Atherosclerosis Flashcards

1
Q

underlying cause of all stages of atherosclerosis

A

endothelial dysfunction

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2
Q

can affect many vascular beds

A

atherosclerosis

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3
Q

rupture of atherosclerotic plaque

A

MI

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4
Q

1st stage in atherosclerotic plaque formation

A

endothelial dysfunction

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5
Q

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

A

endothelial dysfunction

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6
Q

MCP-1

A

attracts monocytes

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7
Q

M-CSF

A

attracts macrophages

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8
Q

2nd stage of atherosclerotic plaque

A

formation of fatty streak

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9
Q

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

A

formation of fatty streak

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10
Q

VSMC migrate into endothelium by

A

PDGF and AngII

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11
Q

macrophages unable to break down oxLDL

A

foam cell formation

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12
Q

3rd stage in atherosclerotic plaque

A

formation of fibrous cap (advanced complicated lesions)

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13
Q

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

A

formation of advanced complicated lesions

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14
Q

degrade matrix

A

MMPs (matrix metalloproteins)

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15
Q

4th stage of atherosclerotic plaque

A

unstable plaque forms

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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
Q

inhibiting dyslipidemia does what to vascular wall

A

HDL prevents LDL to oxLDL, prevents expression of adhesion molecules, prevents foam cell formation

26
Q

reducing inflammation does what to vascular wall

A

no monocytes present (ultimately no foam cell formation)

27
Q

decreasing oxidative stress does what to vascular wall

A

NO stays nice and high; no ROS

28
Q

no ROS oxidative stress leads to what

A

no monocyte adhesion or migration into cell; no endothelial dysfunction

29
Q

decrease in endothelial dysfunction does what to vascular wall

A

NO normal (no EC death)
no monocytes, no platelet aggregation, no LDL oxidation

30
Q

place where people normally form atherosclerotic plaques due to change in laminar flow from bifurcation

A

carotid arteries

31
Q

decrease in PDGF, AGEs, and AngII does what to vascular wall

A

STOPS CAP FORMATION
VSMC stays contractile

32
Q

this is involved in all the steps of atherosclerosis, so if you block this, you won’t get plaque formation

A

AngII

33
Q

drug used to lower AngII

A

Ramapril (ACEI)

34
Q

increase in VSMC and decrease in ECM remodeling effect on vascular wall

A

no cap formation
no rupture b/c no MMP activity

35
Q

drug that blocks AT1R

A

Telmisartan

36
Q

AT1R

A

AngII receptor (ARB)

37
Q

successful drugs to decrease CV disease

A

Ramapril and Telmisartan

38
Q

decrease LDL and CRP=

A

decrease risk for CV disease