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Flashcards in Cardiology Risk Factors Deck (40):
1

What type of cells maintain the integrity and elasticity of arterial vasculature

Endothelial cells and smooth muscle cells.

2

Characteristics of endothelial cells

Impermeable to large molecules (LCL-C)
Anti-inflammatory
Promote vasodilation
Resist thrombosis

3

Characteristics of smooth muscle cells

Control vascular tone
Produce extracellular matrix that maintains vascular integrity.
Within the arterial medial layer.

4

Hallmark of early atherogenesis and its result

Endothelial cell dysfunction -- this allows lipoproteins (LCL) into subintimal space.

5

Progression of early atherogenesis

Endothelial injury
Immunologic recruitment (t-cells, monocytes)
LDL modification -- glycation/oxidation stimulates inflammation
Uptake of mLDL by monocytes to create foam cells
Cellular apoptosis and lesion formation

6

Progression of plaque formation

Smooth muscle cell migration initiated by foam cells and endothelial cells.

Smooth muscle cell proliferation and secretion of ECM (collagen) to create fibrous cap.

7

What type of remodeling is done in early vs late plaque formation.

Early plaque formation is characterized by outward remodeling, which preserves luminal diameter.

Late plaque formation restricts vessel lumen and causes ischemic symptoms.

8

Stable and vulnerable phenotype development

Phenotype determined by the balance between cap degradation and cap synthesis.

9

MMP

An enzyme that degrades the fibrous cap and inhibits matrix synthesis. Stimulated by inflammatory cytokines.

10

Characteristics of a vulnerable plaque

Large lipid cores, thin fibrous cap, many inflammatory cells.

11

Characteristics of a stable plaque

Small lipid pool, thick fibrous cap, preserved arterial lumen.

12

Process of plaque disruption

Fibrous cap rupture (due to hemodynamic stress and matrix degradation)

Subsequent development of superimposed thrombus (that contains fibrin, RBC and platelets)

Clinical manifestation depends on vascular territory and stability of thrombus.

13

Current paradigm of atherosclerosis

A systemic disease that manifests locally.

14

Risk factors for atherosclerosis

Traditional
Nonmodifiable (Age, Sex, Family History)
Modifiable (Dyslipidemia, smoking, DM, physical inactivity, hypertension)

Nontraditional (apolipoprotein a, C reactive protein, homocysteine)

15

Most males with CHD have how many risk factors?

One

16

CVD and age

Increases linearly with age

17

CVD and sex

Males more common early, women more common over 60

18

Function of lipoproteins

Transport cholesterol in the serum

19

Lipoprotein structure

Comprised of outer hydrophilic layer of proteins, phospholipids, cholesterol.

Inner layer has cholesteryl esters, and triglycerides

20

How does density of lipoproteins increase?

With more proteins

21

HCL-C

Good cholesterol
Reverse cholesterol transport
Scavenger delivering cholesterol from periphery to liver
Removes cholesterol from macrophages

22

LDL-C

Bad Cholesterol
Deposits in arterial wall leading to atherosclerosis
Primary goal of pharmacotherapy.

23

How to lower LDL-C?

Diet/exercise

Niacin, bile acid sequestrants, fibric acid.

HMG-CoA reductase inhibitors

24

How do HMG-CoA reductase inhibitors work?

They increase the LDL-C receptor expression in liver and lower serum levels of LDL-C. Also stop liver synthesis of cholesterol

25

Are statins effective? How?

Yes

Lower LDL-C, some elevation of HDL-C, reduce lipid content of the atherosclerotic plaque.

Also modulate vascular tone, stabilize plaques, reduce inflammation

26

Is increasing HDL-C favorable for decreasing CV events?

Hasn't proven useful yet

27

Cardiovascular effects of Dm

Enhanced inflammation, increased platelet reactivity and hypercoagulability, endothelial dysfunction, vascular stiffness

Essentially, accelerated atherosclerosis and a prothrombotic state.

28

Does DM affect CHD mortality?

Yes, increases it at least 2 fold.

29

Why is DM a CHD risk equivalent?

Because risk for coronary heart disease with DM and no prior MI is equal to those without DM with prior MI.

30

What are the treatment objectives in the diabetic patient?

Preventing microvascular complications (retinopathy, neuropathy, nephropathy)

and

Preventing macrovascular complications (stroke, MI, peripheral artery disease)

31

How are diabetics treated to prevent the things above?

Aggressive control of modifiable risk factors like BP, lipids, obesity.

**NOTE, glycemic control may reduce macrovascular risk, but jury is out**

32

Vascular effects of obesity/physical inactivity

Inflammation caused by adipose tissue secreting pro-inflammatory cytokines.

Hypertension -- increased cardiac output to meet the higher metabolic demands of excess body weight, along with changes in vascular tone.

Endothelial dysfunction

Insulin resistance

33

Definition of obesity?

BMI>30

34

Guidelines for activity

30 minutes or more of moderate intensity physical activity on most days of the week.

35

Smoking is a CHD risk factor for young adults because...?

It increases fatty streaks and raised lesions in abdominal aorta in people 15-34.

36

Mechanism of smoking related injury

Endothelial damage
Prothombotic effects on platelets
Coronary vasoconstriction
Oxidative modification of LDL-C.

37

Is LDL-C sufficient alone as a risk factor?

No, think about Tim russert.

38

Role of homocysteine in atherogenesis

CVD patients have elevated levels of plasma homocysteine. May cause oxidative stress, inflammation, platelet aggregations. But reducing homocysteine doesn't have benefit on CV risk.

39

Lipoprotein A and CV risk

variant of LDL, may impair endogenous thrombolysis.

Promotes inflammation.

High LpA levels have higher risk

40

C-reactive protein

Acute phase reactant released by liver that is a marker of inflammation. Associated with cardiac risk independent of cholesterol levels.

Is it a mediator or marker of atherosclerosis?

Has had interesting results suggestion that may be a risk factor