Adult Cardio 2 (Atherosclerosis)

Question 1

____ 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

Answer 1

Atherosclerosis

Question 2

Atherosclerosis is not due to ____, which explains why someone with a diet free of this might still develop atherosclerosis

Answer 2

Cholesterol

Question 3

What are the 4 major classes of lipoproteins?

Answer 3

1. Chylomicrons
2. VLDL
3. LDL
4. HDL

Question 4

The four classes of lipoproteins differ in type and amount of both ___ and ___, as well as size and effect on atherogenicity

Answer 4

Fat and protein

Question 5

Cholesterol is important for building ___ ___

Answer 5

Cell membranes

Question 6

____ delivers cholesterol, which causes the protein to then become more dense (___)

Answer 6

LDL; HDL

Question 7

The HDL might go back to the liver and pick up more cholesterol to be delivered and then once again become ___

Answer 7

LDL

Question 8

What are the triglyceride-rich lipproteins?

Answer 8

-Chylomicrons
-VLDL

Question 9

What are the cholesterol-rich lipoproteins?

Answer 9

-LDL
-HDL

Question 10

A large artery consists of ___ morphologically distinct layers

Answer 10

3

Question 11

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

Answer 11

Intima

Question 12

The normal intima is a very thin region and consists of extracellular connective tissue matrix, primarily ____ and ____

Answer 12

-Proteoglycans
-Collagen

Question 13

The ____, the middle layer, consists of smooth muscle cells (this is where the muscles are)

Answer 13

Media

Question 14

The ____, the outer layer, consists of connective tissues with interspersed fibroblasts and smooth muscle cells

Answer 14

Adventitia

Question 15

First step in the production of atherosclerosis:

Answer 15

LDL enters intima through intact endothelium

Question 16

Second step in the production of atherosclerosis:

Answer 16

Intimal LDL is oxidized into proinflammatory lipids

Question 17

Third step in the production of atherosclerosis:

Answer 17

Oxidized LDL causes adhesion and entry of monocytes and T lymphocytes across endothelium

Question 18

Fourth step in the production of atherosclerosis:

Answer 18

Monocytes differentiate into macrophages and then consume large amount of LDL, transforming into foam cells

Question 19

Fifth step in the production of atherosclerosis:

Answer 19

Foam cells release growth factors (cytokines) that encourage atherosclerosis

Question 20

When the macrophage continues to ingest LDL, it will ___ and nothing will be able to phagocytose it

Answer 20

Die

Question 21

The foam cells can then form a ___ ___ which narrows arteries and causes atherosclerosis

Answer 21

Fatty streak

Question 22

Plaques are unstable and they might tear apart the endothelial layer which might occlude an artery completely causes something like a ___ or ___ ___

Answer 22

Stroke or heart attack

Question 23

Overall pathophysiology of atherosclerosis:

Answer 23

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.

Question 24

Step 1 is lesion formation:

Answer 24

Lipoprotein trapping in the subendothelial matrix

Question 25

Step 2 in lesion formation:

Answer 25

Lipoprotein aggregation and monocyte migration

Question 26

Step 3 in lesion formation:

Answer 26

Foam cell formation

Question 27

Step 4 in lesion formation:

Answer 27

Formation of fibrous plaque

Question 28

Step 5 is lesion formation:

Answer 28

Plaque rupture

Question 29

The intersection of inflammation and lipid metabolism modulates atherosclerosis and provides potential targets for ___ ___

Answer 29

Therapeutic manipulation

Question 30

___ ____ can improve cardiovascular risk factors

Answer 30

Weight loss