Atherosclerosis Flashcards
When does intimal thickening happen
because of injury and aging
Atherosclerosis
hardening of arteries. Specifically fibrofatty lesion in tunica intima which protrude into vascular lumen, weaken tunica media
What does obstruction of vascular lumen lead to
ischemia, infaration - which can lead to development of aneurysm
How does smooth muscle get into the sub-endothelial compartment
- from tunica media through fenestrations
- precursor cells in blood that squeeze between damage in injury
How do foam cells form
- LDL in subendothelial compartment
- becomes oxidized
- phagocytosed by macrophages and smooth muscle cells
fatty streaks
early changes to tunica intima, but not to level of atheroma
How can you tell if it’s a fatty streak (microscopic view)
thickening of intima
separation from internal elastic membrane
foam cells
Atherosclerotic lesions
dark deposits that become calicified, are non reversible
Non-modifiable risks for atherosclerosis
40-60 yo
family history
male
genetic abnormalities
Modifiable risks for atherosclerosis
hyperlipidemia cigarettes c-reactive protein hypertension diabetes
Normal total cholesterol
<200 mg/dl
Normal LDL
<130 gm/dl
Normal HDL
> 45 mg/dl
Normal triglycerides
<150 mg/dl
How does c-reactive protein put you are more risk
- endothelial cells become prethrombotic
- increase their adhesiveness for WBC
- causes inflammation of wall vasculature
What has to happen to cause endothelial cell dysfunction
some injurious event - can be chronic endothelial injury like hyperlipidemia, hypertension, etc
Endothelial dysfunction
increased permeability, leukocyte adhesion
Key events of atherosclerosis
1) Chronic endothelial injury
2) Endothelial dysfunction
3) Smooth muscle recruitment to intima. Macrophage activation
4) Macrophages and smooth muscle cells engulf lipid
5) Smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid
Foam cells
smooth muscle cells or macrophages. Macrophages predominant form
Role of NO in adhesion
prevent adhesion of leukocytes to endothelium, reduce adhesion of platletes
Frequencies of critical stenosis of cornoary arteries (most to least common)
1) anterior interventricular branch of left coronary artery
2) Right coronary artery
3) Circumflex branch of left coronary a
Wavefront phenomenon of necrosis
necrosis happens inner layer of myocardium then outer myocardium
What does triphenyltetrazolium chloride do
stains viable cells red and nonviable white
What are the consequences of myocardial ischemia and infarction
arrythmia
acute rupture of cardiac wall of IV septum
rupture of papillary muscles
ventricular aneurysm
Order of events in cerebral infarction
1) Intense eosinophilia (12-24 hours)
2) neutrophils invade to clean up damage
3) macrophages come in and cause proliferation of glial cells (10 days)
