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Cardiovascular > Atherosclerosis and CHD > Flashcards

Atherosclerosis and CHD Flashcards

1
Q

What is the innermost layer of the artery?

A

Tunica intima

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2
Q

What does the tunica intima consist of?

A

Endothelium, subendothelial layer, and elastic membrane

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3
Q

What is the endothelium?

A
  • Inner lining of tunica intima
  • Thromboresistant layer between blood and thrombogenic subendothelial layer
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4
Q

What is the function of the endothelium?

A
  • Modulates tone, growth, hemostasis, and inflammation throughout circulatory system
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5
Q

What is the middle layer of the artery?

A

Tunica media

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6
Q

What does the tunica media consist of?

A

Smooth muscle and an elastic membrane

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7
Q

What is the outer layer of an artery?

A

Tunica externa/adventitia

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8
Q

What is the tunica externa/adventitia composed of?

A

Extracellular matrix with fibroblasts, mast cells, and nerve terminals

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9
Q

What is the basic function of arteries?

A

Carry oxygenated blood throughout the body

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10
Q

What is the function of the tunic intima?

A

Creates pathway for oxygenated blood to be carried to site of perfusion

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11
Q

What is the function of the tunica media?

A

Comprised of smooth muscle that dilate and constrict in response to cardiac output needs

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12
Q

What is the function of the tunica externa/adventitia?

A

Connects arteries to other structures in the body

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13
Q

What is atherosclerosis?

A
  • Pathologic process that causes disease of the coronary, cerebral, and peripheral arteries
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14
Q

How does atherosclerosis begin?

A

With development of fatty streaks within arterial walls, can begin as early as childhood

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15
Q

What are the 6 histologic steps in the development of atherosclerosis?

A
  • Fatty streak formation
  • Fibrous cap development
  • Disruption of the vasa vasorum
  • Proliferation of the fibrous plaque
  • Development of an advanced lesion
  • Intraplaque hemorrhage
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16
Q

What causes the development of a fatty streak?

A
  • Thickening of intima due to accumulation of foam cells and extracellular matrix (smooth muscle can also deposit)
  • Lipids accumulate causing fatty streak
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17
Q

What can the fatty streak contain?

A

Foam cells, extracellular matrix, smooth muscle cells, T lymphocytes
* Coronary arteries have biglycan and can trap VLDL and LDL

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18
Q

What are the steps in fatty streak formation?

A
  • Vascular injury precipitates monocyte binding to endothelium
  • Monocytes cross endothelium to become macrophages
  • Macrophages eat LDL and become foam cells
  • T cells release cytokines which activate macrophages and cause smooth muscle cells to proliferate
  • Smooth muscle cells move to subendothelial space, producing collagen and taking up LDL, adding to foam cell accumulation
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19
Q

If the plaque remains stable, what will form?

A

A fibrous cap

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20
Q

What is a fibrous cap?

A
  • A dense, collagen-based layer of connective tissue that covers the lipid core of an atherosclerotic plaque
  • Provides stability to plaque
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21
Q

What is the vasa vasorum?

A
  • Micro-vessels originating from tunica adventitia
  • Provide oxygen and nutrients to outer layer of arterial wall
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22
Q

What happens with disruption of the vasa vasorum?

A
  • As atherosclerotic plaques expand, they acquire their own microvasculature
  • Plaque vasculature is thin-walled, leading to increased risk of microvascular hemorrhage and progression of atherosclerosis
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23
Q

What happens during proliferation of the fibrous plaque?

A
  • Connective tissue accumulates from the fatty streak
  • Connective tissue consists of lipid containing smooth muscle and extracellular lipid pool
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24
Q

What happens in the development of advanced lesions?

A
  • Necrotic lipid-rich core and calcified regions develop over time
  • Coronary arteries remodel in response to atheroma formation
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25
Q

What is positive remodeling of advanced lesions?

A
  • Increased vessel size early in CHD to compensate for plaque accumulation in an effort to reduce lumen loss
  • Alters arterial function leading to symptoms of unstable angina (@rest/seated/exercise)
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26
Q

What is negative remodeling?

A
  • Vessel shrinkage resulting in obstructive plaques that lead to stable angina
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27
Q

What happens during the intraplaque hemorrhage stage of atherosclerosis?

A
  • Due to plaque neovascularization
  • leads to accelerated plaque progression, instability, and ischemic vascular events
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28
Q

What factors contribute to the development of atherosclerosis and its complications?

A
  • Endothelial dysfunction
  • Inflammatory and immunologic factors
  • Plaque rupture or erosion
  • Risk factors for development of disease
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29
Q

What is the initial step in the pathogenesis of atherosclerosis?

A

Endothelial vasodilator dysfunction d/t loss of endothelial-derived nitric oxide

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30
Q

What precipitates endothelial vasodilator dysfunction?

A

oxidized LDL

31
Q

What is associated with endothelial dysfunction?

A
  • Hypercholesterolemia
  • Diabetes
  • Hypertension
  • Cigarette smoking
32
Q

What are ways to improve endothelial vasodilator dysfunction?

A
  • Correct HLD
  • ACEI if HTN present
  • High doses of antioxidants (vitamin C, flavonoids)
33
Q

How does inflammation impact atherosclerosis?

A
  • Macrophages eat oxidized LDL
  • Releases inflammatory substances, cytokines, and growth factors leading to plaque proliferation
34
Q

What does chronic inflammation lead to?

A

Stable plaques

35
Q

What does active inflammation lead to?

A

Unstable and ruptured plaques

36
Q

Atherosclerosis is usually asymptomatic until the plaque causes what % stenosis of the vessel lumen?

A

70-80

37
Q

Once the plaque causes 70-80% stenosis of the lumen, what occurs?

A

Blood flow impediment and symptoms of angina pectoris

38
Q

What are the 2 processes that atherosclerotic plaques can progress via?

A

Chronic and acute

39
Q

What happens in chronic atherosclerotic plaque progression?

A

Slow luminal narrowing

40
Q

What happens in acute atherosclerotic plaque progression?

A

Rapid luminal narrowing with plaque hemorrhage and/or luminal thrombosis

41
Q

Plaque erosion can occur in the absence of rupture when what happens?

A

endothelium is missing at plaque site

42
Q

What does it mean for a plaque rupture or erosion to be silent?

A
  • No acute symptoms
  • Repeated ruptures and thrombosis followed by wound healing
  • Leads to increased plaque burden, progression of vessel stenosis, and negative arterial remodeling
43
Q

What are the effects of atherosclerosis?

A
  • Coronary arteries: MI, angina
  • CNS: stroke, TIA
  • Periphery: claudication, limb ischemia/poor healing, aneurysms
  • Renal arteries: RAS
  • GI: mesenteric ischemia
44
Q

Why is it important to manage atherosclerosis?

A
  • Major cause of death
  • # 1 cause of death in US and worldwide
  • 1 person dies every 33 sec from CVD
45
Q

What is the epidemiology of atherosclerosis?

A
  • Prevalence increases with age
  • Average ACS presentation is 68 yrs
46
Q

How do 40-50% of adults in US present with their first sign of heart disease?

A

Sudden death

47
Q

in 2020, _____ deaths in the US was due to CHD

A

1 in 5

805,000 individuals in the US suffer from an MI annually with 1 in 5 heart attacks being silent

48
Q

From 2018-2019 it cost more than _______ billion per year to care for heart disease in the US

A

$239

This is projected to reach $1.1 trillion by 2035

49
Q

What race of ethnic groups has the highest % of deaths due to atherosclerosis?

A

White
Native hawaiian or pacific islander
Black

50
Q

What are CHD risk equivalents?

A
  • Clinical coronary heart disease (CHD)
  • Symptomatic carotid artery disease
  • Peripheral arterial disease
  • Abdominal aortic aneurysm
  • Diabetes mellitus
  • Chronic kidney disease
51
Q

What are modifiable risk factors for atherosclerosis?

A
  • Cigarette smoking
  • Dyslipidemias
  • HTN
  • DM
  • Obesity
  • Sedentary lifestyle
52
Q

What are unmodifiable risk factors for atherosclerosis?

A
  • Premature CHD in 1st degree relative <55 men, <65 women
  • Age >45 men, >55 women
  • Male sex
53
Q

What are additional risk factors for atherosclerosis/CHD?

A
  • High serum levels of CRP
  • High triglycerides
  • Sleep apnea
  • Stress
  • Persistent heavy alcohol use
  • Elevated homocysteine levels
54
Q

How much does cigarette smoking increase risk of heart disease?

A

2-4x

54
Q

On average, smokers die ______ than nonsmokers

A

10 years earlier

55
Q

The #1 preventable cause of death and illness in the US. How much can stopping it reduce the risk of CHD?

A

Cigarette smoking
50%

56
Q

How does cigarette smoking impact severity of atherosclerosis?

A

Higher risk, severity, and extent of atherosclerosis in smokers
Also higher risk of IHD and sudden cardiac death

57
Q

How does smoking promote atherosclerosis?

A
  • Increases platelet adhesiveness
  • Raises endothelial permeability
  • SNS stimulation by nicotine
58
Q

Why is hypercholesterolemia and atherosclerosis/CHD directly proportional?

A
  • Atherosclerotic plaques contain cholesterol and cholesterol esters
  • Risk increases progressively with higher LDL and declines with higher HDL
  • Populations with hypercholesterolemia have higher mortality from CHD
  • Dietary regulation and administration of cholesterol-lowering drugs have beneficial effect on reducing the risk of CHD
59
Q

What groups benefit from statins?

A
  • Individuals with clinical ASCVD
  • Individuals with primary elevations of LDL-C>190 mg/dL
  • Individuals 40-75 yrs with DM and LDL-C 70 to 189 mg/dL w/out clinical ASCVD
  • Individuals w/out clinical ASCVD or DM who are 40-75 yrs with LDL-C 70-189 mg/dL and have an estimated 10-year ASCVD risk of >7.5%
60
Q

What are the high intensity statins?

A

Atorvastatin 40-80 mg
Rosuvastatin 20-40 mg

61
Q

Look at the flowchart for primary prevention with statins and try to figure it out

A

:(

62
Q

What are the moderate intensity statins?

A

Atorvastatin 10-20 mg
Rosuvastatin 5-10 mg
Simvastatin 20-40 mg
Pravastatin 40-80 mg
Lovastatin 40 mg ER
Fluvastatin 80 mg
Pitavastatin 2-4 mg

63
Q

How is hypertension related to atherosclerosis?

A
  • Causes mechanical injury to arterial wall
  • Increases heart’s workload causing heart muscle to thicken and become stiff
  • Endothelial injury from persistent high BP leads to plaque formation as per response to injury hypothesis
64
Q

How is DM related to atherosclerosis?

A
  • Ath develops at an early age in people with both IDDM and NIDDM
  • Diabetes increases risk of heart disease and stroke
  • At least 65% of people with diabetes die of some form of heart or blood vessel disease
  • Considered CHD risk equivalent
65
Q

How is risk for atherosclerosis/CHD different for men?

A

Higher incidence and severity
Presents earlier in life
Risk increases after age 45

66
Q

How is risk for atherosclerosis/CHD different for women?

A
  • Lower incidence in women, especially premenopausal
  • Risk increases after 55 yrs although still lower than men’s despite increased risk post menopause
  • Postmenopausal women on HRT have increased risk of CV events
67
Q

Fully-developed atheromatous plaques usually appear when?

A

40s+

68
Q

What genetic and familial factors are related to CHD and atherosclerosis?

A
  • Increased risk of CHD with family history of premature CHD
  • CHD in male first degree relative <55 years; CHD in female first degree relative <65 years
  • Hereditary genetic derangements of lipoprotein metabolism predispose to high blood lipid level and familial hypercholesterolemia
  • Familial predisposition to atherosclerosis may be related to other risk factors like diabetes, hypertension, and hyperlipidemia
  • Children of parents with heart disease are more likely to develop it themselves
69
Q

What racial and ethnic factors influence atherosclerosis and CHD?

A
  • African americans have more severe high BP than caucasians
  • Heart disease risk is also higher among mexican americans, american indians, native hawaiians, and some asian americans
70
Q

What goes into calculating the 10 year ASCVD risk?

A
  • Age and gender
  • Diabetes
  • Race
  • Smoking
  • Cholesterol
  • Blood pressure
71
Q

What grade is statin use in a patient with 1 or more CV risk factors and 10-year CVD risk of 10% or greater by USPSTF?

A

B

72
Q

What grade is the USPSTF recommendation that adults with CVD risk are offered behavioral counseling interventions to promote a healthy diet and physical activity?

A

B

73
Q

What grade is the USPSTF recommendation that patients are advised to quit tobacco use?

A

A

Cardiovascular (17 decks)

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