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Cardiovascular > 04.07 - Atherosclerosis 1 and 2 (Nichols) > Flashcards

04.07 - Atherosclerosis 1 and 2 (Nichols) Flashcards

1
Q

5 major modifiable risk factors for atherosclerosis

A

Smoking, HTN, Obesity, DM, Dyslipidemia

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2
Q

___ causes 20-25% of fatal acute MI’s

A

Superficial erosion of coronary atheromata

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3
Q

2 most important causes of endothelial dysfunction

A

hemodynamic disturbances; Hypercholesterolemia

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4
Q

3 Characteristics of Endothelial Dysfunction

A

Impaired endothelium-dependent vasodilation, Hypercoagulable states, increased oxygen free radical production

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5
Q

3 Factors that maintain SM cells in quiescent state

A

Heparan, NO, TGF-alpha

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6
Q

3 Major components of ECM in plaque

A

Collagen, Elastic Fibers, Proteoglycans

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7
Q

95% of HTN is

A

Idiopathic (Essential HTN)

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8
Q

Action of Lp-PLA2

A

Travels with circulating LDL and Hydrolyzes oxidized phospholipids in LDL

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9
Q

Action of Products of Lp-PLA2 reaction generated in atherosclerotic lesions

A

Upregulate MCP-1, ICAM-1, and VCAM-1 on endothelial cells

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10
Q

Actions of Myocardial Natriuretic Peptides

A

Inhibit Na resorption –> Diuresis; Also systemic Vasodilation

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11
Q

Arteries v Veins: Which are more prone to penetration by tumors or inflammatory processes?

A

Veins

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12
Q

Arteriosclerosis literally definition

A

Hardening of arteries

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13
Q

Atheroscerlosis is characterized by

A

Presence of intimal lesions called Atheromas

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14
Q

Canakinumab

A

IL-1beta mab

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15
Q

Cause of Homozygous Familial Hypercholesterolemia

A

Defective LDL receptors and inadequate LDL uptake

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16
Q

Cause of Hyaline Arteriolosclerosis

A

Leakage of plasma components across injured endothelial cells; Increased ECM production by SM cells in response to chronic stress

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17
Q

Causes of Artery Amyloidosis (3)

A

Plasma Cell Dyscrasia; Chronic Systemic Inflammation (esp RA); Genetic (esp TTR)

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18
Q

Causes of Fibrinoid Necrosis (2)

A

Malignant HTN; Autoimmune Vasculitis, esp. PAN

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19
Q

Causes of Hyaline Arteriolosclerosis (2)

A

Benign HTN, DM

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20
Q

Causes of Hyperplastic Arteriolosclerosis (2)

A

Malignant HTN; Autoimmune: Scleroderma, Lupus

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21
Q

Cholesterol crystals contribute to development of atherosclerosis by activating

A

Inflammasome in Mac’s –> IL-1 production

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22
Q

Color of young vs old fibrosis

A

Young is clear, Old is dark pink

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23
Q

Complication of Fibromuscular Dysplasia in Renal Arteries

A

Renovascular HTN

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24
Q

Complications of Fibromuscular Dysplasia

A

Luminal Stenosis, Abnormal Vessel Spasm that reduces vascular flow

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25
Q

CRP levels strongly and independently predict risk of

A

MI, Stroke, PVD, SCD

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26
Q

CRP secreted by cells within atherosclerotic plaque can

A

activate endothelial cells –> increase adhesiveness and pro-thrombotic state

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27
Q

Cutoff for Malignant HTN

A

200/120

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28
Q

Darapladib

A

Small molecule inhibitor of Lp-PLA2

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29
Q

Determinants of Plaque Vulnerability

A

Thinness of Fibrous Cap; Size of Lipid Core; Amount of Inflammation, Amount of Calcification

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30
Q

Dominant lipids in atheromatous plaques

A

Cholesterol and Cholesterol Esters

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31
Q

Earliest atherosclerotic lesion is called

A

Fatty streak

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32
Q

Early human atherosclerotic lesions begin at sites of

A

intact, but dysfunctional, endothelium

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33
Q

Effect of Kinins and Prostaglandins on TPR

A

Both Decrease thru Vasodilation

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34
Q

Effect of Lp-PLA2 bioactive lipid products on macrophages

A

Upregulated MCP-1 –> Secrete IL-1beta and undergo apoptosis

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35
Q

Effect of MCP-1 on macrophages

A

Secrete IL-1b and Apoptosis

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36
Q

Extensive AV fistulas can cause

A

high-output cardiac failure

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37
Q

First 3 steps of Atherosclerosis

A

Malfunction of injured endothelial cells; Accumulation of lipid in intima; Leukocyte recruitment

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38
Q

Focal irregular thickening of the walls of medium-sized and large muscular arteries due to combo of medial and intimal hyperplasia

A

What is Fibromuscular Dysplasia

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39
Q

How does Ang II raise BP

A

(1) Vascular SM contraction; (2) stim aldosterone secretion; (3) Increase tubular Na resorption

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40
Q

How does obesity contribute to atherosclerosis

A

Pro-inflammatory, Pro-thrombotic

41
Q

How does Thrombin initiate Inflammation

A

Cleaves PARs on leukocytes, endothelium, and other cells

42
Q

How is LDL modified in Tunica Intima

A

Oxidized and Glycated

43
Q

How is LDL taken up by macrophages

A

Not by LDL-R, but by a Scavenger Receptor

44
Q

Hyaline Arteriolosclerosis in kidney leads to

A

Nephrosclerosis (Glomerular Scarring)

45
Q

IL-1beta mab

A

Canakinumab

46
Q

In general, plaque inflammation increases

A

Collagen degradation and reduces collagen synthesis –> Destabilizing cap

47
Q

In malignant HTN, Hyperplastic Arteriolosclerosis changes are accompanied by

A

Fibrinoid Deposits and Vessel Wall Necrosis (necrotizing arteriolitis)

48
Q

Injured endothelial cells secrete

A

IL-1 and TNFalpha

49
Q

Injured endothelial cells secrete less

A

Superoxide Dismutase, NO, Prostacyclin

50
Q

Last step of Atherosclerosis

A

ECM (wavy collagen) deposition

51
Q

Major clinical consequences of Atherosclerosis

A

MI, Stroke, PVD, AA’s

52
Q

Medial attenuation between focal segments of thickened wall prone to rupture

A

Fibromuscular Dysplasia

53
Q

Monckeberg Medial Sclerosis is characterized by

A

Calcific deposits in muscular arteries (>50, do not encroach on lumen)

54
Q

Morphology of Fatty Streaks

A

Yellow, flat, elongated, minimally raised

55
Q

Most important determinant of stroke volume

A

Filling Pressure (regulated by sodium homeostasis)

56
Q

Most important independent risk factor for atherosclerosis

A

Family History

57
Q

Mutations in ENaC lead to

A

Increased distal tubular resorption of Na induced by Aldosterone

58
Q

Neointimal vs Medial SM cells

A

Neointimal can’t contract; Do have capacity to divide and have great synthetic capacity

59
Q

On its own, HTN can increase risk of IHD by __

A

60%

60
Q

Plaques in individuals taking statins have

A

more fibrous character (resistant to rupture)

61
Q

Problem with modified LDL being taken up by Scavenger Receptor

A

No feedback inhibition –> Take up too much

62
Q

Result of upregulation of MCP-1, ICAM-1, and VCAM-1 on endothelial cells

A

Vasodilate less in response to NO and undergo apoptosis

63
Q

Role of IFN gamma in plaques

A

Strongly inhibits SM cell production of collagen required to repair and maintain integrity of fibrous cap

64
Q

Ruptured plaques tend to have (3 things)

A

Thin Cap, Large Lipid Core, Abundant Inflammatory Cells

65
Q

Stereotypical response of vessel wall to any insult

A

Intimal thickening

66
Q

Superficial erosion causes what percent of fatal acute MI

A

20-25%

67
Q

T/F: Anti-Gout drugs can help atherosclerosis patients

A

True: Colchicine, 60% reduction of 3 year period

68
Q

T/F: Intimal thickening is always pathologic

A

False, part of normal aging

69
Q

T/F: Statins decrease the degree of stenosis as assessed on angiography

A

FALSE

70
Q

T/F: Statins result in significant reductions in atheroma volume

A

FALSE

71
Q

The pro-inflammatory role of Lp-PLA2 is mediated by

A

products of Lp-PLA2 reaction generated in athersclerotic lesions

72
Q

Thin-walled arterial outpouchings in cerebral vessels

A

Berry Aneurysms

73
Q

Top 3 most affected arteries with atherosclerosis

A

Infrareneal AA, Coronaries, Popliteals (Internal Carotids)

74
Q

Triggering the inflammasome results in activation of enzyme called

A

Caspace-1 –> Cleaves Pro-IL1b to IL-1b

75
Q

Two forms of small blood vessel disease that are HTN-related:

A

Hyaline Artiolosclerosis, Hyperplastic Arteriolosclerosis

76
Q

Type of HTN associated with Hyaline Arteriolosclerosis

A

Benign/Mild

77
Q

Up to ___ % of events due to atherosclerosis are from plaque rupture

A

75

78
Q

What activates inflammasome in mac’s

A

Cholesterol Chrystals

79
Q

What boosts production of interstitial collagenases in macrophages?

A

CD 40 ligand on T cells

80
Q

What BP threshold is associated with increased risk of atherosclerosis

A

140/90

81
Q

What causes renin release besides low pressure

A

Circulating Catecholamines, Low Sodium in Distal Convoluted Tubules

82
Q

What does Aldosterone resorp and secrete

A

Resorb Na, Secrete K

83
Q

What else beside IL-1 do Mac’s release

A

ROS –> LDL oxidation and growth factors that stimulate SM cell proliferation

84
Q

What is Fibromuscular Dysplasia

A

Focal irregular thickening of the walls of medium-sized and large muscular arteries due to combo of medial and intimal hyperplasia

85
Q

What is important about vasa vasorum formed in arteries that don’t normally have

A

Prone to rupture

86
Q

What leads to conversion of Fatty Streak to Atheroma

A

Intimal SM cell proliferation and ECM deposition

87
Q

What mediates pro-inflammatory role of Lp-PLA2

A

Bioactive lipid products of Lp-PLA2 rxn generated in athersclerotic lesions

88
Q

What produces the MMPs implicating in degradating plaque collagen

A

Macrophages: MMP-1, MMP-8, MMP-13

89
Q

What regulates Filling Pressure

A

Sodium Homeostasis

90
Q

What T cell product is implicated in inhibiting the ability of SM cells to make new collage

A

Interferon Gamma

91
Q

What upregulates expression of MCP-1, ICAM-1, and VCAM-1 on endothelial cells

A

Bioactive lipid products of Lp-PLA2 rxn generated in athersclerotic lesions

92
Q

What women are protected against Atherosclerosis

A

Premenopausal

93
Q

When can Hyaline Arteriolosclerosis be seen in absence of HTN

A

Old People; Diabetic Microangiopathy

94
Q

When does Fibromuscular Dysplasia typically occur

A

Young women

95
Q

When is there low sodium levels in distal convoluted renal tubules

A

When GFR falls (when CO low) –> Increased Na resorption by proximal tubules, lower levels more distally

96
Q

Which come first in SHODDY

A

Smoking, then Obesity, then HTN

97
Q

Why is inhibiting collagen production by SM cells bad in plaque

A

Collagen needed to maintain integrity of fibrous cap

98
Q

With chronic hyperlipidemia, lipoproteins accumulate within intima, where they generate 2 pathogenic derivatives:

A

Oxidized LDL, Cholesterol Crystals

99
Q

Without appropriate tx, 50% of HTN pts die of

A

IHD or CHF (another 1/3 of stroke)

Cardiovascular (18 decks)

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