atherosclerosis Flashcards

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1
Q

what occurs to the intimal layer of blood vessels as we age?

A

there is intimal thickening and a recruitment of smooth muscle cells
phenotype is proliferative so ECM is elaborated

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2
Q

atherosclerosis

A
  • fibrofatty lesions in the tunica media
  • protrude into the vascular part and the tunica media
  • cause weakening of the tunica media to create aneurysms
  • cause obstruction in the vascular area to cause ischemia or infarction
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3
Q

what are the sources of smooth muscle cells that infiltrate the tunica intima to cause intimal thickening?

A
  • from the tunica media
  • from smooth muscle precursors in blood that infiltrate the weakened endothelial layer and begin thickening the intimal layer in a proliferative fashion
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4
Q

Fatty streaks

A
  • precursor to atheroma seen as a red streak with sudan red stain
  • no fibrosis yet
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5
Q

About how many americans die every year due to ischemic heart disease?

A

500,00

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6
Q

What percentage of decrease have we seen since 1963 in regard to death by IHD and stroke?

A

IHD- 50%

stroke- 70%

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7
Q

incidence of ischemic heart disease increases by how much between the age of 40-60

A

5 fold

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8
Q

How are mens and womens risk for MI different?

A

men’s risk are higher until women hit menopause. after, their risk increase until it is even at age 70-80

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9
Q

Hyperlipidemia and cholesterol guidelines

A

total cholesterol 200

triglycerides 45

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10
Q

how is smoking related to MI?

A

-smoking one pack a day or more increases your risk of ischemic heart disease by 200%

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11
Q

how is diabetes mellitus related to MI?

A

MI risk is twice as high in diabetics compared to nondiabetics
100 fold increase rise with gangrene of lower limb

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12
Q

how is elevated C reactive protein related to MI?

A
  • make endothelial cells prothrombotic

- endothelial cells also become more adhesive to WBC =inflammation

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13
Q

what events occur in the pathogenesis of atherosclerosis?

A

1) injury to endothelial layer of the blood vessel
2) endothelial dysfunction- becomes more permeable to monocytes-leukocytes and platelets, LDL begins to accumulate in the subendothelial dept
3) plt and macrophages and endothelial cells begin to recruit smooth muscle to help heal that intimal layer (from blood stream and tunica media)
- macrophages activated and engulf LDL molecules
4) Macrophages further become engorged with oxidized LDL = FOAM CELLS, also have smooth muscle cells also engorge with oxidized LDL and look foamy but are not the true foam cells
5) SM is proliferative and forms ECM along with collagen that forms a collagen cap.
- also get accumulation of lipid in the center and all are referred to as a FIBROFATTY ATHEROMA

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14
Q

what does nitric oxide normally do in blood vessels? How does that change when there is damage to the endothelial layer of the vessel?

A
  • it prevents adhesion of leukocytes and platelets to the endothelial layer of the vessel
  • when there is damage to the endothelium, there is less NO entering so there is an increase in plt adhesion and leukocyte adhesion
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15
Q

what are the top 3 coronary arteries that are narrowed and thrombosed by ischemic heart disease?

A

LAD
RCA
Circ

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16
Q

wavefront phenomenon of myocardial necrosis

A

when there is blockage, there is ischemia that causes cell death that begins in the inner layer of the myocardium (subendocardium) and works its way out to the subepicardium in a wave
-this is so because inner layer has a greater oxygen demand

17
Q

what is an early microscopic find of a cerebral infarct?

A

-eosinophillic neurons

18
Q

A couple days after infarction, what do neutrophils do?

A

-they infiltrate the infarcted area and clean up the debris

19
Q

Ten days after a cerebral infarct, what can we see microscopically?

A

presence of macrophages and reactive gliosis (scarring of CNS)