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Cell Injury, Ischemia faster than hypoxia dec. O2 to cells, dec. ATP synth Cell Injury -early loss of PM selective perm., Irreversible-depletion of ATP-no return -severe mito. swelling -large densities in matrix -release cytochrome C ->death -Ca influx, esp w/ reperfusion -from inside mito, ER, across PM ->activate enzymes, further kill mito, dmg cytoskeleton->swell/rupture -Lysosomes leak enzymes -Cell contents into extracell. space ->enzyme presence is marker for dz Lethal Hit was inability to reverse mito dmg and huge membrane dysfunction Cell Death Necrosis - from irrev. dmg -2 processes-enzymatic digestion of cell, denaturation of proteins autolysis-enzs from self cell digest self heterolysis-enzs from leukocytes Most commonly coagulative, Necrosis - from irrev. dmg -2 processes-enzymatic digestion of cell, denaturation of proteins autolysis-enzs from self cell digest self heterolysis-enzs from leukocytes Most commonly coagulative Nuclear Changes-all from nonspecific DNA breakdown Karyolysis - pale nucleus fades away Pyknosis (also in apop) - small, dark nuc Karyorrhexis-fragmentation of pyk. nuc., Irreversible-depletion of ATP-no return -severe mito. swelling -large densities in matrix -release cytochrome C ->death -Ca influx, esp w/ reperfusion -from inside mito, ER, across PM ->activate enzymes, further kill mito, dmg cytoskeleton->swell/rupture -Lysosomes leak enzymes -Cell contents into extracell. space ->enzyme presence is marker for dz Lethal Hit was inability to reverse mito dmg and huge membrane dysfunction Cell Death Apoptosis-programmed cell death Physiologic Causes embryogenesis, homeostatic cell #, defense against virus/tumor, aging, immune response (lymphocytes), hormone-dependent involution Pathologic injurious stimuli-radiation, heat, anti-CA drugs - cause necrosis in large doses atrophy after obstruction, virally-dmged cells, Cell Injury -early loss of PM selective perm. Reversibility-longevity of O2 deprivation Irreversible-depletion of ATP-no return -severe mito. swelling -large densities in matrix -release cytochrome C ->death -Ca influx, esp w/ reperfusion -from inside mito, ER, across PM ->activate enzymes, further kill mito, dmg cytoskeleton->swell/rupture -Lysosomes leak enzymes -Cell contents into extracell. space ->enzyme presence is marker for dz Lethal Hit was inability to reverse mito dmg and huge membrane dysfunction, Apoptosis-programmed cell death Physiologic Causes embryogenesis, homeostatic cell #, defense against virus/tumor, aging, immune response (lymphocytes), hormone-dependent involution Pathologic injurious stimuli-radiation, heat, anti-CA drugs - cause necrosis in large doses atrophy after obstruction, virally-dmged cells Precipitating Factors 1. Loss of + signals from other cells Neuron - Growth Factors Lymphocytes - IL-2 2. Receipt of (-) signals inc. oxidants in cells DNA dmg from drugs, UV, radiation receptor-ligand interactions TNF-a, TNF-b, FasL to TNFreceptor, Cell Injury -early loss of PM selective perm. Reversibility-longevity of O2 deprivation Reversible -oxphos down->low ATP synth ->Na/K ATPase on PM down & increased catabolites ->cell swelling -reliance on glycolysis->low pH -ribosomes detach from ER-> protein production decreased -PM blebbing all reversed when O2 restored Light u-scope-hydropic swelling, fatty (esp in fat-metabolizing cells), Ischemia faster than hypoxia Reperfusion Injury (stroke, MI) Initially surviving cells- do not survive reperfusion -make O2 free radicals ->dmg mito->cytokines, adhesion molecules ->destruction, Cell Injury -early loss of PM selective perm. Chemical Injury CCl4-dry cleaning- -P-450 converts to CCl3 free radical ->auto-catalytic membrane lipid peroxidation -very fast dmg to ER-swelling dec. fat export->fatty liver Acetaminophen- -detox in liver via sulfation, glucuronidation -some coverted by P-450 to toxic metabolite -Detox via GSH, which can be saturated -High tylenol doses->toxin buildup->massive hep'cyte necrosis (lipid peroxidation), Apoptosis-programmed cell death Physiologic Causes embryogenesis, homeostatic cell #, defense against virus/tumor, aging, immune response (lymphocytes), hormone-dependent involution Pathologic injurious stimuli-radiation, heat, anti-CA drugs - cause necrosis in large doses atrophy after obstruction, virally-dmged cells Sequence of Events Cell Shrinks, Mito releases Cytochrome c Blebbing/budding on PM surface, Chromatin degrades, Nucleus breaks into fragments, Phospholipids to membrane surface (for phags) Phagocytes secrete cytokines->no inflamm.