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1

what are the plaques of athleroscelorosis made of

made of lipids and cholesterol

2

the soft yellow core of a lipid is mostly made out of

cholesterol and cholesterol esters

3

what are 3 effects of plaques

mechanical obstruction of blood flow

rupture leading to thrombosis

weaken the arterial media leading to aneurism formation

4

what percentage of deaths are related to athleoscleorosis

half

5

what are 3non modifiable risk factors

age
gender
genetics

6

modifodibile risk factor

cigarettes
obesity
HTN
DMII
hyperlipidemia
hypercholesterima

7

LDL good or bad

bad

8

Function of LDL

takes choldesterol to peripheral tissues

9

functon of HDL

transports cholesterol from tissue to the liver

10

Do we want a high or low HDL

High

11

medial portion of arteriery has what kind

endothelial cells

12

What is the initial event in terms of development of a plaque is due to

endothelial injury

13

what are some causes of endothelial cell injury

HTN
Cigarette smoking
hyperlipidemia

14

what does hyperlipidemia or cholesterol spikes specifically do and how does it affect things

it increases local o2 free radical production , this causes impairment in endothelial function

15

what happens in response to the endothelial cell damage

smooth muscle cell recruitment proliferation

16

what do dysfunctional endothelial cells express

adhesion molecules that promote leukocyte adhesion this attracts additional inflammatory cells such as monocytes and macrophages

17

what do activated macrophages prodoces

reactive 02 species which promote growth factors cause further LDL oxidation

18

what happens when plaques rupture

thrombus formation

19

what do fatty streaks develop into

plaques

20

what are the 3 possible outcomes of a plaque

1. aneruysm and rupture

2. occlusion by thrombus

3. critical stenosis

21

at what percent of occlusion do we see clinical manifestations

70%

22

the rupturing or fissuring of a plaque that moves in to fill the lumen is called

thrombosis

23

abdominal aortic anuerisms are most likely caused by

atherosclerosis

24

what are 4 clinical consequences of an athlosclerotic plaque

1. MI
2. Stroke
3. Abdominal aortic aneruysim

4. Peripheral vascular disease (commonly seen in DM)

25

what determines the risk for plaque rupture

fiberous cap

26

what kind of cells are commonly found in plaques

microphages filled lipid called foam cells

27

where is the most common location for athelosclerosis

abdominal aorta

28

why do plaques tend to form where arteries bifurcate

because at this point there is a lot of turbulent flow

29

what is responsible for breaking down the fibrous cap of an atheroma?

Matrix metalloproteinases

30

What is the function of PDGF?

PDGF is released at atherosclerotic lesion sites by platelets and macrophages and stimulates proliferation and migration of smooth muscles cells in the tunica intima, an important step in atherosclerosis that occurs in response to endothelial injury.