Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio > Cardiology Risk Factors > Flashcards

Cardiology Risk Factors Flashcards

1
Q

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

A

Endothelial cells and smooth muscle cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Characteristics of endothelial cells

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Characteristics of smooth muscle cells

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hallmark of early atherogenesis and its result

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Progression of early atherogenesis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Progression of plaque formation

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

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

Late plaque formation restricts vessel lumen and causes ischemic symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Stable and vulnerable phenotype development

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

MMP

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Characteristics of a vulnerable plaque

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Characteristics of a stable plaque

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Process of plaque disruption

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Current paradigm of atherosclerosis

A

A systemic disease that manifests locally.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Risk factors for atherosclerosis

A

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

Nontraditional (apolipoprotein a, C reactive protein, homocysteine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Most males with CHD have how many risk factors?

A

One

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CVD and age

A

Increases linearly with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

CVD and sex

A

Males more common early, women more common over 60

18
Q

Function of lipoproteins

A

Transport cholesterol in the serum

19
Q

Lipoprotein structure

A

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

Inner layer has cholesteryl esters, and triglycerides

20
Q

How does density of lipoproteins increase?

A

With more proteins

21
Q

HCL-C

A

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

22
Q

LDL-C

A

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

23
Q

How to lower LDL-C?

A

Diet/exercise

Niacin, bile acid sequestrants, fibric acid.

HMG-CoA reductase inhibitors

24
Q

How do HMG-CoA reductase inhibitors work?

A

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

25
Q

Are statins effective? How?

A

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
Q

Is increasing HDL-C favorable for decreasing CV events?

A

Hasn’t proven useful yet

27
Q

Cardiovascular effects of Dm

A

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

Essentially, accelerated atherosclerosis and a prothrombotic state.

28
Q

Does DM affect CHD mortality?

A

Yes, increases it at least 2 fold.

29
Q

Why is DM a CHD risk equivalent?

A

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

30
Q

What are the treatment objectives in the diabetic patient?

A

Preventing microvascular complications (retinopathy, neuropathy, nephropathy)

and

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

31
Q

How are diabetics treated to prevent the things above?

A

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

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

32
Q

Vascular effects of obesity/physical inactivity

A

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
Q

Definition of obesity?

A

BMI>30

34
Q

Guidelines for activity

A

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

35
Q

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

A

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

36
Q

Mechanism of smoking related injury

A

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

37
Q

Is LDL-C sufficient alone as a risk factor?

A

No, think about Tim russert.

38
Q

Role of homocysteine in atherogenesis

A

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
Q

Lipoprotein A and CV risk

A

variant of LDL, may impair endogenous thrombolysis.

Promotes inflammation.

High LpA levels have higher risk

40
Q

C-reactive protein

A

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

Cardio (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions