1.3 Cell Death Flashcards
Etymology Karyo-seed hexis- burst pynk- dot apoptosis- falling of leaves (26 cards)
Pyknosis
nuclear shrinking
Karryorrhexis
nuclear disintegration
karylolysis
disintegration of nuclear fragments
necrosis
death of a large group of cells followed by acute inflammation
apoptosis
suicide
coagulative necrosis
cells retain their shape, nucleic are gone
the organ remains intact, wedge-shaped and pale, wedge points to area of infarct
ischemic infarction, EXCEPT THE BRAIN
red infarction
- re-entry of blood
2. into a loosely organized tissue
liquefactive necrosis
morph:
enzymatic lysis fo cells and protein
brain infarction, abcess, pancreatitis
necrosis: brain infarction
microglial cells cause liquefactive necrosis
necrosis: abscess
neutrophils release enzymes that cause liquefactive necrosis
necrosis: pancreatitis
- liquefactive (pancreatic enzymes digest itself)
2. fat necrosis (pancreatic enzymes)
gangrenous necrosis
mummified, ischemia of lower limb and GI
- coagulative necrosis
- wet gangrene: infection of gangrenous tissue
caseous necrosis
cottage cheese appearance, a combination of coagulative and liquefactive necrosis
granulamatous infection due to TB or fungal infection
fat necrosis
chalky white appearance due to deposition of calcium (saponification)
- trauma to fat (breast)
- pancreatitis-mediated damage of peripancreatic fat
saponification
fatty acids released by trauma or lipase join with calcium
dystrophic calcification
a dead or dying tissue becomes a nidus for calcium deposition. normal levels of calciums
metastatic calcification
high serum calcium or serum phosphate cause precipitation of calcium into tissue
fibrinoid necrosis
necrotic damage to the blood vessel wall, results in bright pink staining
- malignant hypertension
- vasculitis
preeclampsia
fibrinoid necrosis of the placenta
apoptosis
morph: pink (eosinophilic), nuclear condensation, apoptotic bodies are removed by macrophages
energy dependent, genetically programmed cell death involving single or small groups of cells
ex. endometrial shedding, embryogenesis, CD8 T cells
caspases
activate proteases that break down the cytoskeleton
intrinsic mitochondrial pathway
an apoptotic pathway due to cellular injury, DNA damage, or decreased hormonal stimulation
Mechanism: Bcl2 is inactivated, cytochrom c leaks into the cytoplasm
Bcl2
stabilizes the mitochondrial membrane to prevent Ctyo c from leaking out
extrinsic ligand-receptor pathway
- Fas lignad binding FAS death receptor on the target cell
2. TNF binds TNF receptor on target cells