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Cardiology > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

What is the innermost layer of an artery and what does it consist of?

A

Tunica intima

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2
Q

Does atherosclerosis effect veins?

A

Just arteries unless vein is used for bypass

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3
Q

What layer of the artery is thromboresistant?

A

Endothelium of tunica intima, which is a Continuous, thromboresistant layer between blood and potentially thrombogenic subendothelial tissue
Modulates tone, growth, hemostasis and inflammation throughout circulatory system

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4
Q

What is the middle layer of an artery, outer layer?

A

Tunica Media
Middle layer of an artery
Consists of smooth muscle cells and an elastic membrane
Tunica Externa / Adventitia
Outer layer of an artery
Composed of extracellular matrix with fibroblasts, mast cells and nerve terminals

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5
Q

Explain arterial physiology in the lens of the tunica intima, media, and externa/adventia?

A

At the most basic level, arteries carry oxygenated blood throughout the body

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

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6
Q

What is atherosclerosis?

A

Athero: porridge, fatty material

sclerosis: hardening d/t walling off the fatty material (Refers to connective tissue in the plaques)

Blood can no longer move, leading to ischemia and death

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7
Q

What are fatty streaks?

A

The first development of althersclerosis that can happen at childhood

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8
Q

What arteries can be affected with atherosclerosis?

A

All of them!

Brain = stroke
Abdominal aneurism
etc

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9
Q

What are the 6 histologic steps of artherosclerosis?

A

Fatty streak formation
Fibrous cap development (covers fat up)
Disruption of the vasa vasorum (outside of artery feeds it)
Proliferation of the fibrous plaque (becomes even thicker)
Development of an advanced lesion
Intraplaque hemorrhage (the fatty substances of blood can break up d/t nicks)

Can kill the patient

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10
Q

Explain the development of a fatty streak

A

The initial histologic step in development of atherosclerosis
Occurs as a result of:
Focal thickening of the intima d/t accumulation of foam cells (looks like fomy beer) 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 lymphocytes²

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

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11
Q

What is a fatty streak composed of?

A

foam cells

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12
Q

If a fatty cap becomes stable, what is formed?

A

Fibrous cap - it is more stable and there can be less pain (as opposed to an unstable fatty streak)

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13
Q

Explain the Disruption of the Vasa Vasorum

A

A network of micro-vessels originating from tunica adventitia of large arteries
Serve to provide oxygen and nutrients to outer layers of arterial wall

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 and the fatty streak

this allows more RBCs to hit and can further the clots

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14
Q

Explain the proliferation of the fibrous plaque?

A

Evolves from the fatty streak
Develops as connective tissue accumulates
Consists of lipid-containing smooth muscle cells and an extracellular lipid pool

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15
Q

What is unstable angina?

A

Chest pain all the time, including at rest

stable angina, chest pain with exertion

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16
Q

Explain positive vs negative remodeling

A

Positive remodeling: increased vessel size occurring early in CHD to compensate for plaque accumulation in an effort to reduce lumen loss
Physiologically, alters arterial function leading to symptoms of unstable angina

Negative remodeling: results in vessel shrinkage
Results in obstructive plaques that lead to stable angina

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17
Q

What is the critical event of artherosclerosis?

A

A result of plaque neovascularization
Critical event that leads to accelerated plaque progression, instability, and ischemic vascular events

all of the blood and fatty tissue occlude the blood flow to the tissue leading to ischemia

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18
Q

What two main things do we need for atherosclerosis?

A

Lipids (hyperlipidemia)
Inflammation

STATINS!!!!!

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19
Q

Apart from lipids and inflammation, what factors can lead to the development of altherscleoris?

A

Endothelial Dysfunction
Inflammatory & Immunologic Factors
Plaque Rupture or Erosion
Risk Factors for Development of Disease

20
Q

What is the initial step of artherosclerosis?

A

Endothelial vasodilator dysfunction (because you cannot vasodilates, leading to more cholestrol build-up)

21
Q

What does endothelial vasodilator dysfunction a result of?

A

Endothelial-derived nitric oxide

22
Q

What can cause endothelial dysfunction?

A

Turbulent BF

hypercholestremia
DM
HTN
smoking

anything that will damamge the lining!

23
Q

Why does inflammation lead to the pathogenesis of acute and chronic atherosclerosis?

A

Release of growth factors

chronic inflammation leads to stable plaques
active inflammation unstable and ruptured plaques

24
Q

When does atherosclerosis lead to symptoms?

A

Typically asymptomatic until 70-80% stenosis (sometimes even 50% though)

this is why we need to treat early and aggressive

chronic = slow luminal narrowing
acute = rapid luminal narrowing associated with plaque hemorrhage and/or luminal thrombosis

25
Q

Does plaque rupture always lead to symptoms?

A

NO

26
Q

What can atherosclerosis lead to?

A

Coronaries – MI, angina
CNS – Stroke, TIA
Periphery – Claudication, limb ischemia/poor healing, aneurysms
Renal Arteries – RAS
GI – mesenteric ischemia (abdominal arteries will need a stent)

all of the arteries can be affected

27
Q

What is the #1 cause of death?

A

CHD/ atherosclerotic CAD
1 US person dies every 33 seconds :(

1 in 5 deaths are caused by

28
Q

What is the average age of death atherosclerosis?

A

68 years

29
Q

What is the MC presentation of CHD?

A

Death :(

silent heart attacks

30
Q

What does a DM female often have as a presentation for heart attack?

A

Just stomach pain

31
Q

What patients have the highest risk of death with atherosclerosis?

A

Men is MC

happens in all ethnicities

32
Q

What is a coronary heart disease (CHD) equivalent?

A

Treated as if they have heart disease

We assume they have it

33
Q

What are the CHD equivalence?

A

Clinical coronary heart disease (CHD)
Symptomatic carotid artery disease
Peripheral arterial disease (PAD)
Abdominal aortic aneurysm (AAA)
Diabetes mellitus
Chronic kidney disease (CKD)

CADCP

34
Q

What are the modifiable risk factors of atherosclerosis?

A

Cigarette smoking
Dyslipidemias (↑LDL or ↓HDL)
HTN
DM
Obesity
Sedentary Lifestyle

High C-reactive protein (inflammation marker)
High triglycerides (esp women)
Sleep apnea (hypoxia, obestiy)
Stress
Persistent heavy alcohol use
elevated homocysteine (low levels of B6, B9, B12 - gastric bypass patients, vegans)

35
Q

What are the unmodifiable risk factors of CHD?

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

36
Q

How much does smoking risk heart disease?

A

Alone
2-4X

37
Q

On average, how many years less do smokers live?

A

10 years less

38
Q

What are the four groups that receive statins?

A

Individuals with clinical ASCVD (secondary prevention)

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%

38
Q

How does HTN lead to atherosclerosis?

A

Mechanical injury to the arterial wall causing it to be thicken and stiff leading to plaque formation

39
Q

DM and atherosclerosis

A

Atherosclerosis develops at an early age in people with both IDDM and NIDDM
Even when glucose levels are under control…
Diabetes increases the risk of heart disease and stroke
Risks are even greater if blood sugar is not well controlled
At least 65% of people with diabetes die of some form of heart or blood vessel disease
CHD risk equivalent

40
Q

What age is concerning of fx of heart attack for males and females?

A

CHD in male first degree relative <55 years; CHD in female first degree relative <65 years

41
Q

Difference between age and gender of coronary heart disease

A

Higher incidence & severity in men
Present with problems earlier in life
Risk increases after age 45
Lower incidence in women, especially in premenopausal age¹
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
Fully-developed atheromatous plaques usually appear in 40s and beyond
About 80% of people who die of CHD are >65

42
Q

Why might AA have a higher risk than caucasians to have cardiovascular disease?

A

higher instance of high BP

43
Q

According to USPSTF, what patient should you screen for AAA?

A

65-75 who have ever smoked

44
Q

What is the recommendation according to the USPSTF for aspirin prophylaxis?

A

C for aspirin use if 40-59 with 10% greater of ASCVD

45
Q

What is USPSTF screening for HTN, DM, tobacco

A

HTN: A for all patients >18

prediabetes T2DM: B

Statin: B
Smoking: A
CRP screening

46
Q

Mr. Jones is a 69-year-old obese male (BMI 40) presenting to your clinic to establish care. He has a 25-pack-year history of smoking and drinks alcohol daily (3 beers/day). His blood pressure is 138/90 today. He is taking no medications and is unsure of his medical history. Based off our lecture discussion regarding cardiovascular risk prevention, what needs to be considered for this patient?

A

No smoking
<15 beers a week

Cardiology (22 decks)

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