Adult Cardio 2 (Atherosclerosis) Flashcards
____ is initiated by injury/inflammation leading to endothelial dysfunction and accumulation of lipid-laden macrophages within arterial wall, eventually leading to lesion formation and plaque rupture
Atherosclerosis
Atherosclerosis is not due to ____, which explains why someone with a diet free of this might still develop atherosclerosis
Cholesterol
What are the 4 major classes of lipoproteins?
- Chylomicrons
- VLDL
- LDL
- HDL
The four classes of lipoproteins differ in type and amount of both ___ and ___, as well as size and effect on atherogenicity
Fat and protein
Cholesterol is important for building ___ ___
Cell membranes
____ delivers cholesterol, which causes the protein to then become more dense (___)
LDL; HDL
The HDL might go back to the liver and pick up more cholesterol to be delivered and then once again become ___
LDL
What are the triglyceride-rich lipproteins?
-Chylomicrons
-VLDL
What are the cholesterol-rich lipoproteins?
-LDL
-HDL
A large artery consists of ___ morphologically distinct layers
3
The ____, the innermost layer, is bounded by a monolayer of endothelial cells on the luminal side and a sheet of elastic fibers, the internal elastic lamina, on the peripheral side
Intima
The normal intima is a very thin region and consists of extracellular connective tissue matrix, primarily ____ and ____
-Proteoglycans
-Collagen
The ____, the middle layer, consists of smooth muscle cells (this is where the muscles are)
Media
The ____, the outer layer, consists of connective tissues with interspersed fibroblasts and smooth muscle cells
Adventitia
First step in the production of atherosclerosis:
LDL enters intima through intact endothelium
Second step in the production of atherosclerosis:
Intimal LDL is oxidized into proinflammatory lipids
Third step in the production of atherosclerosis:
Oxidized LDL causes adhesion and entry of monocytes and T lymphocytes across endothelium
Fourth step in the production of atherosclerosis:
Monocytes differentiate into macrophages and then consume large amount of LDL, transforming into foam cells
Fifth step in the production of atherosclerosis:
Foam cells release growth factors (cytokines) that encourage atherosclerosis
When the macrophage continues to ingest LDL, it will ___ and nothing will be able to phagocytose it
Die
The foam cells can then form a ___ ___ which narrows arteries and causes atherosclerosis
Fatty streak
Plaques are unstable and they might tear apart the endothelial layer which might occlude an artery completely causes something like a ___ or ___ ___
Stroke or heart attack
Overall pathophysiology of atherosclerosis:
Injured endothelial cells release chemotactic agents & growth factors Begin to transport & modify great amounts of lipids in blood (LDL) When sequestered LDL is oxidized– damages nearby cells & attracts monocytes to the area Monocytes cling to altered endothelial cells, migrate to sub-intima & become macrophages Macrophage becomes filled with oxidized-LDL and transform to foam cells Foam cells initiate an inflammatory response which lead to smooth muscle cell (SMC) proliferation SMC can release elastase and collagen which in addition to the generation of toxic products may facilitate plaque rupture or vessel wall damage, thickening the intima, and producing plaques.
Step 1 is lesion formation:
Lipoprotein trapping in the subendothelial matrix
Step 2 in lesion formation:
Lipoprotein aggregation and monocyte migration
Step 3 in lesion formation:
Foam cell formation
Step 4 in lesion formation:
Formation of fibrous plaque
Step 5 is lesion formation:
Plaque rupture
The intersection of inflammation and lipid metabolism modulates atherosclerosis and provides potential targets for ___ ___
Therapeutic manipulation
___ ____ can improve cardiovascular risk factors
Weight loss
