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Cardio > Atherosclerosis - Exam 2 > Flashcards

Atherosclerosis - Exam 2 Flashcards

1
Q

What is the innermost layer of the artery? What does it consist of?

A

Tunica Intima

endothelium, subendothelial layer, and elastic membrane

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2
Q

_____ is the inner lining of the tunica intima. What is its role? What 4 things does it modulate?

A

Endothelium

Thromboresistant layer between blood and subendothelial tissue

tone, growth, hemostasis and inflammation throughout circulatory system

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3
Q

What is the middle layer of the artery? It consists of ______ and ______

A

Tunica Media

smooth muscle cells and elastic membrane

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4
Q

What is the outer layer of the artery? What is it composed of?

A

Tunica Externa / Adventitia

extracellular matrix with fibroblasts, mast cells and nerve terminals

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5
Q

What layer of the artery? ______ creates the pathway for oxygenated blood to be carried to the site of perfusion

A

tunica intima

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6
Q

What layer of the artery? ______ is comprised of smooth muscle that dilates and constricts in response to cardiac output needs

A

Tunica media

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7
Q

What layer of the artery? _______ connects arteries to other structures in the body

A

Tunica externa / adventitia

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8
Q

What are the 6 steps in the progression of atherosclerosis?

A
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9
Q

What does the fatty streak formation occur as a result of? What type of cells specifically?

A

Thickening of the intima due to the accumulation of foam cells (recall from our lipid lecture!) and extracellular matrix

foam cells

When foam cells accumulate in the intima, we see fatty streak formation

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10
Q

During the fatty streak formation, _______ precipitates monocyte binding to endothelium. _______ cross endothelium and become activated tissue ______. ______ “eat” oxidized LDL, becoming ______. T cells release ______, which further activates macrophages and cause smooth muscle cells to proliferate. Smooth muscle cells move to subendothelial space, producing ______ and taking up LDL, adding to foam cell accumulation

A

Vascular injury

monocytes

macrophages

macrophages

foam cells

cytokines

collagen

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11
Q

What is step 2 called? What happens during the phase?

A

plague formation

Plaque eventually evolves from the fatty streak and develops as connective tissue and debris accumulate

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12
Q

During step 2, what does the connective tissue and debris accumulation consist of?

A

Consists of lipid-containing smooth muscle cells and an extracellular lipid pool

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13
Q

What is step 3? What happens during this step?

A

development of advanced lesions

As plaque builds, we see a necrotic lipid–rich core and calcified regions that develop over time

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14
Q

A larger plaque that is building in step 3 is called an _______. What happens as a response?

A

atheroma

Coronary arteries remodel in response to atheroma formation

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15
Q

What is the difference between positive and negative remodeling? What step is this commonly seen in?

A

positive: increased vessel size occurring early in CHD to compensate for plaque accumulation in an effort to reduce lumen loss

aka the vessel gets bigger so blood can continue to flow

negative: results in vessel shrinkage

seen in step 3, development of advanced lesions

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16
Q

What is step 4? What is happening? What is the goal?

A

Step 4: Fibrous Cap Formation

As plaque/atheromas develop, a dense collagen-based layer of connective tissue covers the well-defined lipid core of an atherosclerotic plaque

further provides stability

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17
Q

At what step is the plaque considered stable? What step results in critical changes as a result of continuing developing plaques?

A

step 4

step 5

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18
Q

What is the vasa vasorum? What is its role?

A

The vasa vasorum is a network of micro-vessels that provides oxygen and nutrients to outer layers of arterial wall

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19
Q

What is step 5? What is happening in this step?

A

Step 5: Disruption of the Vasa Vasorum

as the atherosclerotic plaques expand into the vasa vasorum it results in microvascular hemorrhaging, further inflammation, and worsening atherosclerosis/potential thrombosis

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20
Q

What is step 6? This occurs a result of _______. What does this lead to?

A

Step 6: Intraplaque Hemorrhage

A result of plaque neovascularization

Critical event that leads to accelerated plaque progression, instability, and ischemic vascular events → unstable plaque can rupture leading to thrombosis

21
Q

What step is considered the critical event? Why is it considered so harmful?

A

Step 6: Intraplaque Hemorrhage

ischemic vascular events → unstable plaque can rupture leading to thrombosis

22
Q

Why does endothelial dysfunction result in worsening atherosclerosis? What does atherosclerosis impede development of? Why is this important?

A

because endothelial dysfunction FEEDS atherosclerosis through inflammation

impede the availability of nitric oxide (NO)

NO is needed so the vessels can dilate and constrict properly

23
Q

Name 4 additional CV risk factors that decrease the availability of NO. Why are these considered especially harmful?

A

smoking, HTN, HLD, and diabetes

damage precipitates inflammation, leading to worsening atherosclerosis thereby contributing to the cycle

24
Q

______ plays a key role in the pathogenesis of atherosclerosis. What eats oxidized LDL? What happens as an end result?

A

Inflammation

macrophages

This releases inflammatory substances, cytokines, and growth factors leading to further plaque proliferation

25
Q

chronic inflammation results in the _____ plaques and active inflammation results in the ______ plaques

A

Chronic inflammation → stable plaques

Active inflammation → unstable & ruptured plaques

26
Q

Atherosclerosis is usually asymptomatic until the plaque causes _____ stenosis of the vessel lumen. Then what happens?

A

70-80%

blood flow is impeded and s/s of angina may start showing

27
Q

What are the 2 ways atherosclerotic plaques can progress? What is happening in the lumen during each?

A

Chronic → slow luminal narrowing

Acute → rapid luminal narrowing associated with plaque hemorrhage and/or luminal thrombosis

28
Q

______ occurs as the vessel erodes and the plaque continues to grow → this compromises the ______ nature of vessel walls

A

Plaque erosion

antithrombotic

29
Q

How will plaque rupture or erosion present? What is it characterized by? What does it lead to?

A

usually silent with no acute symptoms

Characterized by repeated ruptures and thrombosis followed by wound healing

Leads to increased plaque burden, progression of vessel stenosis, and negative arterial remodeling

30
Q

What is the #1 cause of death in the US? What is the average age of ACS presentation?

A

CHD/Atherosclerotic CAD

68 years

31
Q

**What are the 5 CHD risk equivalent dz?

A

Symptomatic carotid artery disease

Peripheral arterial disease (PAD)

Abdominal aortic aneurysm (AAA)

Diabetes mellitus

Chronic kidney disease (CKD)

32
Q

**What are the 6 modifiable CHD risk factors? What is the highlighted one?

A

Cigarette smoking

33
Q

**What are the 3 unmodifiable risk factors for CHD?

A
34
Q

_____ is the #1 preventable cause of death and illness in the US. Also has higher risk of _____ and ______

A

cigarette smoking

IHD and sudden cardiac death

35
Q

Give 3 reasons smoking promotes atherosclerosis. What is the major one?

A

increasing platelet adhesiveness
raised endothelial permeability
SNS stimulation by nicotine

36
Q

Why does hypercholesterolemia have a directly proportional relationship with atherosclerosis and CHD?

A

-plaques contain cholesterol and cholesterol esters

  • Risk increases progressively with higher levels of LDL and declines with higher levels of HDL
  • Populations having hypercholesterolemia have higher mortality from CHD
37
Q

What 4 groups of people would benefit from taking a statin?

A
38
Q

What are the 4 high-intensity statins?

A

Rosuvastatin (Crestor) 20-40 mg

Atorvastatin (Lipitor) 40-80 mg

39
Q

Why does persistently high HTN lead to plaque formation?

A

Endothelial injury resulting from persistent high BP leads to plaque formation as per response to injury hypothesis

40
Q

What is the trend between DM and atherosclerosis?

A

Atherosclerosis develops at an early age in people with both Type 1 and Type 2 DM even when their BS is well controlled

41
Q

At least ____ of people with diabetes die of some form of heart or blood vessel disease

A

65%

42
Q

At what age does the risk increase for men? for women? Postmenopausal women on ____ have an increased risk of CV events.

A

men: risk increases at 45

women: risk increases at 55

hormone replacement therapy

43
Q

When do fully-developed atheromatous plaques tend to appear?

A

40s and beyond

44
Q

What is the genetic component with regards to CHD and risk? Give both male and female

A

CHD in male first degree relative <55 years

CHD in female first degree relative <65 years

45
Q

What ethnicity has the highest risk for heart disease?

A

black

46
Q

What are the USPSTF recommendations with regards to AAA?

A

men aged 65-75 who have even smoked- grade B

men aged 65-75 who have NEVER smoked - grade C

47
Q

**What are the USPSTF recommendations for ASA use?

A

Grade C

aka must meet the criteria for ASA use and it is NOT recommended to give it just anyone as a preventative measure

48
Q
A

Cardio (24 decks)

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