Cardio-path- atheroscelosis

Question 1

What is the fundamental basis for the vast majority of vascular disorders.?

Answer 1

Injury to the vessel wall—and in particular to endothelial cells

Question 2

Blooc vessel Endotherlial Cell injury/dysfunction may contribute to pathologic processes including thrombosis, hypertensive lesions and atherosclerosis.

Answer 2

vascular

Question 3

Vascular injury leading to Endothelial Cell loss or dysfunction stimulates growth of what?

Answer 3

smooth muscle cells, extra-cellular matrix synthesis, and thickening of the vascular wall.

Question 4

As a result of vascular injury, smooth muscles cells migrate to the ?

Answer 4

intima -SMCs then proliferate, synthesize ECM, forming a neo-intima covered by an intact EC layer.

Question 5

Though Smooth muscle cell proliferation and matrix synthesis can help to repair a damaged vessel wall, it can also cause what negative effect?

Answer 5

lead to luminal occlusion.

Question 6

What ) is characterized by intimal lesions called atheromas (atheromatous/atherosclerotic plaques) that impinge on the vascular lumen, and can rupture to cause sudden occlusion?

Answer 6

atherosclerosis

Question 7

What pathology underlies the pathogenesis of coronary, cerebral, and peripheral vascular disease, and causes more morbidity and mortality in the Western world than any other disorder!*?

Answer 7

atherosclerosis

Question 8

Raised lesions composed of soft friable (crumbly) lipid cores covered by fibrous caps:

Answer 8

Atheromatous plaques

Question 9

Thickness of the intimal lesions also may be sufficient to decrease perfusion of the , leading to ischemia and changes in the ECM caused by subsequent .

Answer 9

media, inflammation.

Question 10

Subsequent tunica media hypoxia and inflammation from thick intimal atherosclerotoc plaques can weaken the media, and lead to the formation of?

Answer 10

aneurysms

Question 11

What are constitutional risk factors?

Answer 11

non-modifiable

Question 12

What is the most important independent risk factor for atherosclerosis?

Answer 12

Family history

Question 13

Most familial risk is not related to , but related to multifactorial traits, including hypertension, and, diabetes

Answer 13

familial hypercholesterolemia

Question 14

Familial hypercholesterolemia is a “receptor disease” caused by of-function mutations in the gene encoding the receptor, which is involved in the transport and metabolism of .

Answer 14

loss; LDL; cholesterol.

Question 15

Describe the LDL receptor disesase familial hypercholesterolemia?

Answer 15

loss-of-function mutations in the gene encoding the LDL receptor

impair the intracellular transport and catabolism of LDL, resulting in accumulation of LDL cholesterol in the plasma.

elevated levels of cholesterol induce premature atherosclerosis and greatly increase the risk of MI.

Question 16

Atherosclerosis is considered silent until about what age?

Answer 16

middle age or later

Question 17

Which group of women are protected against atherosclerosis?

Answer 17

premenopausal women

Question 18

Hyperlipidemial is a major risk factor, why?

Answer 18

The main cholesterol component associated with increased risk is low-density lipoprotein (LDL) cholesterol (“bad cholesterol”); LDL distributes cholesterol to peripheral tissues.

Question 19

How does the liver get rid of excess cholesterol?

Answer 19

through the bile

Question 20

HTN can increase the risk of ischemic heart disease by %

Answer 20

60

Question 21

How does having diabetes affect your risk of MI?

Answer 21

the incidence of myocardial infarction is twice as high in diabetics vs. non-diabetics.

Question 22

Smoking can the risk of IHD related mortality.

Answer 22

double

Question 23

What is the response-to-injury hypothesis views atherosclerosis?

Answer 23

chronic inflammatory response of the arterial wall to endothelial injury.

Question 24

the beginning of the pathogenesis of atherosclerosis begins with endotherial injury, which results in endotherlial - leading to increased , leukocyte , and thrombosis.

Answer 24

dysfunction; permeability; adhesion

Question 25

What are the 3 suspected triggers of early atheromatous lesions?

Answer 25

HTN, hyperlipidemia, and toxins from cigarette smoke.

Question 26

What type of lipoprotein accumulates to the vessel wall during plaque formation?

Answer 26

mainly oxidized LDL and cholesterol crystals

Question 27

Is there platelet adhesion in the pathogenesis of atherosclerosis?

Answer 27

yes

Question 28

Monocytes also adhere to endothelium in the atherosclerotic process, migrate to the , and differentiate into and then cells.

Answer 28

intima; macrophages, foam

Question 29

Foam cells (macrophages with stuff inside) accumulate whiich can then release inflammatory .

Answer 29

lipids; cytokines

Question 30

factors released from activated platelets, macrophages, and vascular wall cells lead to the recruitment of ?

Answer 30

smooth muscle cells to the intima

Question 31

What contributes to the initiation, progression, and complications of atherosclerotic lesions?

Answer 31

inflammation

Question 32

Early in atherogenesis dysfunctional express adhesion molecules that promote adhesion, in particular, monocytes and T cells which migrate into the intima under the influence of .

Answer 32

endothelial cells; leukocyte; chemokines

Question 33

What leads to the "fatty streak" (earliest atherosclerotic lesion) in the vessel?

Answer 33

SMC Proliferation and Matrix Synthesis

Question 34

What begin as minute yellow, flat macules that coalesce into elongated lesions, 1 cm or more in length?

Answer 34

fatty streaks note: the fatty streaks are highlighted in red

Question 35

Fattty streaks are composed of lipid-filled foamy macrophages but are only minimally raised and **do/do not** cause any significant flow disturbance.

Answer 35

do not

Question 36

Answer 36

Foamy cells (macs with lipids) in intima

Question 37

What are the 2 key features of atherosclerotic plaques?

Answer 37

**intimal thickening and lipid accumulation** They are white to yellow raised lesions; they range from 0.3 to 1.5 cm in diameter but can coalesce to form larger masses.

Question 38

Answer 38

**Thrombus** superimposed on **ulcerated plaque**s gives a **red-brown color.**

Question 39

Describe the morphology of an atherosclerotic plaque?

Answer 39

patchy, usually involving only a portion of any given arterial wall. note: the image is a trichrome stain blue is fibrosis C is cholesterol

Question 40

In descending order of severity, atherosclerosis involves mostly which 5 types of arteries?

Answer 40

1. abdominal aorta, 2. the coronary arteries, 3. the popliteal arteries, 4. the internal carotid arteries, 5. the vessels of the circle of Willis.

Question 41

What are the 3 main components of the atherosclerotic plaques?

Answer 41

(1) **Cells**, including SMCs, macrophages, and T cells; (2) **ECM**, including collagen, elastic fibers, and proteoglycans; and (3) Intracellular and extracellular **lipid.** **note: the red circles surround cholesterol (lipids)**

Question 42

Atheromas generally over time. • They also often undergo _._

Answer 42

enlarge; calcification note: calcified plaque

Question 43

Which vessel has the ulcerated plaque and which is occluded by a clot?

Answer 43

left image- rupture of plaque right image- clot or thrombus

Question 44

Which size of arteries are most likely to develop atherosclerosis?

Answer 44

**Large elastic arteries** (eg, aorta, carotid, and iliac arteries), and **large- and mediumsized muscular arteries** (eg, coronary, renal, and popliteal arteries) are the vessels most commonly involved.

Question 45

What are some major consequences of peripheral vascular disease as it concerns the extremities?

Answer 45

gangrene of extremities)

Question 46

ischemia of the heart, brain, kidneys, and lower extremities. • Myocardial infarction (heart attack), cerebral infarction (stroke), aortic aneurysm, and peripheral vascular disease (gangrene of extremities) are the major clinical consequences of?

Answer 46

atherosclerosis

Question 47

What is acute plaque change?

Answer 47

plaque rupture causes mechanical obstruction and exposure of substances that promote platelet activation and thrombus generation

Question 48

What % of a vessel needs to be considered **critical stenosis**, where tissue demand exceeds supply?

Answer 48

70% occlusion

Question 49

What is stable angina?

Answer 49

pts have adequate cardiac perfusion, but with exertion, demand exceeds supply, and chest pain develops because of cardiac ischemia due to atherosclerosis

Question 50

What are some effects of chronic aterial hypoperfusion due to atherosclerosis?

Answer 50

bowel ischemia, sudden cardiac death, chronic IHD, ischemic encephalopathy, and intermittent claudication (ischemic leg pain). -narrowed popliteal arteries

Question 51

What typically triggers thrombosis?

Answer 51

Acute Plaque Change (plaque erosion or rupture)

Question 52

Plaques that have a particularly **high risk of rupturing**, contain large numbers of **foam cells** and **abundant extracellular lipid**, have **thin fibrous caps** containing f**ew smooth muscle cells**, and contain **clusters of inflammatory cells** are considered?

Answer 52

vulnerable plaques