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17 Cards in this Set
- Front
- Back
hypertrophy
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↑ in size of cells due to synthesis of more subcellular components, resulting in ↑ in size of the organ (ex. body builder)
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hyperplasia
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↑ in cell numbers, often accompanied by ↑ in size of the organ or tissue
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hypoplasia
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failure of an organ or tissue to reach normal adult size (cell size usually normal)
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atrophy
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↓ in size of a cell due to loss of subcellular components, usually resulting in shrinkage of the involved tissue or organ
gross: dec. size, wrinkled capsule |
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agenesis
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absence of an organ or tissue due to absence of the primordium
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aplasia
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absence of an organ or tissue due to failure of the primordium to continue development
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degeneration
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morphological manifestations of reversible cell injury
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cell death
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the result of irreversible cell injury
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necrosis
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morphological changes following cell death in a living organism
results largely from degradative action of enzymes on lethally injured cell |
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autolysis
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morphologic changes in cells following death of the host
largely same processes as in necrosis, but normal body responses to necrosis (ex. inflammation, mitosis) are incapable of occurring |
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putrefaction
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degradation/rot of tissue due to action of saprophytic bacteria which are either normal flora or invade from gut at time of or after death (commonly occurs w/ autolysis)
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morphology of necrosis vs. autolysis
1. distribution 2. staining 3. inflammation? 4. cadaver bacteria? 5. preservation of tissue pattern/cellular detail 6. consistency |
1. N: patchy, A: generalized/diffuse
2. N: good to poor, A: poor 3. N: present, A: absent 4. N: rare, A: frequent 5. N: focally lost, A: diffusely lost 6. N: variable (friable), A: friable, soft, wet, gas filled |
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ischemia
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inadequate tissue perfusion
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lesions indicative of irreversible cell injury
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amorphous densities in mitochondrial matrices
massive swelling of mitochondria nuclear change (pyknosis, karyolysis, karyorrhexis) lysosomal rupture (occurs later) |
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lesions indicative of reversible cell injury
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cell swelling d/t inc. Na, H2O intracellularly
fatty change: abnormal accumulation of trigylcerides w/in parenchymal cells detachment of ribosomes from RER cell surface blebs mitochondrial swelling dec. protein synthesis |
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2 phenomena associated w/ irreversible cell injury
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inability to reverse mitochondrial dysfunction upon reperfusion
cell membrane damage |
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coagulation necrosis
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often precedes other types of necrosis
gross & microscopic architecture of necrotic tissue are still recognizable usually caused by hypoxia, ischemia, or acute toxicity ex. infarction, Zenker's necrosis (coag necrosis of skeletal muscle) |