Lecture DetailsEdit

Anthony Longano; Week 10 MED1011; Pathology

Lecture ContentEdit

Cell injury can be from ischaemia, hypoxia, physical agents (mechanical trauma, extreme temperature, electricity), chemical agents, infectious agents, immunologic reactions, genetic derangement. Four intracellular mechanisms commonly lead to cell death: maintenance of cell membrane integrity (failure of membrane ion pumps, cytotoxic cytokines, complement activation); aerobic respiration and production of ATP (impairment of cellular respiration), interruption of protein synthesis, DNA damage/loss.

Morphological changes can be light after ultrastructural alterations. Lethal cell damage can take some time to show compared to reversible damage (cell swelling can occur in minutes, necrotic myocytes 10-12 hours after ischaemia). General cellular changes in necrosis are cell swelling, mitochondrial and lysosomal swelling, rupture of lysosomes, nuclear damage (pyknosis, karyolysis, karryorrhexis), inflammatory response.

Apoptosis occurs in ageing, homeostatic mechanism to maintain cell population in tissues, defence mechanism in immune reactions, damage by disease, aging. Looks like cell shrinkage, chromatin condensation, formation of apoptotic blebs and bodies, phagocytosis of apoptotic cells/bodies by macrophages. Involves single cells and small clusters of cells, and elicits minimal inflammation.

Major regulating pathways of apoptosis are 1. Fas-Fas ligand binding (membrane bound Fas binds to Fas on apoptotic T cells), 2. Bcl-2 protein activation (Bcl-2 suppresses apoptosis, prevents increase in mitochondrial permeability).

Necrosis can be coagulative, colliquative (liquefactive), caseous, gangrene, fibrinoid, fat necrosis. Coagulative is the most common, devitalised tissue retains its architechture, macroscopically there is a region of pallor that gradually becomes softer, and there may be secondary haemmorhage. There may be no changes in the first few hours which leads to loss of nuclear staining, preservation of cell architecture, inflammatory response, phagocytosis and repair/regeneration.

Colliquative (liquefactive) necrosis is marked by liquefaction of tissue, can occur in brain due to a lack of supporting stroma and the site of necrosis is eventually marked by a cavity. Caseous necrosis is where the dead tissue lacks any structure, has amorphous eisonophilic area containing nuclear debris, is typically caused by TB infection. Gangrene is putrefaction of tissue usually caused by bacterial infection complicating necrosis. Fibrinoid necrosis is usually fibrin deposit in damaged blood vessel wall, indicator of vasculitis. Fat necrosis is release of intracellular fat which creates an inflammatory response and eventually fibrosis. Can be caused by trauma or enzymatic lysis of fat (lipase). May result in a mass being formed.


Underwood 102-108Edit

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