Test 3 summary - Test 3 Material Physical factors for blood...

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Test 3 Material Physical factors for blood vessels —some factors constant like length, others are variable. Flow=pressure/resistance o Vessel radius —most important variable factor because resistance=1/radius 4 so a small constriction causes a large increase in resistance. Same pressure gradient throughout. o Viscosity— thickness of blood controlled by the hematocrit (% of RBCs in blood, 45% in males, 42% in females) A large change is needed to influence blood flow. Above ~48%, RBCs will interact with arteriole walls and greatly increase resistance Atherosclerosis— can lead to hardening of artery because of excess fatty acids o Stage I— LDL (bad cholesterol) lays down fatty streak (forms plaque) Alcohol effect— modest alcohol consumption can solubilize the fatty streak, reducing the effects of stage I, a biophysical effect o Stage II— white blood cells and fibroblasts overgrow the fatty streak and reduce diameter of blood vessel o Stage III— calcium infiltration hardens overgrowth and hardens arteries Capillary fluid exchange— balance of BP forcing fluid out at the arterial end and osmotic pressure form plasma proteins drawing fluid in at the venous end. Fluid moves through capillary pores and some hydrophobic gases move across the membrane wall. There is a net outward at the arterial end of 11mmHg, which creates filtration. At venuous end, there is a net inward of 9mmHg. o Reabsorption— at venous end you have a lower BP so that BP<osmotic pressure and fluid reenters. There is a slightly more fluid filtered than absorbed Lymph flow— returns excess filtered fluid to circulation. Fluid enters closed-ended lymph vessels and merges with others. Lymph nodes are sites of large lymph vessel merger. Lymph enters vena cava where the BP=0 through the thoracic duct o Edema— swelling, excess filtration because of broken capillaries or low blood protein from starvation or alcoholism). Occurs when filtration exceeds return or bacteria causes pressure and destruction that draws on osmotically. Cardiovascular regulation o Nitric oxide (NO)— important in the moment to moment regulation. Activated by hormones/neurons. Increased NO release relaxes vascular smooth muscle which increases blood flow. Can be factor of hypertension if you don’t have enough o Baroreceptors— stretch receptors in carotid sinus and aortic arch. Changes in BP alter baroreceptor activity o Resetting— body adjusts to own normal BP, adaptation to prolonged BP changes over days Drug treatments for hypertension o ACE inhibitors— block conversion of Angiotensin I to angiotensin II, most common initial Rx treatment o α-adrenergic receptor blockers— stops sympathetic constriction of vascular smooth muscle and blocks NE effects. Fewer Ca+2 channels open so there is less Ca+2 entry and less force
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Test 3 Material o β-adrenergic receptor blockers— blocks NE/Epi effects on the heart so there is less Ca+2 entry and contracts less strongly. Decreases force of cardiac contractions.
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