236b cell death Flashcards Preview

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Flashcards in 236b cell death Deck (7)
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1
Q

apoptosis - overview? cell appearance? E required? pathways? final activator? radiation involvement?

A

programmed cell death without inflammation

red cytoplasm, cell shrinkage, pyknosis, membrane blebbing, apoptotic bodies (engulfed by adjacent cells)

ATP required

intrinsic + extrinsic pathways

both activate cytosolic caspases –> cell breakdown (endonuclease yield 180 bp fragments)

radiation causes apoptosis via free radicals and dsDNA breaks –> rapidly dividing cells (skin, GI mucosa) very susceptible

2
Q

intrinsic pathway for apoptosis - when does it normally occur? how? factors involved? final step?

A

tissue remodeling in embryogenesis

regulating factor withdrawn (IL-2 after immuno reaction leads to cell death) OR injury (radiation, toxins, hypoxia)

BAX and BAK –> apoptosis
bcl-2 –I apoptosis (via –I Apaf-1)

increases mito permeability and cytochrome c release

3
Q

extrinsic pathway for apoptosis - pathways?

A

2 pathways

1) FasL binds to Fas (CD95) – occurs in thymic medullary negative selection (defect = autoimmune disease) –> forms death domain FADD binding site, FADD activates caspases
2) immune cell (cytotoxic cell release of perforin and granzyme B)

4
Q

necrosis - overview? test? inflammation? E required?

A

enzymatic degradation and protein denaturation from exogenous injury

intracellular components leak (tropin, LFTs)

inflammatory process

no E required

5
Q

irreversible cell injury markers

A

nuclear pyknosis, karyorrhexis, karyolysis

plasma membrane damage (PL degradation)

lysosomal rupture

mito permeability –> see amorphous densities within mito

6
Q

reversible cell injury with return on O2

A

ATP depletion –> membrane bleebing and swelling due to loss of Na/K pump activity -> ribosome detachment –> lower protein synthesis

nuclear chromatin clumping

fatty change

7
Q

what cytokines mediate systemic inflammation (thus increas ESR via hepatic production of acute phase reactants)?

what makes them?

A

TNF-a
IL-1
IL-6

from macrophages and neutrophils activation during injury