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124 Cards in this Set
- Front
- Back
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What are the 3 concentric layers of a blood vessel?
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-Intima
-Media -Adventitia |
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What are the layers of blood vessels composed of?
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-Endothelial cells
-Smooth muscle cells -ECM |
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What is ECM made up of?
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-Collagen
-Proteoglycans -Elastic fibers |
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What is the intima?
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-Endothelial cells
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What lies between the intima and media?
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Internal elastic lamina
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What is the Media?
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Smooth muscle cells
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What lies between the media and adventitia?
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External elastic lamina
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What is the outermost layer of a blood vessel?
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The adventitia
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What is the hallmark of large arteries?
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Elasticity
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What is the largest artery and why is it elastic?
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The aorta - so that it can expand and recoil during systole and diastole.
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What is the hallmark of medium arteries?
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Muscular
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What are 2 examples of medium arteries? Why are they muscular?
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-Renal arteries
-Coronary arteries Muscle allows them to vasoconstrict and dilate and regulate regional bloodflow. |
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What are the smallest of the arteries?
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Arterioles
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What function do arterioles serve?
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To change bloodflow from pulsatile to steady
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What do arterioles lead into?
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Capillaries
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What vessels provide the most resistance to bloodflow?
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Arterioles
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What supplies oxygen and nutrients to the inner media of arteries?
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Fenestrations in the internal elastic lamina, allowing oxygen to diffuse in from the lumen of the vessel.
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What supplies oxygen and nutrients to the outer media of arteries?
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Vasa vasorum
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What is the diameter of capillaries?
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1 RBC width; 7-8 micra
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What makes capillaries different from arterioles?
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-Only made of endothelial cells
-NOT three layers |
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What is the function of capillaries?
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To allow diffusion and exchange of nutrients.
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How do capillaries achieve their function?
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By having slow flow (due to lack of media) and very large cross sectional area collectively.
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What organs have the highest density of capillaries?
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Highly metabolic organs:
-heart -adrenals -thyroid |
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How much blood is in the veins at any given moment?
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2/3
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What are 3 ways in which veins differ from arteries?
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-Larger diameters
-Larger lumens -Thinner, less organized walls |
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To what 3 changes are veins prone?
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-Irregular dilation
-Compression -Easy penetration |
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What are irregularly dilated veins called?
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Varicose veins
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What prevents reverse flow in veins?
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Valves
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What causes bloodflow in veins?
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Contraction of skeletal muscles around the veins.
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What do we see happening at postcapillary venules in certain conditions?
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Vascular leakage and WBC extravasation during inflammation
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What are 3 congenital anomalies of blood vessels?
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-Aberrant branching patterns
-Berry aneurysms -Arteriovenous fistulas |
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Are aberrations in the usual anatomic branching patterns of arteries usually symptomatic?
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Rarely
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When are blood vessel congenital anomalies symptomatic?
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When the anomalous artery is a coronary artery.
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What can an anomalous coronary artery result in?
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Sudden death
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What is an arteriovenous fistula?
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A direct communication between an artery and a vein without a capillary in between. (abnormal)
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Are AV fistulas always developed in utero?
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No, they can be acquired.
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What are 3 things that can cause acquired AV fistulas?
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-Penetrating injuries
-Arterial aneurysm rupture into the adjacent vein -Inflammatory necrosis of adjacent vessels |
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What is the result of an AV fistula? Longterm?
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Shunting - high-output cardiac failure (lose out on all the resistance of the capillaries)
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What are AV fistulas susceptible to?
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Rupture with ensuing hemorrhage
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What lines blood vessels?
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Endothelial cells
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What unique organelle do endothelial cells contain?
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Weibel-Palade bodies
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What are Weibel-Palade bodies?
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Organelles that store vWF and other substances.
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What is the major function of endothelial cells?
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To maintain the permeability barrier between circulation and the rest of the peripheral tissues.
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What are 4 anticoagulant molecules made by ECs?
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-Prostacyclin
-Thrombomodulin -Heparin-like molecules -Plasminogen activator |
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What are 3 prothrombotic molecules made by ECs?
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-vWF
-Tissue factor -PAI (inhibitor) |
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What ECM components do ECs produce?
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-Collagen
-Proteoglycans |
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What vasoconstrictors do ECs make?
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-Endothelin
-ACE |
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What vasodilators do ECs make?
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-Nitric oxide
-Prostacyclin |
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What inflammatory mediators are produced from ECs?
-cytokines -adhesion molecules |
-IL1, IL6, chemokines
-VCAM1, ICAM1, E/P-selectins |
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What growth stimulators do ECs produce? Growth inhibitors?
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Stimulators: PDGF, CSF, FGF
Inhibitors: Heparin, TGF-beta |
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What important metabolic function do ECs serve?
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Oxidation of LDL
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What is required for proper EC function?
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The right balance between EC activators, and induced genes in responding ECs
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What are 3 major consequences of EC dysfunction?
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-Initiation of thrombus formation
-Atherosclerosis -Vascular lesions of hypertension |
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When is EC dysfunction rapid and reversible?
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When it is independent of new protein synthesis.
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When is dysfunction longer in onset and development?
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When it results from altered gene expression and protein synthesis.
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What is the predominant cellular component of the media of vessels?
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Smooth muscle cells
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What is the function of smooth muscle?
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Vasoconstriction and dilation
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What else does smooth muscle synthesize?
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-Collagen
-Elastin -Proteoglycans |
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What are 3 factors elaborated by smooth muscle cells?
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-PDGF
-IFN-y -TGF-b |
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What are 4 things that regulate vascular smooth muscle cells?
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-Renin-angiotensin system
-Catecholamines -Estrogen -Osteopontin |
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In what process do vascular smooth muscle cells play an integral part?
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Atherosclerotic plaque formation
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What regulates the migration and proliferation of vascular smooth muscle cells?
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-PDGF
-IL-1 |
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What are 3 inhibitors of vascular smooth muscle?
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-nitric oxide
-IFN-y -TGF-beta |
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What IS arteriosclerosis?
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Hardening of the arteries due to thickening and loss of elasticity.
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What are the 3 types of arteriosclerosis?
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1. Atherosclerosis
2. Monckeberg medial calcific sclerosis 3. Arteriolosclerosis (2 kinds) |
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What are the 2 kinds of arteriolosclerosis?
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-Hyaline
-Hyperplastic |
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What is the most common and important type of arteriosclerosis?
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Atherosclerosis
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What is the hallmark feature of atherosclerosis?
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Intimal lesions that protrude into and obstruct the lumen of vessels
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What adverse effect do fibrofatty plaques and atheromas have on vessels?
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Weakening of the underlying media
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Why do we care about atherosclerosis?
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It is responsible for >1/2 of all deaths in the western world.
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What are 4 common sites of atherosclerosis?
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-Infrarenal aorta
-Coronary arteries -Popliteal arteries -ICA and circle of willis |
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When does atherosclerosis start? When does it become symptomatic?
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Start: in childhood
Symptoms: in adulthood |
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What are common organs fed by atherosclerotic vessels when symptomatic disease occurs?
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-Heart
-Brain -Kidneys -Lower extremities -Small intestine |
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What are 5 adverse vascular changes that result from progressive atheromas?
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-Stenosis
-Thrombosis/obstruction -Aneurysm -Rupture -Embolization |
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What are the 3 major consequences of atherosclerosis?
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-MI
-Stroke -Aneurysm |
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What does chronic endothelial injury cause?
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Endothelial dysfunctino
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What are 7 causes of chronic endothelial injury?
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-Hyperlipidemia
-Hypertension -Viruses -Smoking -Homocysteine -Immune reactions -Toxins |
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What is the result of injury to endothelial cells?
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Inflammation
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What inflammatory cells respond to injured endothelium? What do they do?
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-Monocytes
-Macrophages Adhere to damaged endothelium |
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What do monos/macrophages do after adhering to the damaged endothelium?
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Penetrate the vessel wall and interact with smooth myocytes.
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What dangerous molecules are lurking in the circulation?
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LDL and VLDL
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What is it bad to have lots of LDL and VLDL when endothelial injury is happening?
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They bind to vascular matrix proteins and get eaten by the monos/macrophages
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What are monos and macrophages that are engorged with LDL and VLDL called?
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Foam cells
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What does growth factor release from platelets and macrophages during endothelial inflammation cause?
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Migration of smooth muscle to the intima
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What do smooth muscle cells DO after migrating to the intima?
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-Proliferate
-Accumulate collagen -Form a fibrous cap |
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What is the end result of chronic endothelial injury and inflammation?
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Formation of a plaque
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What accumulates in the plaque to make it unstable and prone to rupture?
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Lipid
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What propagates the inflammatory response in plaque formation?
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Tcells evolving into Th1's
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What is the earliest form of an atherosclerotic plaque?
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Fatty streak
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When does formation of plaques begin?
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At young ages
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What are the 3 types of clinical consequences of atherosclerosis seen in middle age to elderly age?
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STARE
-Stenosis -Thrombosis -Aneurysm -Rupture -Embolism |
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What happens in atherosclerosis if risk factors are not taken care of?
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The lipid core will continue to grow and push the arterial wall outward.
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What is at the center of large atherosclerotic plaques?
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Yellow grumous debris
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What does grumous mean?
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Gruel
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What eventually happens to the grumus debris?
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It calcifies
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Result of calcified atherosclerotic plaques?
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Stiff, brittle, noncompliant arteries.
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What are 4 specific complications of Atherosclerosis?
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HEAT
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HEAT:
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-Hemorrhage into the plaque or hematoma formation
-Embolization -Aneurysmal dilation -Thrombosis |
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What can hemorrhage, embolization, and thrombosis all result in?
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Myocardial infarction
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What are 4 general complications of acute or chronically diminised arterial perfusion?
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-Mesenteric occlusion
-Ischemic encephalopathy -Chronic ischemic heart disesae -Sudden cardiac death |
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What are 4 major nonmodifiable risk factors for atherosclerosis?
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-Increasing age
-Male gender -Family history -Genetic abnormalities |
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What are 4 potentially controllable risk factors for atherosclerosis?
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-Hyperlipidemia
-Hypertension -Cigarette smoking -Diabetes |
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What increases the risk for atherosclerosis more; increased diastolic or systolic BP?
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Both
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At what blood pressure are men at a >5 fold greater risk for developing atherosclerosis?
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169/95
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What is the number 1 preventable risk factor for atherosclerosis?
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Smoking
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In what patients is the risk of MI due to atherosclerosis DOUBLED?
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Diabetes mellitus patients
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Why are patients with Diabetes mellitus at increased risk of MI and atherosclerosis?
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The disease induces hypercholesterolemia
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What are diabetes mellitus patients at a 100X increased risk of getting?
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Gangrene in their lower extremities due to atherosclerosis
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What do we get from the Framingham Heart Study?
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A 10-year risk calculator based on risk factors in the patient.
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What is Monckenberg medial calcific sclerosis?
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Calcifications in muscular arteries
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In what age of patients do we typically see Monckenberg medial calcific sclerosis?
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>50 years
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Does Monckenberg medial calcific sclerosis result in occlusion?
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no
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What is Arteriolosclerosis most often associated with?
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-Hypertension
-Diabetes mellitus |
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Do we see occlusion of the vessels in arteriolosclerosis?
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Not quite but there is vessel wall thickening and luminal narrowing.
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Does hypertension affect blood vessels?
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YES - it causes hypertensive vascular disease.
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For what 2 conditions is hypertensive vascular disease one of the most important risk factors?
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-Coronary artery disease (CAD)
-Cerebrovascular accidents |
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What are the 4 main complications that hypertensive vascular disease leads to?
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-Cardiac hypertrophy
-Heart failure -Aortic dissection -Renal failure |
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With what 2 forms of arteriolar disease is Hypertensive Vascular Disease associated?
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-Hyaline arteriolosclerosis
-Hyperplastic arteriolosclerosis |
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What 3 changes do we see in Hyaline arteriolosclerosis?
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-Pink hyaline thickening of the arteriolar wall
-Loss of underlying structural detail -Narrowing of the lumen |
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What are the 2 things that cause hyaline thickening of arterioles?
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-Leaking plasma proteins
-Excess ECM production from smooth muscle cells |
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What 2 conditions lead to hyaline arteriolosclerosis?
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-Hypertension
-Diabetes mellitus |
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What condition leads to HYPERPLASTIC arteriolosclerosis?
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Malignant hypertension - severe acutely elevated blood pressure.
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What are the histologic features seen in hyperplastic arteriolosclerosis?
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-Onionskin
-Laminated thickening of the arteriolar wall -Progressive narrowing of the lumen |
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Which is more common; hyperplastic or hyaline arteriolosclerosis?
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Hyaline
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