Cell death is the ultimate result of irreversible injury. It may be:
a. Physiological –e.g. during embryogenesis
b. Therapeutic –e.g. cancer radiotherapy/chemotherapy
Cell death occurs by:
Normal programmed cell death without inflammation, e.g. during embryogenesis.
Premature cell death accompanied with inflammation during evolution of disease.
Autolysis is dissolution of dead cells by own enzymes.
Cell death is recognized by:
• Margination or progressive loss of nuclear chromatin
• Focal rupture of the nuclear membrane
• Breakdown of the plasma membrane.
• Development of flocculent densities in mitochondria.
Changes in the Nucleus
• Pyknosis: condensation of chromatin of chromatin and shrinkage of the nucleus.
• Karyorrhexis: fragmentation of the nucleus.
• Karyolysis: dissolution of the nucleus.
Changes in Cytoplasm Staining
• Positive staining with vital dyes such as Trepan blue which reflects abnormal membrane permeability.
• Opacification: denaturation of proteins lead to aggregation with resultant opacification of the cytoplasm.
• Eosinophilia: exposure of basic amino groups results in increased affinity for acidic dyes such as eosin.
• Release of K+ by dead cells.
• Release of enzymes into the blood. e. g. increased plasma levels of creatine kinases, lactic dehydrogenase and aspartate aminotransferase.
• Release of protein or protein breakdown products into the blood.
Degeneration autolysis of normal tissues occurring in dead body, generally distinguished from necrosis by being diffuse and not associated with inflammatory response.
Digestion of cell by enzymes released from lysosome; occurs after cell dies.
After cell death
Leakage of enzymes & protein into extracellular fluid occurs, which is useful in diagnosis:
– CK-NAC, troponin in MI
– ALT in hepatitis
– ALK PO4ase in biliary obstruction
Dead cells form myelin figures with accumulation of free fatty acids leading to calcifications.