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57 Cards in this Set
- Front
- Back
single largest killer of men and women in US
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coronary artery disease (CAD)
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3 layers of arteries, from innermost to outermost
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Intima, Media, Adventitia
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What's the anatomy of an atherosclerotic plaque?
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1) fibrous cap : consists of activated smooth muscle cells and T cells
2)lipid-filled core : with macrophage foam cells |
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What effect does NO have on growht of endothelial cells?
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It inhibits growth
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Endothelial Derived Relaxing Factor (EDRF) is also known as:
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NO
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What does EDRF/NO do in the endothelium?
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It causes vasodilation, inhibition of growth, is antithrombotic, and anti-inflammatory
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What causes EDRF/NO to be released?
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Biochemical mediators: Ach, ADP, bradykinin, histamine
Biomechanical forces: shear stress Also released tonically. |
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Ach, ADP, bradykinin, histamine: how are these related to NO release?
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They all cause NO release from endothelium
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What does ACh normally do to arteries? How is this changed in conditions that are risk factors for CAD (hi cholesterol, smoking, etc)?
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Normally promotes release of NO, which causes an increase in blood flow thru vasodilation. This is decreased with risk factors.
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T/F Endothelial dysfunction and decreased NO availability is one of the first events in atherogenesis
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T
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What is the effect of free radicals like superoxide on NO?
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Breaks it down
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What is the effect of shear stress on NO?
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Increases release. This is why plaques tend to accumulate in bifurcations which are areas of low shear stress.
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NO effect on Monocytes
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Inhibits chemotaxis and activation (antiinflammatory)
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T/F One of the earliest changes associated with these risk factors is an increase in oxidative stress in the vessel wall.
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T
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What does the increase in oxidative stress do to the vessel wall?
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Causes decreased production of NO.
Causes increased production of vasoconstrictive substances, such as endothelin and angiotensin II. |
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T/F Most of the ACE in the body is circulating.
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F. Only 10% is circulating. The remainder is in the tissues.
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T/F Increased AII leads to increased production of superoxide ion.
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T. This results in Reduced NO availability.
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What "activates" the SM cells of the vessel intima and causes them to grow?
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angiotensin II
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What happens in LDL infiltration to the intima?
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LDL gets oxidized and is taken up by macrophages which become foam cells and form early plaques.
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OX-LDL- leads to expression of what adhesion molecules on endothelial surface?
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(ICAM-1, VCAM-1, P-selectin)
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What happens when the adhesion molecules on the endothelial surface are upregulated by OX-LDL?
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Adhesion of monocytes and T-lymphocytes to endothelium
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MCP-1 (monocyte chemoattractant protein-1): role in atherogenesis
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Endothelial-derived cytokine that facilitates movement of monocytes & certain T-lymphocytes into the intima (transmigration)
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M-CSF (monocyte colony stimulating factor): role in atherogenesis
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Endothelial-derived cytokine that promotes activation and maturation of monocytes & macrophages in the intima
expression of scavenger receptors allows uptake of ox-LDL by macrophages |
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T/F A low shear state is prothrombotic
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T
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a one cell thick layer that lines the intima
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endothelium
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T/F Enhanced permeability to lipoproteins is an important and possibly first step in the development of atherogenesis
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T
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How does NO cause dilation of arteries?
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Stimulates guanylate cyclase to produce gGMP. This causes SM relaxation and dilation of the artery.
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NO effect on platelets
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Inhibitions aggregation and adhesion (antithrombotic)
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What two systems generate angiotensin II (AII?)
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1) Renin-angiotensin (tissue)
2) Circulating |
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T/F The renin-angiotensin system contributes to a reduction in NO and therefore anti-atherosclerotic effects
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F. These are pro-atherosclerotic.
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earliest lesion in atherosclerosis
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foam cell (lipid laden macrophage)
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accumulation of foam cells in the intima is known as ______
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fatty streaks
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T/F in an MI, the culprit lesion is usually large and focal
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F. Size of lesion isn't necessarily related to risk of causing MI.
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What % of patients with an MI have at least one risk factor of HTN, hyperlipidemia, diabetes, or current smoking?
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80%
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T/F Risk modification is important because it reduces development and progression of atherosclerosis.
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Kinda T, Kinda F.
Risk mgmt also reduces the conversion of stable plaques to unstable plaques that have a tendency to rupture. |
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Non-modifiable risk factors for CV risk
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Male gender
Age Family history |
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Primary prevention : defn
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preventive tx before recognized CV events
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Secondary prevention: defn
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tx focused on patients with existing CVD or diabetes
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A ratio of total cholesterol:HDL <___ is associated with a reduced risk of coronary events
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4.0
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LDL should be lowered to ____ for primary prevention and ____ for secondary prevention
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less than 100, <70mg/dl
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T/F Effective therapies to raise HDL don't yet exist
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T
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What are some lifestyle factors that raise HDL?
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Exercise and moderate alcohol intake.
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How does risk for atherosclerosis and MI change when one quits using tobacco?
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Stopping smoking for one year reduces the risk of having an MI in the next year to nearly that of a nonsmoker.
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What type of exercise is best for reducing CV risk?
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Regular (3x/week) and aerobic. Weights are acceptable if done in rhythmic reps and without breath-holding.
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T/F Diabetics without recognized CAD have an equally increased risk of events compared to patients who've had a recent MI
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T
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T/F benefits of tight BP control and tight glucose control are equal in diabetes
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F. BP control is more important, but both are very important.
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Obesity, in particular truncal obesity, increases CV mortality risk by _______ over normal weight
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50-100%
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T/F Young age obesity appears to have a greater CV risk than older persons
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T
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What do the Framingham point score quantify?
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10 year risk for developing CHD
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What are the 6 risk factors accounted for in the Framingham point score?
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1) Smoking
2) Age 3) HDL level 4) Systolic BP 5)Total cholesterol 6) Sum of the points |
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What are the additional benefits beyond blood pressure lowering effects of ACE inhibitors?
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Improves vascular function.
Reduces risk of CVD death, nonfatal MI, Stroke, and new onset diabetes. |
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T/F Systemic measures fo inflammation correlate with risk of coronary events
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T
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How does CRP level affect mortality risk?
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they're positively correlated
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What is the role of statins in CV risk reduction?
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They reduce the acute and chronic risk of coronary events.
They lower LDL predominantly, but also lower triglycerides and slightly increase HDL. They also reduce CRP (ie, reduce inflammation). |
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Can cholesterol treatment cause a regression in plaques?
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There is an arresting of plaque progression at LDL levels <70, but not a regression.
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Risk factors adversely affect endothelial function resulting in paradoxical ____ mediated vasoconstriction.
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acetylcholine
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T/F primary proinflammatory risk factors result in hepatic production of acute-phase reactants, such as CRP.
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T
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