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35 Cards in this Set
- Front
- Back
necrosis
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gross and microscopic manifestations that indicate cell death in living tissue -
enzyme degradation mainly - always pathological |
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apoptosis
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programmed cell death -
genetically controlled - eliminates unwanted cells - physiological and pathological |
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autolysis
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degradation of cell and contents caused by own enzymes
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heterolysis
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degradation of cell and contents by extrinsic enzymes
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putrefaction
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lysis of dead tissue by bacterial enzymes
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necrotic changes
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hypereosinophilic cytoplasm (RNA loss + coagulated proteins),
glycogen loss (smaller cell, more pink), nuclear changes |
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morphologic necrotic types
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coagulative,
liquefactive, caseous, fat, fibrinoid, gangrenous, gummatous |
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coagulative necrosis
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microscopic: cell outline and tissue architecture preserved,nucleus loss, increased eosinophilia; macroscopic: dense and dry appearance, white-grey when cut |
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liquefactive necrosis
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microscopic: complete loss of cell and tissue structure,no cell outlines, neutrophils; macroscopic: soft and filled with fluid |
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caseous necrosis
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no cell outlines or tissue architecture but firm consistency;
macroscopic: yellowish-white, cheese-like from lipid release from cell walls; microscopic: eosinophilic material surrounded by inflammatory cells |
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enzymatic fat necrosis
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focal areas of fat destruction, due to pancreatic enzyme actions;
pale outlines, hematoxylin stains calcium blue; pancreatitis --> fatty acids + Ca = saponification and chalky white calcium deposits |
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traumatic fat necrosis
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trauma --> healing by fibrous tissue and calcification
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fibrinoid necrosis
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immunologic injury;
smudgy pink staining of fibrin-like protein material |
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gangrenous necrosis
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loss of blood supply = form of infarction;
dry (coagulative) wet (with infection and liquefactive); in lower limbs and bowels |
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infarction
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localized area of tissue necrosis from loss of or reduced blood supply;
coagulative in most tissues, liquefactive in brain |
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Physiologic apoptosis
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embyrogenesis,
hormone-dependent involution, thymus involution in adults, cells programmed to die (epidermis, gut), inflammatory cell destruction |
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Pathologic apoptosis
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toxin induced,
councilman bodies, psammoma bodies, tumor cell death by cyt T cells, neuronal loss in Alzheimer's, HIV+ T-lymphocyte death |
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councilman bodies
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dead hepatocytes in viral hepatitis
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psammoma bodies
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apoptosis of neoplastic cell with subsequent calcification
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neoplastic
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abnormally growing cell
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apoptosis initiation
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extrinsic or intrinsic caspase activation,
gene regulation |
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apoptosis execution
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cell death caused by activated enzymes
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removal of cells in apoptosis
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cytoplasmic buds form on membrane that contain nuclear fragments,
mitochondria and protein fragments |
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extrinsic pathway
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receptor-ligand interactions:
TNF + TNF1, Fas + Fas ligand --> caspase activation |
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intrinsic pathway
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withdrawal of hormones or growth factors, damage to DNA --> release of cyt c --> caspase activation
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Bcl-2
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inhibits apoptosis by preventing release of cyt c from mitochondria
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p53
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tumor suppressor gene = stimulates apoptosis; elevated by DNA injury and pauses cell cycle to repair; activates Bax if repair is impossible
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Bax
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stimulates apoptosis
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caspases
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group of proteases that mediates execution phase
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executioner caspases
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activate endonucleases (DNA degradation) and proteases (cytoskeleton breakdown)
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apoptotic bodies
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broken off cytoplasmic buds
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phagocytosis
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absorbtion of apoptotic bodies by adjacent cells or macrophages
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apoptotic morphology
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eosinophilic cytoplasm,
pyknotic nucleus, small cells, apoptotic bodies, phagocytosis, lack of inflammatory response |
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dysregulated apoptosis
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too much or too little apoptosis;
decreased = cancers, autoimmunity; increased = neurodegenerative, death of infected cells (AIDS) |
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enzyme markers of cell death
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AST aspartate aminotransferase (liver necrosis),
ALT alanine aminotransferase (liver necrosis), CK-MB creatine kinase MB (AMI, myocarditis), amylase and lipase (pancreatitis) |