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63 Cards in this Set
- Front
- Back
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As arteries become arterioles and capillaries, the ratio of wall thickness:lumen size (increases or decreases)?
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increases
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3 layers of blood vessels
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intima, media, adventitia
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Membrane separating intima and media in arteries
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internal elastic lamina
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How do cells of the endothelium layer receive oxygen?
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diffusion from the blood flow
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How do cells of the adventitial layer receive oxygen?
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vasa vasorum (blood vessels within the blood vessel wall)
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3 types of arteries
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Large/Elastic, Medium/Muscular, Small/Arterioles
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Resistance is a function of vessel diameter. What is the relationship?
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Resistance = 1/(diameter^4). If the diameter is doubled, resistance drops 16x. If diameter is cut in half, resistance increases 16x
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In which types of arteries is resistance a major component?
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arterioles, since they are the smallest and most affected by smooth muscle contraction
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In which blood vessels are valves found?
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veins that move blood against gravity
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What is vasculogenesis?
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embryonic formation of blood vessels form scratch
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What is angiogenesis?
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formation of new blood vessels from existing ones in a mature adult
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What is arteriogenesis?
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maintenance of arteries during chronic changes of flow and pressure
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What are arteriovenois fistulas?
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congenital defect; connections between veins and arteries that bypass the capillary beds
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What is fibromuscular dysplasia?
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congenital defect; focal thickening of artery walls
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What is endothelial activation?
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response to injury where endothelium can bind leukocytes or platelets via adhesion proteins
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How is von Willebrand factor stored in endothelial cells before they are activated?
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in Weibel-Pallade bodies
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PDGF has what affect on smooth muscle?
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promotes proliferation
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Vascular injury most commonly leads to thickening of which layer?
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intima
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Why do vessels have a mechanism of auto-regulation?
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to prevent hyperperfusion. with high cardiac output, some vessels constrict to maintain normal blood flow
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Renin function
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convert angiotensinogen into angiotensin 1; leading to aldosterone release
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2 mechanisms by which angiotensin II increases blood pressure?
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potent vasoconstriction and releases aldosterone from zona glomerulosa of adrenal cortex
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Natriuretic peptides have what effect on sodium in the the kidney?
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they promote sodium excretion; inhibit sodium reabsorption
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What is Liddle Syndrome?
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genetic defect in Na channel leads to higher reabsorption of Na with aldosterone = high BP
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Generic factors that lead to essential hypertension.
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genetics, vasoconstriction, reduced sodium excretion, environment (obesity, smoking)
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How does BP increase in renovascular hypertension?
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stenosis of renal artery = low BP in afferent arteriole of glomerulus = JG cells release renin = angiotensin pathway = aldosterone = salt/water reabsorption = high BP
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What is arteriosclerosis?
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hardening of arteries
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What is Monckberg medial sclerosis?
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calcification of muscular arteries
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Why does atherosclerosis cause hypertension?
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intimal lesions (atherosclerotic plaques of cholesterol) increase resistance
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How does atherosclerosis increase chances of aneurysm?
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intimal thickening leads to a weakening of the media layer. the vessel can now bulge and burst
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What are some uncontrollable risk factors for atherosclerosis?
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Age, gender, family genetics
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What are some controllable risk factors for atherosclerosis?
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Diet/Cholesterol/lipids, hypertension, smoking
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How do Statins (class of drugs) help to reduce atherosclerosis?
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HMG-Coa Reductase inhibitors prevent cholesterol formation in the body, reducing cholesterol levels and making atherosclerotic plaques less likely
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Why is C reactive protein a good indicator of heart attacks, strokes etc.?
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it is detected early and correlates strongly with a prothrombotic state and endothelial activation. it is released from the endothelial cells in the atherosclerotic plaque
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Once endothelial injury occurs, how does atherosclerosis form?
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LDL accumulates in the vessel wall, WBCs migrate to endothelium and become foam cells, platelet adhesion and smooth muscle proliferation, plaque growth
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How would genetic defects in LDL receptors lead to atherosclerosis?
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bad LDL receptor = LDL stays in blood vessels/can't be taken into cells. This LDL will then be more likely to accumulate in the vessel walls
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What are foam cells?
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phagocytes or smooth muscle cells that have accumulated cholesterol or lipids to form atherosclerotic plaques
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How do monocytes become foam cells under the intimal layer?
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first they become macrophages, then engulf lipoproteins (like LDL)
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How do foam cells promote endothelial activation?
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oxidized LDL taken up by the foam cells increase cytokine production and augments macrophage activation. smooth muscle proliferation also occurs as oxidized LDL aggravates the endothelium
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How to T cells contribute to atherosclerosis?
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during chronic endothelial inflammation, T cells migrate under the intima and signal cytokine release = macrophage, endothelial activation + smooth muscle proliferation
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What is an atheroma?
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cholesterol/atherosclerotic plaque
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What is a fatty streak?
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precusror to a full atherosclerotic plaque
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3 components of atherosclerotic plaques
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cells (smooth muscle/macrophages/T cells), ECM (collagen changes), lipids (intra/extracellular)
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What is an atheroembolism?
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plaque rupture leading to debris in the blood stream that can become micro-emboli
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What is stable angina?
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chest pain on exertion; likely caused by atherosclerotic blockage of 70%
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Why is plaque rupture bad for the patient?
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formation of micro-emboli as plaque debris disperses throughout the body
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Why is plaque erosion bad for the patient?
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the subendothelium is now exposed to blood and highly thrombogenic, a new clot/stenosis can form
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Why is hemorrhage into the plaque bad for the patient?
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expands the plaque's volume
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Where does the collagen (that forms the fibrous cap of a plaque) come from?
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smooth muscle cells
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Would increased metallo-protease activity make an atherosclerotic plaque (more or less) stable?
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less stable; the protease will cleave the collagen in the fibrous cap and make it more likely to rupture
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Why are myocardial infarctions more likely between 6AM and noon?
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The sympathetic reaction of waking up may induce vasoconstriction, contributing to vascular stress
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What is an aneurysm?
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localized dilation of a vessel or the heart
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What is a false aneurysm?
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extravasation of blood to form an extravascular hematoma. this may appear similar to an aneurysm (dilated blood vessel)
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What is an arterial dissection?
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blood enters the artery itself (between intima and media)
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Why would poor vascular connective tissue lead to aneurysm?
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the walls of the artery will not be able to resist the forces of the blood and begin to dilate
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What is Loeys-Deitz Syndrome?
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mutated TGF-B receptors = collagen and elastic fiber problems = likely aneurysms
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Why does Ehler-Danlos Syndrome cause aneurysms?
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collagen III fiber problems = weak vascular walls = likely aneurysms
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Why do elevated levels of metallo-proteases lead to aneurysms?
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they degrade collagen of the vessel walls
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Why do decreased levels of TIMPs (tissue inhibitor of metallo-proteases) lead to aneurysms?
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they are not high levels enough to stop the proteases from degrading collagen of the vessel walls = aneurysm
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What is a mycotic Abdominal Aortic Aneurysm?
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infection in the AA leads to rapid dilation and potential rupture
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What is an inflammatory Abdominal Aortic Aneurysm?
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migration of lymphocytes/macrophages into vessel wall causes dilation
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Most aortic dissections begin with a tear in the intimal layer. If a patient had a dissection without a tear in the intimal layer, where would the blood be entering the wall of the vessel from?
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vasa vasorum
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Herpesvirus, cytomegalovirus, and chlamydia pneumoniae have been detected in what?
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Atherosclerotic plaques
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What are the classifications of dissections?
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DeBakey1- extensive proximal dissection
DeBakey2- isolated proximal DeBakey3- distal dissection |
