Gangrenous necrosis Surgical term,usually applied to a limb which has lost its blood supply resulting in coagulative necrosis. Superadded bacterial infection causes liquefaction by bacterial enzymes,resulting in wet gangrene.

Caseous necrosis A distinct form of coagulative necrosis,most often seen in TB infection. Gross:cheesy appearance. Micro-obliterated tissue architecture,granulomatous reaction.

Fat necrosis Descriptive of focal areas of fat destruction. Classical eg is in pancreatitis,where lipases act on intra abdominal fat. Chalky white areas are seen in the fat,grossly.This is due to saponification(fatty acids combined with calcium salts). Micro:shadowy outlines of cells with basophilic calcium deposits,surrounded by an inflammatory reaction.

Apoptosis Literally means falling off. It is programmed cell death. Induced by a tightly regulated intracellular program. Cells destined to die,activate enzymes that degrade the cells’own nuclear DNA & nuclear and cytoplasmic protein. Plasma membrane remains intact. The dead cell is rapidly replaced by phagocytes before its contents leak out. Therefore does not elicit an inflammatory reaction. It can occur normally or in pathologic conditions.

Apoptosis in physiologic situations: During embryogenesis. Hormone-dependant involution in the adult. Cell deletion in proliferating cell populations. Death of inflammatory cells after the immune response. Elimination of potentially harmful self-reacting lymphocytes. Cell death induced by cytotoxic T-cells.

Mechanisms of apoptosis: - End result is activation of caspases - Too little apoptosis is abnormal - Too much apoptosis is abnormal Nematode Caenorhabtidis elegans is the perfect example of cell growth and death by apoptosis.

Apoptosis in pathologic conditions: Radiation. Cytotoxic cancer drugs. Certain viruses eg;viral hepatitis. Parenchymal atrophy,post ductal obstruction,in salivary gland,pancreas. Cell death in tumors.

Morphologic features of apoptosis: Cell shrinkage-cytoplasm is dense,with tightly packed organelles. Chromatin condensation-characteristic. Formation of cytoplasmic blebs and apoptotic bodies. Phagocytosis of apoptotic cells or cell bodies by macrophages.

Bio-chemical features of apoptosis Protein cleavage-with nuclear & cytoplasmic alterations. DNA breakdown-by endonucleases. Phagocytic recognition-occurs soon after cell death,without release of proinflammatory cellular components.

Mechanisms of apoptosis The extrinsic (death receptor-initiated pathway)-by engagement of cell surface death receptors. The intrinsic(mitochondrial pathway)-as a result of increased mitochondrial permeability.There is release of pro-apoptotic molecules into the cytoplasm. The execution phase-mediated by proteolytic cascade. Removal of dead cells-recruitment of phagocytes by secretion of soluble factors by dying cells.

Disorders with defective apoptosis and increased cell survival: Cancers,especially of breast,prostate and ovary. Auto-immune disorders.

Disorders with increased apoptosis and excessive cell death: Neuro-degenerative diseases. Ischaemic injury. Death of virus infected cells.

What you need to know: Consequences of cell injury. Reversible and irreversible injury. Free radicals. Types of cell death. Morphological patterns of necrosis. Apoptosis in various conditions.

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