Pathology Final Exam
Terms
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- hypertrophy
- ↑ in size of cells due to synthesis of more subcellular components, resulting in ↑ in size of the organ (ex. body builder)
- hyperplasia
- ↑ in cell numbers, often accompanied by ↑ in size of the organ or tissue
- hypoplasia
- failure of an organ or tissue to reach normal adult size (cell size usually normal)
- 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 - agenesis
- absence of an organ or tissue due to absence of the primordium
- aplasia
- absence of an organ or tissue due to failure of the primordium to continue development
- degeneration
- morphological manifestations of reversible cell injury
- cell death
- the result of irreversible cell injury
- necrosis
-
morphological changes following cell death in a living organism
results largely from degradative action of enzymes on lethally injured cell - 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 - putrefaction
- 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 - ischemia
- inadequate tissue perfusion
- 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) - 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 - 2 phenomena associated w/ irreversible cell injury
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inability to reverse mitochondrial dysfunction upon reperfusion
cell membrane damage - 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)