CAD Flashcards
Where does atherosclerosis occur?
branch pts, exiting vessels, post abd aorta
hemodynamic turbulence is a indicator
inflamm markers
high sensitivity C-reactive protein (HSCRP) *** acute phase interleukins (IL-1, IL-6) serum amyloid a**** prego assoc plasma protein a chronic infection
risk factors for atherosclerosis
genetic abn
family history
increase age
male
modifiable - hyperlipidemia, HTN, smoke, diabetes, vit def, obese, sedentary life, inflamm
where do lipids accum at
intima by macrophages and oxidation
oxidized ldl forms
foam cells and a lesion called fatty streak
proteins in flamm exudate are
clotting prot
complement
kinin cascade (vasodiliation)
fibrinolytic protein
what receptor takes in oxidized lipids
scavenger receptor CD36, TLR-4
what does inflammasomes produce
IL-1 and IL-18
inflam cytokines
what does neutrophil NETosis do?
scaffold for platelet/rbc activation, aggregation, thrombosis, elastase
what contributes to smooth m cell proliferation
pdgf fibroblast growth factor transforming growth factor-a intima changes thickness breakdown elastic mem (decrease contractile/ Venous Pressure)
adaptive immunity mechanisms increase what, with what cells and mediators
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
gen of lipid reactive T and B cells
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
what happens to a fatty streak over time
covers with a fibrous cap (dense collagen fibers)
center necrotic, lipid, debris, foam cells, thrombus, surrounded by zone of inflammatory and smooth m cells
thrombosis due to erosion vs due to rupture
thick, angina and non-stemi, white platelet rich thrombus
thin, STEMI, red fibrin rich thrombus
phases of atherosclerosis
norm -> fatty streak -> fibrofatty plaque -> advanced vul plaque -> aneurysm and rupture, occlusion by thrombus, critical stenosis (middle age)
pro-coagulant markers and process marker
plasma homocysteine, tissue plasminogen activator, plasminogen activator inhibitor
process markers - fibrinogen
can you use non-specific anti-inflammatories and selective inhibitor COX2 to treat atherosclerosis?
NO
it makes things worse and increase mortality
destabilizes the plaques
arterial wall response to injury
- chronic endothelial injury (risk factors)
- endothelial dysfunction (increased perm, leukocyte adhesion, monocyte adhesion, emigration)
- macrophage activation, sm recruit
- macrophages and sm cells engulf lipid
- sm proliferation, collagen and matrix deposition, extracellular lipid
Frequently Affected Arteries
Abdominal aorta > Coronary arteries > Popliteal arteries > Internal carotid arteries > Circle of Willis
cardiac risk based on levels of hs-CRP
high >3 mg/L
avg 1-3 mg
low <1 mg
