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Pathology 1-3
Duke PA pathology
Question | Answer |
---|---|
When is control of intracellular environment lost in apoptosis? | maintained in early stages |
What happens to cell shape in necrosis? | cells swell and organelles swell |
What happens to cell shape in apoptosis? | cells contract |
**add in slide 68,71** | |
How can you tell when a cell is in early apoptosis? | chromatin margination and condensation |
How can you tell when a cell is later in apoptosis? | nucleus is fragmented |
What happens to a cell after apoptosis? | phagocytosis of apoptotic cellular remnants by adjacent cell |
When does apoptosis happen in the thymus? | stress - body releases corticosteroids causing apoptosis of t-cells |
How is apoptosis regulated? | the balance between factors that stimulate apoptosis and factors that inhibit apoptosis |
What role does bcl-2 have in apoptosis? | pro-survival |
What role does bax have in apoptosis? | pro-apoptosis |
What does p53 do? | helps cells respond to injury, if cells have too much damage, p53 up-regulates bax, tipping the scale to apoptosis |
What are various ways cells can be signaled to undergo apoptosis? | injury, withdrawal of growth factors, hormones, cytotoxic T lymphocytes, receptor-ligand interactions |
What role do caspases play in apoptosis? | initiator caspases signal executioner caspases which cause breakdown of cytoskeleten, forming the bleb |
What two things can happen when a cell is exposed to a noxious agent in necrosis? | excess of normal cell constituents or edema |
At what point does a cell considered to have irreversible injury? | when the cell becomes necrotic |
What happens to a necrotic cell? | autolysis, replacement, then regeneration or fibrosis….OR calcification |
What are the types of necrosis? | coagulative, liquefactive, fat, caseous, fibrinoid |
What changes characterize necrosis? | changes in cytoplasmic staining, in nuclear morphology and/or staining characteristics |
In necrosis how does cytoplasm look? | more eosinophilic |
pyknosis | nucleus shrinks and chromatin condenses; nucleus becomes more deeply basophilic (very dark blue with H&E stain) |
Karyorrhexis | nucleus breaks up into small pieces |
Karyolysis | nucleus becomes progressively paler staining and eventually disappears |
Liquefactive necrosis | pattern of cell death characterized by dissolution of necrotic cells |
Where is liquefactive necrosis typically seen? | in an abscess - large numbers of neutrophils release hydrolytic enzymes, break down dead cells |
Pus | liquified remnants of dead cells, including neutrophils |
fat necrosis | result of release of lipases into adipose tissue |
In fat necrosis, what are triglycerides cleaved into? | fatty acids |
What do fatty acids bind to? | bind to and precipitate calcium ions, forming insoluble salts |
caseous necrosis | occurs with granulomatous inflammation in response to certain microorangisms |
Where is fat necrosis most commonly found? | in pancreas injury |
What is the most common microorganism that causes caseous necrosis? | tuberculosis |
What is the host response to microorganisms that cause caseous necrosis? | chronic inflammatory response |
Fibrinoid necrosis | occurs in the wall of arteries in cases of vasculitis |
What does fibroid necrosis cause? | endothelial damage and necrosis of smooth muscle cells of the media |
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 |
Infarction | cell death and coagulative necrosis due to prolonged ischemia |
What do renal and splenic infarcts typically look like? | wedge-shaped |
What do liver infarcts look like? | central lobular necrosis - area around central vein undergoes necrosis |
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 |