IMED2004 Lecture Notes - Lecture 34: Lung Transplantation, Ischemia, Metaplasia
26 Mar 2020
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Document Summary
Possible outcomes of cellular stress or injury: non-lethal, reversible injury (short term/acute or mild, cell-swelling/membrane damage/organelle dysfunction- return to normal state, non-lethal stress (long-term/chronic) adaptation, hyperplasia, hypertrophy, atrophy, metaplasia, metabolic derangement. Intracellular accumulation (e. g. calcification: lethal or irreversible injury cell death, necrosis, apoptosis, autophagy, causes of cell injury, oxygen deprivation, hypoxia. Ischaemia: physical agents, trauma, heat, cold, pressure, radiation, electric shock, chemical agents, drugs, toxins. Immunologic reactions: autoimmunity, excessive/uncontrolled inflammation, genetic derangements, nutritional imbalances, deficiency, excess. Increased demand, increased stimulation (e. g. by growth factors, hormones) Cumulative sub lethal injury over long life span: reversible cell injury: Cellular ageing: cell injury impedes function of energy dependent ion pumps in the plasma membrane. +/- vacuolar change, membrane blebs, increased eosinophilia of cytoplasm: altered cellular metabolism. Intracellular accumulation: even if changes have been reversed, some damaged cells/tissues may accumulate by-products: Proteins (e. g. neurofibrillary tangles in ad, amyloid) Endogenous pigment (melanin in skin/lymph nodes, haemosiderin from old blood)
