Term
| slowly progressive abnormal fibrous thickening and hardening of arterial vessel walls |
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Definition
| atherosclerosis, thickened by lipids, smooth myo cell proliferation and extracellular matrix of intima, then calcifies. |
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Term
| Risk factors for? Age, gender, genetic, hyperlipidemia, hypertension, smoking, inflammation by C-reactive protein and measured by Lp-PLA2, diabetes, infections, high plasma homocysteine, lifestyle of obesity and stress |
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Definition
| athersclerosis: age causes chronic injury, more men |
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Term
| How is genetics a risk factor for atherosclerosis? |
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Definition
| derangements in lipoprotein metabolism |
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Term
| How is hyperlipidemia a risk factor for atherosclerosis? |
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Definition
| hypercholesterolemia, hih LDL. 20% chol comes from diet, 80% made in liver. |
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Term
| How is HDL RT to risk of atherosclerosis? |
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Definition
| Inversely. HDL scavenges cholesterol and removes cholesterol and triglycerides from other tissues and returns to liver for excretion |
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Term
| How does hypertension increase risk for atherosclerosis? |
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Definition
| Produces endothelial injury |
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Term
| How does smoking increase risk for atherosclerosis |
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Definition
| endothelial injury due to CO2 induced hypoxia |
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Term
| How is diabetes a risk for atheroclerosis? |
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Definition
| decreased hepatic removal of LDL from circ |
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Term
| How are infections a risk for atherosclerosis |
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Definition
| maybe RT to inflammation (chlamydia, pneumoniae, peridontal disease. H pylori |
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Term
| How is elevated plasma homocysteine (hyperhomocysteinemia) a risk factor for atherosclerosis? |
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Definition
| significant source of oxygen free radicals, H2O2 and ROS, that causes endothelial dysfunction/damage. AND interferes with action of NO |
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Term
| How is obesity a risk factor for atherosclerosis? |
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Definition
| Adipocytes produce inflamm cytokines |
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Term
| Chronic inflamm response of arterial wall initiated by endothelial injury and sustained by interaction between lipoproteins, macrophages, T cells and cell wall |
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Definition
| Response to injury theory |
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Term
| Patho: injury from risk factors and shear, hemodynamic disturbance, inflammatory response |
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Definition
| Endothelial injury, leads to dysfunction |
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Term
| Patho: LDL accumulates in arterial intima at points where artery branches and sites of endothelial permeability. |
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Definition
| Role of lipids in atherosclerosis-one of the roles |
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Term
| Patho: LDL produces ROS, directly impairs endothelial cell function |
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Definition
| Role of lipids in atherosclerosis-one of the roles |
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Term
| Intimal LDL is oxidized: chemotactic for circ monocytes, ingested by macrophages through scavenger receptors and form foam cells. Inhibits NO production by endoth cells, cytotoxic to endo the cells and smooth myo cells, stimulates SMC movement to intima |
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Definition
| Role of lipids in atherosclerosis-one of the roles |
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Term
| Oxidized LDL in the role of lipids |
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Definition
form foam cells by macrophages
Inhibits NO production
cytotoxic to endothelial cells and smooth myo cells, moves them to intima |
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Term
| Patho: monocyte recruitment, transmigration to intima and activation to macrophages |
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Definition
| Role of inflammation/macrophages in atheroclerosis |
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Term
| Patho: macros take up oxidized LDL through special scavenger receptors to become foam cells |
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Definition
| Role of inflammation/macrophages in atheroclerosis |
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Term
| Patho: secrete IL-1, TNF alpha and other cytokine to continue inflamm process |
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Definition
| Role of inflammation/macrophages in atheroclerosis |
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Term
| Patho: elaborate growth factors: stimulates smooth myo cell proliferation |
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Definition
| Role of inflammation/macrophages in atheroclerosis |
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Term
| Patho: T cells recruited to area by chemoattractants, Th1 active with release of proinflamm cytokines, Th2 stimulates prod of antibodies to oxidized lipoproteins |
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Definition
| Role of immune system in atherosclerosis |
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Term
| Patho: elaborate growth factors, PDGF that stimulates smooth myo cell proliferation, participates in clotting cascade |
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Definition
| Role of platelets in atherosclerosis |
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Term
| Patho: migrate from media to intima and proliferates, synthesize and deposits collagen, elastin and glycoproteins (extracellular matrix), Takes up oxidized LDL and becomes foam cells, migrates over fatty streak to make caps |
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Definition
| Role of smooth muscle proliferation in atheroclerosis |
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Term
| Etiology: multifactors: interaction of genetic, environment and neurohormonal |
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Definition
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Term
| Patho: 5 parts of primary hypertension |
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Definition
reduced renal Na secretion w/normal press
renin-angiotensin-aldol system problem
functional vasoconstriction
vascular smooth myo growth/structure
symp NS dysfunction |
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Term
| Patho: --reduced renal Na excretion, --more Water retention-increased fluid vol, then hi CO plus peripheral vasoconstriction, get hi BP and Na excretion--reset pressure natriuresis, but at higher BP |
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Definition
| Reduced renal Na excretion w/normal arterial pressure: One part patho of Primary hypertension |
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Term
| Patho: genetic disorder affects renin/angiotensin/aldosterone, allele variation in genes encoding R/A/A system (known racial diff), Outcome: arterial smooth muscle remodeling and HTN |
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Definition
| Problem with R/A/A system in primary hypertension |
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Term
| Patho: risk factors of stress/smoling with repeated episodes of VC that causes structural thickening of art walls and HTN |
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Definition
| Functional Vasoconstriction of primary hypertension |
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Term
| Patho: environmental factors high salt diet causes water retention, then hi fluid volume, high CO with peripheral VC, and HTN |
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Definition
| Functional VC of primary hyptertension |
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Term
| Patho: increased wall thickness, genetic defects in intracellular signalling in smooth myo cells: tone does not return to normal, with VC and remodeling of structural thickening of arterial walls |
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Definition
| Defect in Vascular smooth Myo growth and structure |
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Term
| Patho: genetic changes causes increase in # of adrenergic receptors in SMC--increased response to symp stimulation--VC--remodeling |
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Definition
| Altered sympathetic NS function in primary hypertension |
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Term
| What do these 5 things affect?--prolonged VC, increased Total peripheral resistance, injury, increased permeability, increased Ca effects |
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Definition
| Vascular effect of primary hypertension |
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Term
| What is the vascular effect of prolonged vasoconstriction? |
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Definition
| arterial smooth myo hypertrophy and hyperplasia, decreased arterial lumen size |
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Term
| Vascular effect of increased total peripheral resistance |
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Definition
vessel wall injury
vascular effect of primary hypertension |
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Term
| Vascular effect of injury to vessel |
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Definition
| inflammation, increased vascular permeability |
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Term
| vascular effect of increased permeability to injury |
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Definition
| Na, Ca, water, Plasma proteins enter vessel walls and cause further thickening |
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Term
| Vascular effect of increased Ca |
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Definition
| Increased smooth myo contraction, further VC of vascular effect of hypertension |
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Term
| End Organ damage: HF, angina, MI, stroke, aneurysms, hemorrhagic stroke, renal failure, retinopathy |
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Definition
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Term
| Sx: severe HTN >200/>100, severe cerebral damage, or damage to heart, kidney, eye |
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Definition
| Hypertensive crisis, maglignant HTN |
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Term
| Etiology: atheroslerosis, degeneration of arterial media/production of nonfunctional elastin, trauma, genetic susceptibility, infections, hypertension |
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Definition
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Term
| Why does atheroclerosis lead to aneurysm? |
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Definition
| Most common reason, casuses arterial wall thinning thru MEDIAL destruction, and compromises nutrient/O2 supply to arterial wall |
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Term
| How does genetics play into aneurysms? |
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Definition
| congenital defect in connective tissue (collagen or collagen-elastin), marfan syndrome, altered extra cellular matrix production |
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Term
| aneurysm bounded by complete vessel wall |
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Definition
| True aneurysm, remains in system |
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Term
| etiology: tension against a thinned wall, blood remains within the confines of circ system. |
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Definition
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Term
| chronic pain, common men after 50, atherosclerosis most freqt cause, risk for rupture depends on size |
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Definition
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Term
| Sx: pulsating mass, larger than usual pulsation, abd/lower back pain, shock with rupture |
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Definition
| abdominal aneurysm (true) |
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Term
| Breach in vascular wall--extravascular hematoma, free communication between intravascular space and hematoma |
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Definition
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Term
| Most common in men 40+ with HTN |
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Definition
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Term
| Intimal tear, blood enteres wall of artery, dissecting between layers and creating a cavity in the vessel wall. tension against outer arterial wall produces it. |
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Definition
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Term
| Sudden onset, ripping chest or back pain |
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Definition
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Term
| Patho: inadequate tissue perfusion--anaerobic metabolism and production of lactic acid, Lactic acidosis depressed myocardium and decreases peripheral vascular responsiveness to catecholamines--hypoxic cell injury and death |
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Definition
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Term
| What happens with inadequate tissue perfusion? |
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Definition
| Anaerobic metabolism and production of lactic acid |
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Term
| What happens with lactic acidosis? |
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Definition
| depressed the myocardium and decreases peripheral vascular responsiveness to catecholamines--hypoxic cell injury and death |
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Term
| Blood flow is slowed and clotting cascade is activated |
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Definition
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Term
| cells soak up water and further depletion of intravascular volume; lysosomal enzymes leak out and destroy neighbor cells |
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Definition
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Term
| Vasodilated, decreased CO, |
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Definition
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Term
| Etiology: increased and prolonged intraluminal pressusre from venous stasis, obesity, dependent position of legs, tumor masses, damage to saphenous valves, herediary defects in venous wall development |
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Definition
| Chronic venous insufficiency |
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Term
Patho: 1. increased and prolonged intraluminal pressure (oressure breaks valve)
2. Valvular damage/defect in venous wall (hereditary) |
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Definition
| Chronic venous insufficiency |
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Term
| How does increased and prolonged intraluminal pressure cause chronic venous insufficiency? |
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Definition
| causes dilation, renders valves incompetent, further dilates and venous stasis: tortuous veins, clots, edema |
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Term
| How does valvular damage/defects cause chronic venous insufficiency? |
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Definition
| permits backflow/regurgitation, large volume of blood causes incr pressure, dilation and venous stasis: tortuous veins, clots, edema |
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Term
| Have more elastic fibers/elastin |
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Definition
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Term
| Have muscular branches, like renal arteries |
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Definition
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Term
| Have more smooth muscle innervation, principal point of physiologic resistance to blood flow |
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Definition
| Small arteries/arterioles |
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Term
| single layer of endothelial cells, exhange diffusible substances |
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Definition
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Term
| hold up to 2/3 of systemic blood, easily distended, thin walls |
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Definition
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Term
| drains excess fluid in tissues back to vascular system |
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Definition
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Term
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Definition
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Term
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Definition
| single layer of endothelial cells, subendothelial layer connective tissue, internal elastic lamina--more prominent in large arteries |
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Term
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Definition
| smooth myo cells: circular or spiraled, elastin, have actina nd myosin but now always organized in parallel, don't have sarcomeres, Ca binding to calmodulin--facilitates actin/myosin crossbinding, O2 nutrient provided by diffusion , has external elastic lamina |
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Term
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Definition
| connective tissue, nerve fibers, vaso vasorum |
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Term
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Definition
| pressure= quantity of blood flowing thru vessel per minute x resistance of vessels wall to flow (radius) |
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Term
| BP translation to poiseuilli's law |
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Definition
| arterial BP= CO x Peripheral resistance |
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Term
| Increase pre-load does what to CO? |
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Definition
| INcrease preload= increase CO |
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Term
| Increase volume = ? outward pressure |
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Definition
| Increase outward pressure |
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Term
| Poiseuilli's Law--blood or air can cause pressure |
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Definition
| Quantity change by radius (like river flowing thru wall opening or narrow opening) Pressure + CO x Resistance P(F) x R |
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Term
| Net filtration is determined by forces favoring filtration - forces opposing filtration |
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Definition
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Term
| Two parts of autoregulation of vascular system control |
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Definition
Smooth myo cells contract in response to stretch (myogenic response)
-maintain constant blood flow in presence of altered perfusion pressure |
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Term
| What substances promote vasoconstriction that are secreted by the endothelium |
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Definition
Endothelin
Angiotensin converting enzyme ACE |
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Term
| Substances that promote VasoDILATION secreted by endothelium |
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Definition
| Prostacyclin (PG12), Nitric Oxide (shear, stres, Ach, bradykinin, substance P, vasoactive intestinal polypeptide make NO) |
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Term
| What do these stimulate production of: shear, stress, Ach, bradykinin, substance P, vasoactive intestinal polypeptide |
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Definition
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|
Term
| Nitric oxide-dilates or constricts? |
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Definition
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|
Term
| Calcium and arginine is needed for production of ? |
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Definition
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|
Term
| NO acts with cGMP to do what? |
|
Definition
| relaxes vascular smooth myo cells and produces vasodilation |
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Term
| NO acts chronically to keep vascular system? |
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Definition
| dilated, responsible for reactive hyperemia |
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Term
| What happens to BP when NO is inhibited? |
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Definition
| Higher BP--vascular control of system |
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Term
| When are thromboxane and leukotrienes released and what do they do? |
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Definition
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|
Term
| Mediators released on injury, which ones vasodilate? |
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Definition
| Prostaglandins of control of vascular system |
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Term
| Vasoconstrictors of Vascular control of vessels |
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Definition
Norepi, Epi, Vasopressin, Angiotension II
(NEVA--constrictors) Boa constrictors |
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Term
| Vasodilators of vessel controls? |
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Definition
| Kinins (bradykinin), produced from inflammation, InActivated by kininase II (ACE--VC)), if ACE inhibited for tx of HTN or HF, higher plasma and tissue kinens (VD) |
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Term
| ACE: dilator or constrictor? |
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Definition
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|
Term
| Angiotension II--VC, or VD |
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Definition
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|
Term
| Where is angiotension II formed? |
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Definition
| renin from kidneys transforms angiotensinogen (from liver) to angiotensin I within vasculature. ACE converts I to II that is attached to plasma membrane of endothelial cells. |
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Term
| ACE causes VC and excreted by? |
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Definition
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|
Term
| Function of Angiotension II |
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Definition
| VC thru direct action on vascular smooth myo, stimulates aldosterone secretion, growth factor for smooth myo, and hypertrophy and remodeling, stimulates fibroblast production, STOPS NO production and prostacyclin |
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Term
| What chemical inhibits the release of NO? |
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Definition
NO dilates, so something that VC:
angiotension II |
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Term
|
Definition
| VD. increases glomerular filtration rate, antagonize angiotensin II, VD. |
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