CAD Flashcards

1
Q

Where does atherosclerosis occur?

A

branch pts, exiting vessels, post abd aorta

hemodynamic turbulence is a indicator

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2
Q

inflamm markers

A
high sensitivity C-reactive protein (HSCRP) ***
acute phase interleukins (IL-1, IL-6)
serum amyloid a****
prego assoc plasma protein a
chronic infection
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3
Q

risk factors for atherosclerosis

A

genetic abn
family history
increase age
male

modifiable - hyperlipidemia, HTN, smoke, diabetes, vit def, obese, sedentary life, inflamm

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4
Q

where do lipids accum at

A

intima by macrophages and oxidation

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5
Q

oxidized ldl forms

A

foam cells and a lesion called fatty streak

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6
Q

proteins in flamm exudate are

A

clotting prot
complement
kinin cascade (vasodiliation)
fibrinolytic protein

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7
Q

what receptor takes in oxidized lipids

A

scavenger receptor CD36, TLR-4

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8
Q

what does inflammasomes produce

A

IL-1 and IL-18

inflam cytokines

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9
Q

what does neutrophil NETosis do?

A

scaffold for platelet/rbc activation, aggregation, thrombosis, elastase

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10
Q

what contributes to smooth m cell proliferation

A
pdgf
fibroblast growth factor
transforming growth factor-a
intima changes thickness 
breakdown elastic mem (decrease contractile/ Venous Pressure)
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11
Q

adaptive immunity mechanisms increase what, with what cells and mediators

A

cells: Th1, Th17, B cells
mediators: IFNy, TNF, IL-17
increase: adhesion mol expression, release cytokines/chemokines, mch/hla ii expression, ag presentation, oxldl uptake, marcophage activation

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12
Q

gen of lipid reactive T and B cells

A

hypercholesterolemia leads to build up of LDL in intima, mod to look like intruder, taken by macro and presented to T cells, self reactive now and lead to vascular inflammation and atherosclerosis

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13
Q

what happens to a fatty streak over time

A

covers with a fibrous cap (dense collagen fibers)

center necrotic, lipid, debris, foam cells, thrombus, surrounded by zone of inflammatory and smooth m cells

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14
Q

thrombosis due to erosion vs due to rupture

A

thick, angina and non-stemi, white platelet rich thrombus

thin, STEMI, red fibrin rich thrombus

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15
Q

phases of atherosclerosis

A

norm -> fatty streak -> fibrofatty plaque -> advanced vul plaque -> aneurysm and rupture, occlusion by thrombus, critical stenosis (middle age)

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16
Q

pro-coagulant markers and process marker

A

plasma homocysteine, tissue plasminogen activator, plasminogen activator inhibitor

process markers - fibrinogen

17
Q

can you use non-specific anti-inflammatories and selective inhibitor COX2 to treat atherosclerosis?

A

NO
it makes things worse and increase mortality
destabilizes the plaques

18
Q

arterial wall response to injury

A
  1. chronic endothelial injury (risk factors)
  2. endothelial dysfunction (increased perm, leukocyte adhesion, monocyte adhesion, emigration)
  3. macrophage activation, sm recruit
  4. macrophages and sm cells engulf lipid
  5. sm proliferation, collagen and matrix deposition, extracellular lipid
19
Q

Frequently Affected Arteries

A

Abdominal aorta > Coronary arteries > Popliteal arteries > Internal carotid arteries > Circle of Willis

20
Q

cardiac risk based on levels of hs-CRP

A

high >3 mg/L
avg 1-3 mg
low <1 mg