Week 6A: Atherosclerosis, Aneurysm, Cholesterol Flashcards
HC 30, 31, 32
What structures are made extra in atherosclerosis to support new tissue?
Capillaries
Lethal infarctions in atherosclerosis
Myocardial or brain infraction
Important role endothelial cells
Barrier function, determine what does to the tissues
What do endothelial cells have on their cell surface to recognize etc
Proteins
Smoking risk factor for atherosclerosis
Smoking induces ROS formation in the blood
> Inflammation and activation monocytes in blood
How does LDL induce subendothelial inflammation in atherosclerosis? Explain all the steps
There is too much LDL in the low stressed vessel inner curvatures
> Too much ROS formation
> LDL goes into vessel wall and becomes minimally modified LDL (mLDL)
> Activation monocytes and extravasation to become activated macrophages
> Macrophages import mLDL with scavenger receptors
> Macrophages make cytokines and growth factors
Why do macrophages absorb mLDL with scavenger receptors instead of LDLR
LDLR does not recognize mLDL
Activated macrophages make products. Name them with their effects.
-Cytokines: attract more immune cells like monocytes and T-cells
-Growth factors: induce smooth muscle cell (SMC) migration and proliferation
Foam cell formation
Too much mLDL is taken up by macrophages
> Become immobile
> All lipids dissolve
> Cholesterol accumulates
> Very big cells: mechanically trapped in vessel wall: keep producing cytokines and growth factors
Atherosclerosis is a multi-factorial disease. Name the environmental factors, risk factors (molecular) and genetic components
Environment
> Smoking
> Diet
> Lack of exercise
Risk factors
> High cholesterol (LDL)
> Hypertension
> Diabetes
Genetic components
> Familiar Hypercholesterolemia (FH)
> Tangiers Disease
> others
Name treatment for the risk factors diabetes and high LDL and for environmental factors
Environmental > prevention
Diabetes > Insulin
High cholesterol/LDL > statins
Why do statins decrease cholesterol (LDL)
Promote the LDLR mostly
FH is caused by a mutation in the gene for:
LDL receptor
Acute myocardial infarction is caused by which process?
Blood coagulation
What does the plaque consist of in atherosclerosis
Cells > immune cells, SMCs, ECs (endothelial cells)
Risk factor for acute infarction
Exercise
> more blood flow > higher risk for rupture of the plaques
> ECs damaged > coagulation
> thrombus in the narrow vessel lumen: infarction
Which sex has the higher risk to get atherosclerosis?
Men
Symptoms myocardial infarct in women
Pain, shortness breath, fatigue, dizziness, restless feeling, fear, vomiting
Important with myocardial infarct symtoms men and women in atherosclerosis
Different symptoms!
Cell types in atherosclerotic plaque
-Endothelial cells (ECs)
-Monocytes/macrophages
-Smooth muscle cells (SMCs)
- T-cells
Stent treatment in atherosclerosis
Bring in stent around a balloon
> inflate balloon: stent sets out and widens vessel lumen
> deflate and remove balloon, stent remains in place
Explain why 1/3 of patients with stent treatment in atherosclerosis comes back with symptoms after light exercise after a while
SMC proliferation in the stent
> In-stent restenosis
In-stent restenosis is a pathology of the … cells
smooth muscle cells
Drug-eluting stent
Stent with a drug on the outside of the stent
> low dose: to prevent overgrowth of SMCs in the stent