Duke PA pathology
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| When is control of intracellular environment lost in apoptosis? | maintained in early stages
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| What happens to cell shape in necrosis? | cells swell and organelles swell
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| What happens to cell shape in apoptosis? | cells contract
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| **add in slide 68,71** |
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| How can you tell when a cell is in early apoptosis? | chromatin margination and condensation
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| How can you tell when a cell is later in apoptosis? | nucleus is fragmented
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| What happens to a cell after apoptosis? | phagocytosis of apoptotic cellular remnants by adjacent cell
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| When does apoptosis happen in the thymus? | stress - body releases corticosteroids causing apoptosis of t-cells
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| How is apoptosis regulated? | the balance between factors that stimulate apoptosis and factors that inhibit apoptosis
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| What role does bcl-2 have in apoptosis? | pro-survival
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| What role does bax have in apoptosis? | pro-apoptosis
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| What does p53 do? | helps cells respond to injury, if cells have too much damage, p53 up-regulates bax, tipping the scale to apoptosis
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| What are various ways cells can be signaled to undergo apoptosis? | injury, withdrawal of growth factors, hormones, cytotoxic T lymphocytes, receptor-ligand interactions
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| What role do caspases play in apoptosis? | initiator caspases signal executioner caspases which cause breakdown of cytoskeleten, forming the bleb
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| What two things can happen when a cell is exposed to a noxious agent in necrosis? | excess of normal cell constituents or edema
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| At what point does a cell considered to have irreversible injury? | when the cell becomes necrotic
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| What happens to a necrotic cell? | autolysis, replacement, then regeneration or fibrosis….OR calcification
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| What are the types of necrosis? | coagulative, liquefactive, fat, caseous, fibrinoid
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| What changes characterize necrosis? | changes in cytoplasmic staining, in nuclear morphology and/or staining characteristics
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| In necrosis how does cytoplasm look? | more eosinophilic
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| pyknosis | nucleus shrinks and chromatin condenses; nucleus becomes more deeply basophilic (very dark blue with H&E stain)
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| Karyorrhexis | nucleus breaks up into small pieces
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| Karyolysis | nucleus becomes progressively paler staining and eventually disappears
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| Liquefactive necrosis | pattern of cell death characterized by dissolution of necrotic cells
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| Where is liquefactive necrosis typically seen? | in an abscess - large numbers of neutrophils release hydrolytic enzymes, break down dead cells
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| Pus | liquified remnants of dead cells, including neutrophils
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| fat necrosis | result of release of lipases into adipose tissue
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| In fat necrosis, what are triglycerides cleaved into? | fatty acids
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| What do fatty acids bind to? | bind to and precipitate calcium ions, forming insoluble salts
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| caseous necrosis | occurs with granulomatous inflammation in response to certain microorangisms
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| Where is fat necrosis most commonly found? | in pancreas injury
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| What is the most common microorganism that causes caseous necrosis? | tuberculosis
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| What is the host response to microorganisms that cause caseous necrosis? | chronic inflammatory response
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| Fibrinoid necrosis | occurs in the wall of arteries in cases of vasculitis
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| What does fibroid necrosis cause? | endothelial damage and necrosis of smooth muscle cells of the media
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| What does necrosis of smooth muscle cells and endothelial damage cause in fibrinoid necrosis? | allows plasma proteins, primarily fibrin, to be deposited in the area of medial necrosis
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| Infarction | cell death and coagulative necrosis due to prolonged ischemia
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| What do renal and splenic infarcts typically look like? | wedge-shaped
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| What do liver infarcts look like? | central lobular necrosis - area around central vein undergoes necrosis
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| What histologic changes occur in infarcts? | cytoplasmic hyper-eosinophilia, karyolysis (complete at 2 days), acute inflammatory cell infiltration begins at 12 hours after coronary occlusion and peaks at 2-3 days
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