CVD 1 Flashcards

1
Q
  1. What is the prevelence of death due to CvD in the U.S.?
A

1 in every 2.9 deaths is due to cardiovascular disease

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2
Q
  1. As a systemic disease, most coronary artery disease patients also have…
A

concomitant peripheral or cerebrovascular disease or cerebrovascular disease; if a patient has one plaque its likely they have plaques elsewhere although plaques are not homogenous.

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3
Q
  1. Name the risk factors for atherosclerosis (6 main)
A

age (men>45 women>55), DM, family hx (1st deg relative male <65), hypertension, cigarette smoking, dyslipidemia

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4
Q
  1. How is age such an important factor in development of CVD?
A

age is important because it measures the time the patient has been exposed to risk factors, also natural aging processes cause changes in the vasculature

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5
Q
  1. How do factors like cig. Smoke , dyslipidemia or family hx. Contribute to disease?
A

chemicals in smoke can lead to damage to b.v.; dyslipidemia adds to the pool of cholesterol and lipids that contribute to plaques and genetic factors can effect the way people metabolize lipids

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6
Q
  1. What are characteristics of a “normal” artery? (describe normal 3 layers)
A

endothelium resting on a thin basal lamina, subendothelial space containing thin elastic and collagenous fibers, longitudinally oriented smooth muscle cells

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7
Q
  1. Name two factors that are produce by endothelial cells that contribute to the normal functioning of the b.v.
A

normal levels of NO (promotes constitutive vasodilation), normal t-PA: PAI-1 promotes fibrinolysis (prevents platelet adhesion); damaged endothelium can attrach leukocytes to adhear and migrate into vessel wall

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8
Q
  1. Name the enzyme that produces constitutive NO.
A

constitutive membrane-associated Nosynthase (eNOS), note higher levels of shear stress induce higher levels of NO (O2+ L-arginine is converted to NO and L-citrulline)

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9
Q
  1. What is meant by the expression NO supply is “quenched”?
A

supply of NO reacts with excess oxidative free radicals which converts NO to oxidative compounds

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10
Q
  1. Describe the steps in atherosclerosis where lipoproteins eventually cause an inflammatory response.
A

lipoprotein gets in the subendothelial cells and are modified (glycosolation and oxidation) and oxidized LDL causes inflammatory response via MCP-1 and M-CSF factors

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11
Q
  1. What immune cells mediate the inflammatory response during atherosclerosis?
A

oxidation of LDL causes expression of monocyte scavenger receptors which enter into the subendothelial space and eat debris, causing a coalescence of cholesterol inside the macrophage, creating a foam cell which further produces IL, and proteases which activate SM migration

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12
Q
  1. How is atherothrombosis part of the formation of a plaque?
A

occuring concurrently with the addition of lipoproteins, factors produced by endothelium like t-PA keep platelets from sticking but damage or sloughing of endothelial cells can cause platelets to stick , clot formation causes release of factors that activate SM cells

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13
Q
  1. Name the critical cytoine-regulated adhesion molecule that binds mononuclear leukocytes and where/why is it expressed.
A

vascular cell adhensin molecule (VCAM-1) is expressed over damaged endothelium (fatty streaks due to athrogenic diet) (note atherogenic diet rapidly induces VCAM-1 in rabbit aortic endothelium)

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14
Q
  1. Once adheard to the vascular wall, monocytes respond to this chemotactic stimuli by penetrating from the endothelial surface into the arterial intima
A

monocyte chemoatractant protein-1, produced by endothelial and smooth muscle cells (even in the excess of LDL, MCP-1 seems key in causing development of atherosclerosis)

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15
Q
  1. An activated macrophage expresses this, it leads to the formation of a foam cell.
A

expression of scavenger receptors that internalized modified LDL promotes foam cell formation

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16
Q
  1. Name the factors that promote mitosis of macrophages in a atherosclerotic plaque.
A

macrophage colony-stimulating factor, produced by endothelial and smooth muscle cells

17
Q
  1. When a fatty streak is present, is the endothelium normally intact?
A

yes, the tunica meida may show some disarray due to the beginnings of smooth muscle migration

18
Q
  1. What is the key characteristic of the vessel that denotes a plaque has formed.
A

discontinous endothelium with the formation of a fibrous cap