Lecture 16: Risk Factors and Lipids Flashcards

1
Q

What two cell types maintain integrity/elasticity of arterial vasculature?

A

Endothelial cells and smooth muscle cells

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2
Q

Endothelial cells = normal function

A

Impermeable (to large molecules, like LDL-C), anti-inflammatory, promote vasodilation, resist thrombosis

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3
Q

Smooth muscle = normal function

A

Cause vasoconstriction/dilation, produce extracellular matrix to maintain vascular integrity (collagen and elastin)

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4
Q

What is the first step of atherosclerosis

A

Endothelial cell dysfunction = particles (e.g. LDL) allowed into subendothelial space

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5
Q

What is the second step of atherosclerosis

A

Recruitment of immunologic mediators. This actually causes more LDL to be deposited

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6
Q

What happens to the LDL?

A

Modification –> oxidation/glycation

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7
Q

What happens to immune cells?

A

Uptake of mLDL by monocytes –> “foam cells”

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8
Q

All of the above leads to the formation of __________. When does this happen?

A

Lesions! Late teans

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9
Q

What happens to the smooth muscle cells?

A

Smooth muscle cell migration across the tunica intima into the plaque

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10
Q

Three key features of atherosclerotic lesions

A
  1. Fibrous cap; 2. Lipid material (cholesterol); 3. Inflammation
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11
Q

Two atherosclerotic categories and features

A

Vulnerable plaque: large lipid core, thin fibrous cap, many inflammatory cells; Stable plaque: small lipid pool, thick fibrous cap, preserved arterial lumen

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12
Q

What happens if a fibrous plaque breaks open?

A

Released cholesterol can cause blood to clot –> thrombus

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13
Q

What is the most common mechanism for an atherosclerotic-induced MI?

A

Fibrous cap rupture

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14
Q

What is another (besides MI) consequence of a ruptured fibrous cap?

A

Healed rupture = narrow lumen and fibrous intima

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15
Q

Traditional risk factors for atherosclerosis (two categories: 3, 4)

A

Non-modifiable: age, sex, family history; modifiable: dyslipidemia, smoking, DM, physical inactivity

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16
Q

Non-traditional risk factors for atherosclerosis (3)

A

Apoplipoprotein, c-reactive protein, homocysteine

17
Q

Density of lipoprotein increases as the ratio of…

A

Protein/lipid increases (LDL = more cholesterol)

18
Q

HDL-C (describe)

A

“Good cholesterol” = reverse cholesterol transport by scavenging for deposited cholesterol from periphery to liver

19
Q

LDL-C (describe)

A

“Bad cholesterol” = deposits cholesterol into arterial walls, target of pharmacotherapy

20
Q

T/F: Diet and exercise can help lower LDL-C

21
Q

Four classes of LDL-C lowering pharm agents

A

Niacin, bile acid seqestrants, fibric acid, statins

22
Q

What are statins?

A

HMG-CoA Reductase Inhibitors = increased expression of LDL-C receptor in liver, lowering serum LDL-C

23
Q

Other benefits of statins (4)

A

Modest raise in HDL-C, favorably modulate vascular tone, stabilize plaque, reduce inflammation

24
Q

Major risk factors for coronary heart disease (5)

A

Cigarette smoking, HT, low HDL, family history of premature CHD (male relative 45, females >55)

25
If 10-year risk of a heart attack is higher than _____% prescribe...
7.5%; statins
26
Are there current pharm agents to raise HDL-C?
No: due to SEs and toxicity
27
What is one way to raise HDL modestly?
Statins, niacin
28
What is the best way to raise HDL?
Diet and exercise
29
Cardiovascular effects of DM (5) which lead to...(2)
Enhanced inflammation, hypercoagulability, endothelial dysfunction, glycation of lipoproteins, vascular stiffness/calcification --> accelerated atherosclerosis and prothrombotic state
30
By how much does diabetes increase risk for CVD?
Men: 8 --> 17%; Women: 4 --> 17%
31
All diabetic patients should be treated for...why?
Heart disease; patients with diabetes with no prior heart attack are at the same risk for a heart attack as a non-diabetic patient with a prior heart attack
32
How do we treat patients with diabetes to reduce macrovascular risk?
Control: blood pressure, lipids, obesity (controlling glucose does not decrease risk)
33
Describe obesity and vascular effects (4)
1. Inflammation = adipose releases pro-inflammatory cytokines; 2. Hypertension due to increased CO; 3. Endothelial dysfunction; 4. Insulin resistance
34
What are the current physical activity recommendations?
30 minutes or more of moderate activity on most days
35
Smoking related mechanisms of injury (4)
Endothelial damage, prothrombotic effects on platelet function, coronary vasoconstriction, oxidative modification of LDL-C
36
Describe homocysteine's role in atherogenesis
Elevated homocysteine linked to pathophysiology of atherosclerosis but lowering does not help
37
Describe lipoportein (a)'s role in atherogenesis
Higher levels of lipoprotein (a) associated with higher CV risk but not good therapies
38
Describe c-reative protein's (CRP) role in atherogenesis
Maker of inflammation, statin therapy might lower CRP (prescribe even if there LDL-C is not high)