Atherosclerosis Flashcards

(38 cards)

1
Q

underlying cause of all stages of atherosclerosis

A

endothelial dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

can affect many vascular beds

A

atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

rupture of atherosclerotic plaque

A

MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

1st stage in atherosclerotic plaque formation

A

endothelial dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

decrease in NO
increase in selectins and integrins
monocytes in
EC apoptosis

A

endothelial dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MCP-1

A

attracts monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

M-CSF

A

attracts macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

2nd stage of atherosclerotic plaque

A

formation of fatty streak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

platelets show up and aggregate
VSMC migration by PDGF
T cells show up
foam cell formation

A

formation of fatty streak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

VSMC migrate into endothelium by

A

PDGF and AngII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

macrophages unable to break down oxLDL

A

foam cell formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

3rd stage in atherosclerotic plaque

A

formation of fibrous cap (advanced complicated lesions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

VSMC grow over (fibrous cap)
necrosis and apoptosis from MMPs, ROS, oxLDL mediated cell damage

A

formation of advanced complicated lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

degrade matrix

A

MMPs (matrix metalloproteins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

4th stage of atherosclerotic plaque

A

unstable plaque forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

cap unstable–> rupture

A

unstable plaque

17
Q

what makes unstable plaque

A

VSMC’s die on surface and wall thins

18
Q

thin cap
MMP activity
VSMC death
lipid rich plaque

A

vulnerable plaque (unstable)

19
Q

thick cap
VSMC content high
low MMP activity
lipid poor plaque

A

stable plaque

20
Q

stable plaque consequences

A

angina and intermittent claudication (transient)

21
Q

unstable plaque consequences

A

MI
ischemic stroke
CV death

22
Q

endothelial dysfunction
dyslipidemia
inflammation
oxidative stress
PDGF, Ang II, AGEs
VSMC dysfunction
ECM remodeling

A

factors that promote atherosclerosis

23
Q

convert LDL to oxLDL

A

ROS and AngII

24
Q

what causes VSMC’s to switch from contractile to migratory and synthetic

A

AngII, AGE, PDGF

25
inhibiting dyslipidemia does what to vascular wall
HDL prevents LDL to oxLDL, prevents expression of adhesion molecules, prevents foam cell formation
26
reducing inflammation does what to vascular wall
no monocytes present (ultimately no foam cell formation)
27
decreasing oxidative stress does what to vascular wall
NO stays nice and high; no ROS
28
no ROS oxidative stress leads to what
no monocyte adhesion or migration into cell; no endothelial dysfunction
29
decrease in endothelial dysfunction does what to vascular wall
NO normal (no EC death) no monocytes, no platelet aggregation, no LDL oxidation
30
place where people normally form atherosclerotic plaques due to change in laminar flow from bifurcation
carotid arteries
31
decrease in PDGF, AGEs, and AngII does what to vascular wall
STOPS CAP FORMATION VSMC stays contractile
32
this is involved in all the steps of atherosclerosis, so if you block this, you won't get plaque formation
AngII
33
drug used to lower AngII
Ramapril (ACEI)
34
increase in VSMC and decrease in ECM remodeling effect on vascular wall
no cap formation no rupture b/c no MMP activity
35
drug that blocks AT1R
Telmisartan
36
AT1R
AngII receptor (ARB)
37
successful drugs to decrease CV disease
Ramapril and Telmisartan
38
decrease LDL and CRP=
decrease risk for CV disease