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CV <3 > Lecture 8: Atherosclerosis & CHD > Flashcards

Lecture 8: Atherosclerosis & CHD Flashcards

1
Q

What are the layers of an artery?

A
  • Tunica Intima: Elastic
  • Endothelium: Inner lining of the tunica intima and the Thromboresistant layer
  • Tunica Media: Smooth
  • Tunica Externa/Adventitia
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2
Q

Define atherosclerosis.

A
  • Athero = soft, lipid-rich material in the center of atheroma.
  • Sclerosis = scarring, referring to the connective tissue in a plaque.
  • A pathological process that results in coronary, cerebral and peripheral artery disease.
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3
Q

What are the first signs of atherosclerosis?

A

Fatty streaks within the arterial walls.

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4
Q

What are the 6 histologic steps to atherosclerosis development?

A
  1. Fatty streak formation
  2. Fibrous cap formation
  3. Disruption of the vasa vasorum
  4. Proliferation of the fibrous plaque
  5. Development of an advanced lesion
  6. Intraplaque hemorrhage
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5
Q

What makes fatty streaks?

A

Accumulation of foam cells and ECM, leading to lipid accumulation.

Specifically biglycan is the protein that traps LDL and VLDL in coronary arteries.
The foam cells can also trap T lymphocytes.

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6
Q

Why does a fibrous cap develop?

A
  • If a plaque appears and remains stable.
  • It will wall it off with a collagen tissue layer.

Makes the plaque even more stable ):

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7
Q

How is the vasa vasorum disrupted by a plaque?

A
  • Expansion of plaque
  • Rupture of plaque vasculature, extending to the arterial wall.
  • Microvascular hemorrhage and occur and neovascularization will occur.
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8
Q

Why does proliferation of the fibrous plaque occur?

A

Accumulation of connective tissue

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9
Q

What characterizes an advanced lesion?

A
  • Necrotic, lipid-rich core.
  • Calcified regions
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10
Q

What is positive remodeling?

A

Increased vessel size in early CHD to compensate for loss of lumen. (Leads to unstable angina)

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11
Q

What is negative remodeling?

A

Vessel shrinks due to obstructive plaques, leading to stable angina.

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12
Q

What is the critical event in atherosclerosis?

A
  • Intraplaque hemorrhage due to plaque neovascularization.
  • The plaque will rupture and lead to ischemic events.
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13
Q

What factors contribute to the pathogenesis of atherosclerosis?

A
  1. Endothelial dysfunction
  2. Inflammatory & Immunologic factors
  3. Plaque rupture or erosion
  4. Risk factors for development of disease
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14
Q

What is the primary underlying etiology of endothelial vasodilation dysfunction?

A

Errors in nitric oxide, which is precipitated by oxidized LDL.

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15
Q

How can we improve endothelial vasodilator dysfuction?

A
  1. Correct HLD via diet/statins
  2. ACEi if HTN present
  3. (ehhhh) High dose of antioxidants (Vit C, flavonoids)
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16
Q

What is endothelial dysfunction associated with in terms of risk factors?

A
  • Hypercholesterolemia
  • Diabetes
  • HTN
  • Cigarette smoking
17
Q

What causes chronic inflammation and active inflammation in terms of atherosclerosis?

A
  • Chronic: Stable plaques
  • Active: unstable & ruptured plaques
18
Q

Eating of what by macrophages makes them release inflammatory stuff?

A

Eating oxidized LDL

19
Q

When does atherosclerosis tend to become symptomatic in terms of stenosis %?

A

70-80% usually.

20
Q

What occurs as a result of a silent plaque rupture/erosion?

A
  • Increased plaque burden
  • Vessel stenosis
  • Negative remodeling
21
Q

What is the #1 cause of death in the US and worldwide!

A

CHD/CAD :(

22
Q

What are the CHD risk equivalents?

A
  • Clinical CHD
  • Symptomatic carotid artery disease
  • Peripheral arterial disease (PAD)
  • AAA
  • DM
  • CKD
23
Q

What are the modifiable risk factors?

A
  • Cigarette smoking
  • Dyslipidemias
  • HTN
  • DM
  • Obesity
  • Sedentary lifestyle
24
Q

What are the 3 unmodifiable risk factors?

A
  1. Premature CHD in 1st degree relatives (males younger)
  2. Age (males younger)
  3. Male
25
Q

What gender is high triglycerides a risk factor for CHD in?

A

Females

26
Q

What vitamin deficiency is elevated homocysteine seen in?

A

Low B6, B9, B12

27
Q

How does smoking promote atherosclerosis?

A
  • Increasing platelet adhesiveness
  • Raised endothelial permeability
  • SNS stimulation by nicotine
28
Q

What are the 4 categories of people that would benefit from statin use?

A
  1. Clinical ASCVD
  2. LDL >= 190
  3. 40-75 w/ DM and LDL 70-189 w/o clinical ASCVD
  4. 40-75 w/o DM or clinical ASCVD with LDL 70-189 w/ 10 year risk >= 7.5%

3 and 4 are essentially people who dont meet the previous indication above them.

29
Q

What are the two high intensity statins?

A
  • Atorvastatin 40/80
  • Rosuvastatin 20/40
30
Q

How does hypertension cause plaque formation?

A

Thickening and stiffening of heart muscle results in endothelial injury.

31
Q

What therapy is common in postmenopausal women that may result in increased ASCVD risk?

A

Hormone replacement therapy.

Natural estrogen is beneficial at preventing ASCVD.

32
Q

What age is considered premature CHD for 1st degree relatives?

A
  • Males < 55
  • Females < 65
33
Q

When is AAA screening recommended?

A

65-75 males with prior smoking history via US.

34
Q

What recommendation is not always recommended in terms of HTN management?

A

ASA 81mg daily is only for people who are not at an increased risk for bleeding.

C recommendation only.

35
Q

When should DM screening be done?

A

35-70 who are overweight or obese.

36
Q

What USPSTF recommendation is an A for CVD risk prevention?

A

Tobacco cessation!

37
Q

What are the biggest things that affect ASCVD risk?

A
  • Smoking
  • DM
  • HDL levels

CV <3 (25 decks)

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