3: Cell Death Flashcards

1
Q

leaking cellular contents

A

necrosis

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2
Q

cell fragmentation and phagocytosis

A

apoptosis

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3
Q

cytoplasmic changes with necrosis

A

esoinophilia
glassy appearance
vauolation

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4
Q

nuclear changes with necrosis

A

pyknosis
karyorrhexis
karyolysis

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5
Q

pyknosis

A

shrinkage of nucleus

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6
Q

karyolysis

A

fading of nuclear fragments

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7
Q

karyorrhexis

A

fragmentation of nucleus

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8
Q

usually seen in death due to ischeia, hypoxia, reperfusion injury in most organs except brain

A

coagulative necrosis

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9
Q

basic outline of cell preserved but with no nuclei

A

coagulative necrosis

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10
Q

death of brain tissue, typically

A

liquefactive necrosis

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11
Q

seen in abscess where the center is made up of enzymatic digested PMNs (pus)

A

liquefactive necrosis

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12
Q

amorhpous, granular under the microscope with loss of cells and tissue structure

A

liquefactive necrosis

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13
Q

accumulation of mononuclear cells that mediate the CHRONIC inflammatory rxn and GRANULOMA formation

A

caseous necrosis

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14
Q

lipid in wall of the organism can’t be fully broken down

A

caseous necrosis

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15
Q

dead cell persist indefinitely as amorphous, coarsely granular, eosinophilic debris

A

caseous necrosis

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16
Q

caseous necrosis is characteristic of what organisms

A

TB and fungi

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17
Q

fat is changed due to action of lipases

A

enzymatic fat necrosis

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18
Q

FA released from enzymatic fat necrosis react with calcium to form

A

soap like substance that appears white, chalky

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19
Q

why can you see some enzymatic fat necrosis on x-ray

A

enough calcium deposition (this will also make them basophilic)

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20
Q

where is enzymatic fat necrosis most commonly seen

A

pancreatitis

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21
Q

injury in blood vessels with accumulation of plasma prtn (cause wall to stain eosinophilic)

A

fibrinoid necrosis

22
Q

vasculitis is associated with…

A

fibrinoid necrosis

23
Q

not specific pattern of cell death usually applied to limb died due to loss of circulation or bowel

A

gangrenous necrosis

24
Q

wet gangrene

A

combination of gangrene with superimposed bacterial infection

25
associated with diabetes
gangrene
26
reduction of available oxygen
ischemia
27
TPA
tissue plasminogen activator | - given to help reperfusion during first 30 min of heart attack/stroke or transplantation
28
blood flow/oxygenation of tissue is restored
reperfusion
29
clinical observations during a heart attack
- lavine sign - no 'P' - ST elevation - elevations in creatine kinase CK-MB - elevations in troponin I or T (TnI or TnT)
30
physiological roles of apoptosis
- embryogenesis - hormone dependent involution - cell deletion in proliferating cell population - normal immune defense against infected/transformed cells - removal of self-reactive lymph clones
31
pathologic apoptosis conditions
- cytotoxic anticancer drugs - low doses of radiation, temp. drugs - transplant rejection - duct obstruction atrophy - some viruses
32
basic outline of apoptosis
- signaling pathways initiate apoptosis - itnracellular signals further commit cell to apoptotic pathway - execution caspases catabolize cytoskeleton and activate endonucleases (DNA breakdown) - removal of dead cells
33
apoptotic pathway from within the cell
mitochondrial intrinsic pathway
34
apoptotic pathway that uses receptors
death receptor extrinsic pathway
35
Bax and Bak
proapoptotic family members of Bcl-2 family
36
action of Bax and Bak
dimerize and form holes in mitochondria
37
what role does cytochrome c play in apoptosis
leaks out of holey mitochondria and stimulates initiator capsases
38
Bcl-2 and Bcl-x
anti-proapoptotic prtns (block proapoptotic prtns)
39
describe the extrinsic pathway of apoptosis
Bcl-2 family sensors recognize cell injury - Bax and bak attack mitochondria - cytochrome c activates initiator capsaes which activate executioner capsases which do the degrading
40
describe the intrinsic pathway of apoptosis
receptor-ligand interactions with Fas and TNF receptor activate adapter proteins - adapter prtns activates initiator capsases which activate executioner capsases which do the degrading
41
wher do the intrinsic and extrinsic apoptotic pathways converge
initiator capsases
42
how does p53 respond to DNA damage
p53 will activate pro-apoptotic forms of the Bcl-2 family (Bax and Bak)
43
low v. high doses of radiation
``` low= apoptosis (gets the proliferationg cells) high= necrosis (gets all cells) ```
44
do viruses induce apoptosis or necrosis
both if nutrient deficiency or complement activation... necrosis if changes in p53, granzyme, or Tcells.... apoptosis
45
tylenol suicide
massive liver necrosis
46
acetaminophen
highly reactive quinone metabolite that reacts w/ prtn, DNA and causes oxygen stress
47
carbon tetrachloride CCL4
metabolite CCl3- reacts with membrane and ER
48
heavy metals and cyanide
injure the mitochondria
49
phalloidin, paclitaxel
injure cytoskeleton and prevent replication
50
chemoterapeutic alkylating agents
direct damage to DNA
51
most vulnerable liver zone for necrosis
3