Necrosis and Atherosclerosis Flashcards

(50 cards)

1
Q

what are the 2 pathways for cell death?

A

apoptosis (planned)

necrosis (pathological)

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2
Q

What are some unique features of necrosis?

A

swelling and karyolysis

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3
Q

What are some unique features of apoptosis?

A

shrinkage and apoptotic bodies

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4
Q

How can ischemia lead to necrosis?

A

mitochondria damage, increased glycolysis and running out of ATP

sodium pump stops working (needs ATP)

osmosis causes cell to start to swell

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5
Q

coagulative necrosis

A

architecture of cell is preserved but cell contents are condensed and hyperdense

this causes cell to stain eosinophilic

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6
Q

liquefactive necrosis

A

complete loss of cell and tissue architecture

creates pus in infection

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7
Q

Where does liquefactive necrosis always take place?

A

the brain

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8
Q

What type of necrosis creates abscesses?

A

liquefactive necrosis

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9
Q

What type of necrosis creates granuloma?

A

caseous necrosis

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10
Q

caseous necrosis

A

cannot clear pathogen so you in case it in layers of fibroblasts to wall it off

looks like cheese in gross anatomy

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11
Q

common cause of caseous necrosis

A

TB

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12
Q

where does saponification occur? and specifically?

A

fat necrosis

specifically, pancreatitis

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13
Q

How does fat necrosis appear? Why

A

appears basophilic due to accumulation of calcium lipid salts

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14
Q

fibrinoid necrosis

A

fibrin leaks into vessels

fibrin stains bright pink

often due to autoimmune disease attacking vessel walls

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15
Q

wet gangrene is caused by …

A

liquefactive necrosis

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16
Q

dry gangrene is caused by …

A

coagulative necrosis

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17
Q

how can you differentiate apoptotic bodies from blebs

A

apoptotic bodies are rounder and nicer looking

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18
Q

what type of cell clears apoptotic bodies?

A

macrophages

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19
Q

what is a chemotactic factor released by apoptotic cells? what do they attract?

A

ADP / UTP produced by connexon channels

attract macrophages

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20
Q

Does apoptosis produce an inflammatory response?

A

no, for this reason it is considered “sterile”

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21
Q

what serves as signal for phagocytosis in apoptosis cell?

A

phosphatidyl serine (PS)

22
Q

What class of enzyme is the critical effector molecule for apoptosis?

23
Q

What is the active site of caspases?

24
Q

How do you active caspases?

A

need to cleave them

25
3 isoforms of caspases to know
3, 8, 9
26
What can caspase activation lead to?
organellar fragmentation, translational shutdown, actin depolymerization, detachment of cells from ECM and inactivation of flipases
27
Intrinsinc pathway of apoptosis
mitochondrial damage and formation of apoptosome *also recognize cytochrome C as part of this
28
Extrinsic pathway of apoptosis
DISC (death inducing complex) caspase 8 binding of death ligands NK cells and cytotoxic T cells can signal extrinsic, death, pathway
29
What is common between intrinsinc and extrinsic apoptosis pathways?
caspase 3
30
What cells express the FasL ligand to trigger the extrinsic death pathway?
NK cells and activated T-cells
31
Caspase 9 is part of ...
intrinsic (mitochrondrial) apoptosis pathway
32
Caspase 8 is part of ...
extrinsic apoptosis pathway
33
Caspase 3 is part of ...
both intrinsic and extrinsic apoptosis pathway
34
Which requires ATP, apoptosis or necrosis?
apoptosis
35
Difference between ischemia and infarction
infarction is irreversible injury
36
white infarct
not hemorrhagic typically seen in dense tissues (heart + kidneys)
37
red infact
has some collateral blood flow blood is able to re-enter the tissue to some extent
38
What type of vessels does atherosclerosis occur in?
arteries only
39
6 steps of forming an atherosclerotic plaque
1) endothelial injury 2) endothelial dysfunction leading to monocytes and platelet adhesion 3) macrophage activation and smooth muscle recruitment 4) accumulation of cholesterol in intima and foam cells 5) smooth muscle proliferation and deposition of ECM 6) formation of distinct fibrous cap and necrotic center
40
Where do plaques commonly form?
at turbulent flow sites
41
difference between pathogenesis and etiology
pathogenesis: process by which disease develops etiology: cause of disease
42
How do foam cells form?
LDL is transported across endothelial barrier LDL particles are oxidized in region of forming atheroma Oxidized LDL are taken up by macrophages forming smooth muscle cells Foam cells release growth factors and cytokines which recruit additional monocytes/smooth muscle cells to plaque
43
transcytosis
transporting LDL across endothelial barrier
44
What is the earliest lesion seen in formation of atherosclerotic plaque?
fatty streak *does not always form atherosclerosis*
45
primary cellular component of fatty streak?
foam cells
46
where is fatty streak?
subendothelial
47
2 parts of atherosclerosis
1) necrotic center 2) fibrous cap
48
what can lead to thrombosis?
an ulcerated atherosclerotic plaque
49
nitroglycerin
nitrogen oxide activates guanyl-cyclases which causes vasodilation of chest vessels
50
how does area of infarct stain?
stains blue on trichrome due to replacement by connective tissue in infarcted area