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Pathology > 1.3 Apoptosis > Flashcards

1.3 Apoptosis Flashcards

0
Q

Apoptosis is seen in…(4)

A

Senescent cells
Embryo development
Immune mediated death…..cytotoxic t cells
Hormonal or cytokine withdrawl….results in dec cells via apop

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1
Q

Apoptosis literally means

A

leaves falling from the tree

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2
Q

Cell swelling is seen in…..

A

Necrosis

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3
Q

Cell shrinking is seen in….

A

Apoptosis

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4
Q

A morphological expression of cell death

A

necrosis

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5
Q

controlled by specific genes

A

apoptosis

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6
Q

physiological cell death or programmed cell death

A

apoptosis

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7
Q

generally initiated by overwhelming stress

A

necrosis

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8
Q

Inflammatory response

A

necrosis

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9
Q

fragmentation of DNA and nucleus with blebbing

A

apoptosis (apoptotic bodies)

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10
Q

how are apoptotic bodies cleared?

A

phagocytized quickly

  • -phosphatidyl serine put on surface to tag it for phagocytosis
  • -no inflammation
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11
Q

Defining features of apoptosis (6)

A 
cell shrinkage
membrane blebs
nuclear shrinkage/pyknosis-------look for size--shrinking says apop
nuclear fragmentation
phagocytosis by neighbor cells
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12
Q

steps in apoptosis (3)

A
  • early–chromatin margination and condensation
  • later–nuclear fragmentation
  • phagocytosis by adjacent cells
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13
Q

stimulus for necrosis vs apoptosis

A

more severe vs less severe

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14
Q

consequences of necrosis (3)

A

loss of functional tissue
impaired organ fn (transient or permanent)
inflammation

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15
Q

consequences of apoptosiss

A

removal of damaged or unnecessary cells

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16
Q

cell number/stages of necrosis

A

all cells

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17
Q

cell number/ stages of apoptosis

A

different levels and stages

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18
Q

pathological apoptosis (10)

A 
ionizing radiation
free radical generation
mild thermal injury <43 deg C
steroids
glucocorticoids induce apop in lymphocytes
viral infection
cell mediated immunity
autoimmune diseases
degenerative diseases of the CNS azheimers, parkinsons 
neoplasia (if apop is inhibited)
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19
Q

control of intracellular environment is lost

A

necrosis

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20
Q

chromatin marginates early while injury is still reversible

A

necrosis

21
Q

cleavage at multiples of 200 bp (ladder on gel)

A

apoptosis

22
Q

loss of membrane integrity….necrosis vs apoptosis

A

early vs late

23
Q

nuclear events …..necrosis vs apoptosis

A

nuclear disintegration vs (condensation +fragmentation)

24
Q

Mechanisms of apoptosis (4)

A

signaling pathways
control and integration
common execution pathways
phagocytosis and removal of dead cells

25
Q

Extrinsic pathway/receptor pathway uses

A

TRAILs (tumor necrosis factor related apoptosis inducing ligands)
ex. TNF, FAS(CD95)/FASL

26
Q

Intrinsic pathway (mitochondrial) uses

A

Bcl2, Bax, p53 release Cyt c, Smac, DIABLO

27
Q

extrinsic initiating caspases

A

8 and 10

28
Q

intrinsic initiating caspases

A

9 and 12

29
Q

Execution caspases

A

3, 6, 7

30
Q

TNF does what?

A

depends on the receptor signaling….different things for different cells

31
Q

potential induced activity vs inhibitor capacity

A

>

inhibition is mostly jut to prevent accidental activation

32
Q

in nematodes ced3 an ced 4

A

are required for apoptosis

not transcriptionally regulated, always around–>zymogens

33
Q

in nematodes ced 9

A

blocks apoptosis – if absent then lethal and excess will disrupt development

34
Q

Bcl2 blocks apop by…..and is found in….

A

inhibiting mitochondrial permeability keeping cyt c in mito; also binds apaf1

B cells
translocation linking gene for IgG promoter leads to B cell lymphoma

35
Q

Bax

A

causes apoptosis
upregulaated by p53
homo and heterodimers of bcl2 and bax determine if apop is blocked or not

36
Q

bid

A

helps bridge extrinsic and intrinsic pathways

37
Q

human homolog of ced 4

A

Apaf 1…..w/ cyt C it activatees caspase 9

38
Q

caspases are …….. proteases thta cleave proteins at …….residues

A

cysteine

aspartic acid

homologs too ced 3

39
Q

how do caspases disassemble a cell

A

inactivate inhibitors of apoptosis
cleave structural proteins
deregulate proteins by separating regulatory and catalytic subunits

40
Q

Caspase Activation (6)

A 
protein cleavage
protein cross links
cell shrinkage
nuclease activation
nuclear shrinkage
DNA fragmentation
41
Q

Extrinsic Pathway is mainly involved in…..mediated by…….

A

normal control of cell/growth survival

TRAIL ligands binding death receptors; receptors aggregate, death domains of these receptors bind adaptor proteins with death domains (FADD and TRADD); bind several caspase 8 molecules inducing proximity and autocatalytic activation

42
Q

FADD

A

fas associated death domain

43
Q

TRADD

A

tnf receptor associated death domain

44
Q

cflip

A

competitively binds death domains preventing procaspase 8 from binding and getting activated……need overwhelming signal to overrcome

45
Q

intrinsic pathway is mainly involved in… and is mediated by……

A

injury induced apoptosis (to mitochondria, dna damage, protein damage, or T cell mediated kill)

mitochondrial leakage of Cyt C, smac, diablo

46
Q

smac and diablo

A

eat up inhibitory capacity

47
Q

p53

A

facilitates apoptosis; inc bax that eats up bcl2, stopping inhibition, promoting apop

not req. for steroid induced apop of lymphocytes

radiation inc. p53–> tumors

48
Q

how are denatured/misfolded proteins handled (3)

A

heat-shock proteins—-refold them
ubiquitin tag/proteosome—degraded them
caspase 12 activation—when other 2 systems are overloaded

49
Q

t-cell grazymes kill by

A

activating caspase 3

50
Q

IAPs

A

inhibitors of apoptosis proteins
inhibit caspase 3 activation
ex. survivin
inhibited by smac/deablo

Pathology (26 decks)

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