Atherosclerosis Flashcards
(55 cards)
1
Q
CHD Risk Equivalents (6)
A
- Clinical coronary heart disease (CHD)
- Symptomatic carotid artery disease
- Peripheral arterial disease (PAD)
- Abdominal aortic aneurysm (AAA)
- Diabetes mellitus
- Chronic kidney disease (CKD)
Pts without known CHD have risk of CV events comparable to pts WITH established CHD
2
Q
Atherosclerosis / CHD MODIFIABLE Risk Factors
A
- Cigarette smoking
- Dyslipidemias (↑LDL or ↓HDL)
- HTN
- DM
- Obesity
- Sedentary Lifestyle
3
Q
Atherosclerosis / CHD UNMODIFIABLE Risk Factors
A
- Premature CHD in 1st degree relative (age < 55 in men, < 65 in women)
- Age (men ≥ 45 y/o, women ≥ 55 y/o)
- Male sex
4
Q
Other Risk Factors for Atherosclerosis / CHD
A
- High serum levels of C-reactive protein (CRP)
- High Triglycerides (esp in women)
- Sleep apnea
- Stress
- Persistent Heavy Alcohol Use
- Elevated Homocysteine levels
5
Q
- Innermost layer of an artery
- Consists of the endothelium, subendothelial layer, and elastic membrane
Which layer of the artery is this
A
tunica intima
6
Q
- Inner lining of the tunica intima
- Continuous, thromboresistant layer between blood and potentially thrombogenic subendothelial tissue
which artery layer is this
A
endothelium
7
Q
3 actions/responsiblities of the endothelium of an artery
A
- Modulates tone
- growth
- hemostasis and inflammation throughout circulatory system
8
Q
- Middle layer of an artery
- Consists of smooth muscle cells and an elastic membrane
which layer of the artery is this
A
tunica media
9
Q
- Outer layer of an artery
- Composed of extracellular matrix with fibroblasts, mast cells and nerve terminals
which layer of the artery is this
A
Tunica Externa / Adventitia
10
Q
how do arteries carry oxygenated blood throughout the body?
Arterial Physiology
A
- Tunica intima creates the pathway for oxygenated blood to be carried to the site of perfusion
- Tunica media is comprised of smooth muscle that dilates and constricts in response to cardiac output needs
- Tunica externa / adventitia connects arteries to other structures in the body
11
Q
What is Atherosclerosis?
A
- A pathologic process that causes disease of the coronary, cerebral, and peripheral arteries
- Begins with the development of “fatty streaks” within arterial walls
12
Q
6 Histologic Steps 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
13
Q
The initial histologic step in development of atherosclerosis occurs as a result of: (3)
A
- Focal thickening of the intima d/t accumulation of foam cells and extracellular matrix
- Smooth muscle cells can also deposit in the intima - Lipids accumulate, creating the fatty streak
- Coronary arteries have a specific protein, biglycan, that can trap VLDL and LDL - Fatty streaks may also contain T lymphocytes
14
Q
Fatty Streak Formation
A
- Vascular injury precipitates monocyte binding to endothelium
- Monocytes cross endothelium and become activated tissue macrophages
- Macrophages “eat” oxidized LDL, becoming foam cells
- T cells release cytokines, which further activates 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
15
Q
how does a fibrous cap develop?
A
- Develops if plaque remains stable
- A dense, collagen-based layer of connective tissue that covers the well-defined lipid core of an atherosclerotic plaque
- Provides further stability to the atherosclerotic plaque
16
Q
how is there a disruption of the vasa vasorum?
A
- A network of micro-vessels originating from tunica adventitia of large arteries
- provides oxygen and nutrients - As atherosclerotic plaques expand, they acquire their own microvasculature
- Plaque vasculature is thin-walled, extending through all layers of the arterial wall
— Increased risk of microvascular hemorrhage, leading to progression of atherosclerosis
17
Q
how does the proliferation of the fibrous plaque happen?
A
- Evolves from the fatty streak
- Develops as connective tissue accumulates
- Consists of lipid-containing smooth muscle cells and an extracellular lipid pool
18
Q
how do advanced lesions develop in atherosclerosis
A
- Characterized by a necrotic lipid–rich core and calcified regions that develop over time
- Coronary arteries remodel in response to atheroma formation
- Positive remodeling
- Negative remodeling
19
Q
which type of artery remodeling results in:
Increased vessel size occurring early in CHD
Alters arterial function leading to symptoms of unstable angina
A
positive remodeling
increases size to compensate for plaque accumulation in an effort to reduce lumen loss
20
Q
which type of artery remodeling results in:
vessel shrinkage
Results in obstructive plaques that lead to stable angina
A
negative remodeling
21
Q
- A result of plaque neovascularization
- Critical event that leads to accelerated plaque progression, instability, and ischemic vascular events
what is this event?
A
Intraplaque Hemorrhage
22
Q
2 general Pathogenesis of Atherosclerosis
A
- lipid metabolism disorder
- inflammation
23
Q
Multiple factors contribute to the development of atherosclerosis and its complications, but what are the 4 main stages/factors?
A
- endothelial dysfunction
- inflammatory and immunologic factors
- plaque rupture or erosion
- risk factors for development of dz
24
Q
how is there Endothelial Vasodilator Dysfunction in atherosclerosis
A
- Occurs d/t loss of endothelial-derived nitric oxide
- This process is precipitated by oxidized LDL
25
Endothelial dysfunction is associated with what disorders
Hypercholesterolemia
Diabetes
Hypertension
Cigarette smoking
26
Ways to Improve Endothelial Vasodilator Dysfunction:
Correct HLD (diet or statins)
ACEI if HTN present
High doses of antioxidants (Vitamin C, flavonoids)
27
what is the role of inflammation in atherosclerosis
1. Macrophages “eat” oxidized LDL
- releases inflammatory substances, cytokines, and growth factors → further plaque proliferation
2. Chronic inflammation → stable plaques
3. Active inflammation → unstable & ruptured plaques
28
Atherosclerosis is usually asx until the plaque causes what percent of stenosis of the vessel lumen
70-80%
_blood flow is impeded_ and sx of angina pectoris may ensue
29
Atherosclerotic plaques can progress via two processes:
1. Chronic → slow luminal narrowing
2. Acute → rapid luminal narrowing associated with plaque hemorrhage and/or luminal thrombosis
30
Plaque erosion occurs how?
in the absence of rupture when endothelium is missing at the plaque site
31
how can plaque rupture or erosion be silent?
- No acute symptoms may occur
- Characterized by repeated ruptures and thrombosis followed by wound healing
- Leads to increased plaque burden, progression of vessel stenosis, and negative arterial remodeling
32
what are The Effects of Atherosclerosis
can affect _different regions of circulation_, predominantly arterial, resulting in different presentations/complications:
- Coronaries – MI, angina
- CNS – Stroke, TIA
- Periphery – Claudication, limb ischemia/poor healing, aneurysms
- Renal Arteries – RAS
- GI – mesenteric ischemia
33
Average of ACS presentation in the US is what age?
68 yrs
_Prevalence increases with age_
34
what race/ethnic groups are most at risk for atherosclerosis?
1. white (non-hispanic) - 21.3%
2. native hawaiian/pacific islander - 20.8%
3. black (non-hispanic) - 20.7%
35
smoking increases risk of HD by what?
2-4x
Also higher risk of IHD and sudden cardiac death
36
on avg, smokers die __ yrs earlier than nonsmokers
10 yrs
37
The #1 preventable cause of death and illness in the US
smoking
38
According to the WHO, one year after quitting smoking, risk of CHD can ↓ by what percent?
50%
39
how does smoking promote atherosclerosis
increasing platelet adhesiveness, raised endothelial permeability, SNS stimulation by nicotine
40
Hypercholesterolemia has a directly proportional relationship with atherosclerosis and CHD because:
1. Atherosclerotic plaques contain cholesterol and cholesterol esters
- Derived from the lipoproteins in the blood
1. Risk increases progressively with higher levels of LDL and declines with higher levels of HDL
3. Populations having hypercholesterolemia have higher mortality from CHD
4. Dietary regulation and administration of cholesterol-lowering drugs have beneficial effect on reducing the risk of CHD
41
Statin Benefit Groups
1. clinical ASCVD (secondary prevention)
2. primary elevations of LDL–C ≥190 mg/dL
3. 40-75 yrs with DM and LDL–C 70 to 189 mg/dL w/out clinical ASCVD
4. 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%
42
what are the two high-intensity statins
Atorvastatin (Lipitor) 40-80 mg
Rosuvastatin (Crestor) 20-40 mg
(everything else is moderate)
43
how does HTN contribute to atherosclerosis/CHD
1. causes mechanical injury to the arterial wall
2. increases the heart’s workload causing the heart muscle to thicken and become stiff
3. Endothelial injury resulting from persistent high BP leads to plaque formation as per response to injury hypothesis
44
Atherosclerosis develops at an early age in people with both ___ and ____
IDDM and NIDDM
45
Even when glucose levels are under control, how is DM a risk factor for atherosclerosis/CHD
1. DM increases the risk of heart disease and stroke
2. Risks are even greater if blood sugar is not well controlled
3. At least 65% DM die of some form of heart or blood vessel disease
4. CHD risk equivalent
46
how is age & gender a risk factor for atherosclerosis/CHD
1. _Higher incidence & severity in men_
- Presents **earlier** in life
- Risk increases **after age 45**
2. _Lower incidence in women_, esp in premenopausal age
- Risk increases **after 55 yrs**, although still lower than men’s risk despite increased risk after menopause
- Postmenopausal women on HRT have an increased risk of CV events
3. Fully-developed atheromatous plaques usually appear in **+40s**
- About 80% of people who die of CHD are >65
47
how do genetic and familial factors contribute to atherosclerosis/CHD?
1. Increased risk of CHD with family history of premature CHD
- CHD in _male first degree relative <55 yrs_; CHD in _female first degree relative <65 yrs
2. Hereditary _genetic derangements of lipoprotein metabolism_ predispose the individuals to high blood lipid level and familial hypercholesterolemia
3. Familial predisposition to atherosclerosis may be related to _other risk factors_ like DM, HTN, and HLD
4. Children of parents with HD are more likely to develop it themselves
48
how do Racial and Ethnic Factors
contribute to atherosclerosis/CHD
1. African Americans have more severe high BP than Caucasians
- Also higher risk of heart disease
2. HD risk is also higher among Mexican Americans, American Indians, native Hawaiians, and some Asian Americans
- Partly due to higher rates of obesity and DM
49
what risk factors are part of the 10-yr risk stratification?
1. age & gender
2. race
3. DM
4. smoking
5. cholesterol
6. BP
50
Screening for abdominal aortic aneurysm (AAA) - USPSTF
65-75 who have never smoked - 1 time screening with US
51
USPSTF Recommendations for Blood Pressure Screening
>18 without known HTN - screening for HTN with office BP measurement and outside of clinical setting for diagnostic confirmation before starting tx
52
USPSTF Recommendations for preDM and T2DM screening
asx 35-70 who have overweight or obesity - should offer or refer pts with preDM to effective preventive interventions
53
USPSTF Recommendations for Statin Use
40-75 who have 1 or more CV risk factors and an estimated 10-year CVD risk of 10% or more
54
USPSTF Recommendations for Healthy Diet & Physical Activity
adults with CVD risk factors are recommended to behavioral counseling interventions to promote heathy lifestyle
55
USPSTF Recommendations for tobacco smoking cessation
- non-pregnant
- pregnant persons
stop/don't do it
