Atherosclerosis Flashcards

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1
Q

When does intimal thickening happen

A

because of injury and aging

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2
Q

Atherosclerosis

A

hardening of arteries. Specifically fibrofatty lesion in tunica intima which protrude into vascular lumen, weaken tunica media

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3
Q

What does obstruction of vascular lumen lead to

A

ischemia, infaration - which can lead to development of aneurysm

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4
Q

How does smooth muscle get into the sub-endothelial compartment

A
  • from tunica media through fenestrations

- precursor cells in blood that squeeze between damage in injury

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5
Q

How do foam cells form

A
  • LDL in subendothelial compartment
  • becomes oxidized
  • phagocytosed by macrophages and smooth muscle cells
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6
Q

fatty streaks

A

early changes to tunica intima, but not to level of atheroma

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7
Q

How can you tell if it’s a fatty streak (microscopic view)

A

thickening of intima
separation from internal elastic membrane
foam cells

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8
Q

Atherosclerotic lesions

A

dark deposits that become calicified, are non reversible

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9
Q

Non-modifiable risks for atherosclerosis

A

40-60 yo
family history
male
genetic abnormalities

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10
Q

Modifiable risks for atherosclerosis

A
hyperlipidemia
cigarettes
c-reactive protein
hypertension
diabetes
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11
Q

Normal total cholesterol

A

<200 mg/dl

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12
Q

Normal LDL

A

<130 gm/dl

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13
Q

Normal HDL

A

> 45 mg/dl

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14
Q

Normal triglycerides

A

<150 mg/dl

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15
Q

How does c-reactive protein put you are more risk

A
  • endothelial cells become prethrombotic
  • increase their adhesiveness for WBC
  • causes inflammation of wall vasculature
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16
Q

What has to happen to cause endothelial cell dysfunction

A

some injurious event - can be chronic endothelial injury like hyperlipidemia, hypertension, etc

17
Q

Endothelial dysfunction

A

increased permeability, leukocyte adhesion

18
Q

Key events of atherosclerosis

A

1) Chronic endothelial injury
2) Endothelial dysfunction
3) Smooth muscle recruitment to intima. Macrophage activation
4) Macrophages and smooth muscle cells engulf lipid
5) Smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid

19
Q

Foam cells

A

smooth muscle cells or macrophages. Macrophages predominant form

20
Q

Role of NO in adhesion

A

prevent adhesion of leukocytes to endothelium, reduce adhesion of platletes

21
Q

Frequencies of critical stenosis of cornoary arteries (most to least common)

A

1) anterior interventricular branch of left coronary artery
2) Right coronary artery
3) Circumflex branch of left coronary a

22
Q

Wavefront phenomenon of necrosis

A

necrosis happens inner layer of myocardium then outer myocardium

23
Q

What does triphenyltetrazolium chloride do

A

stains viable cells red and nonviable white

24
Q

What are the consequences of myocardial ischemia and infarction

A

arrythmia
acute rupture of cardiac wall of IV septum
rupture of papillary muscles
ventricular aneurysm

25
Q

Order of events in cerebral infarction

A

1) Intense eosinophilia (12-24 hours)
2) neutrophils invade to clean up damage
3) macrophages come in and cause proliferation of glial cells (10 days)