrosis or apoptosis.

Types of Cell Injury

• Hypoxia: Insufficient oxygen supply, caused by ischemia (poor blood flow) or inadequate oxygenation/anemia.
• Physical agents: Trauma, heat, cold, radiation, electric shock.
• Chemical agents and drugs: Therapeutic drugs, poisons, environmental pollutants, alcohol.
• Infectious agents: Viruses, bacteria, fungi, parasites.
• Immunologic reactions: Autoimmune diseases.
• Genetic derangements.
• Nutritional imbalances: Protein-calorie deficiency, vitamin deficiencies or excesses.

Reversible Cell Injury (Degeneration)

• Cloudy swelling (Hydropic change): Earliest change, characterized by water accumulation within cells, particularly seen in liver and myocardial cells.
• Hydropic (ballooning or vacuolar change): Similar to cloudy swelling, but more severe and advanced, with increased water accumulation causing swelling and vacuole formation within the cytoplasm.
• Fatty change: Occurs in hypoxic or toxic injury, affecting cells involved in fat metabolism like liver and myocardial cells. Lipids accumulate as empty vacuoles in the cytoplasm.

Irreversible Cell Injury (Necrosis)

• Necrosis: Death of a group of cells, causing inflammation in surrounding tissues.
• Morphological Changes:
  • Nuclear changes:
    • Pyknosis: Nuclear shrinkage.
    • Karyorrhexis: Fragmentation of the nucleus.
    • Karyolysis: Disappearance of the nucleus's basophilia (staining).
  • Cytoplasmic changes: Loss of cell border and eventually structural loss of the necrotic tissue.
• Types of Necrosis:
  • Coagulative: Resulting from ischemia (insufficient blood supply); necrotic tissue appears firm and dry, missing cellular detail under microscopy.
  • Liquefactive: Necrotic tissue appears liquid due to high lipid and fluid content (like in CNS infarction), or enzymatic lysis (like in pyogenic abscesses).
  • Caseous: Begins as coagulative necrosis, then proceeds to slow partial liquefaction; necrotic tissue appears semi-solid, yellowish, and cheese-like (casein), often seen in tuberculosis.
  • Fat necrosis: Two types:
    • Traumatic: Trauma to adipose tissue releasing intracellular fat triggers an inflammatory response, leading to fibrosis. Commonly observed in the breast.
    • Enzymatic: Leakage of pancreatic lipase in acute pancreatitis, causing fat breakdown; glycerol is absorbed, fatty acids combine with Ca+, resulting in white deposits and fibrosis.

Irreversible Cell Injury (Apoptosis)

• Apoptosis: Programmed cell death, energy-dependent.
• Morphological changes:
  • Cell shrinkage with intact plasma membrane.
  • Nucleus shrinkage and fragmentation.
  • Formation of apoptotic bodies (membrane-bound fragments of the cell).
  • Removal of apoptotic cells and bodies by macrophages.
  • No inflammation in surrounding tissues.
• Causes:
  • Physiological: Normal cell turnover, embryonic development, endocrine-dependent tissue involution (e.g., menstrual cycle).
  • Pathological: Radiation injury, cell death by cytotoxic lymphocytes, liver cells in viral hepatitis, pathological atrophy.