Health
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Title: Health

Essay Details:

Subject: Science
Author: Delilah S
Date: April 15, 2013
Level:
Grade: A
Length: 18 / 5284

Essay text:

Renin-Angiotensin-Aldosterone System ? ACEI and pregnancy ? Mechanism of action ? Monitoring of ACEI ? Hypokalemia/hyperkalemia as result of RAAS 2. Hypertension ? Classification of primary and secondary & etiology ? DEEPICT secondary HTN ? Symptoms, labs, when to admit? ? Treatments ? Beta-blockers, Ca2+ channel blockers, diuretics ? Refractory HTN ? Atherosclerosis and HTN 3. Review of Case ? Silver wiring ? Creatinine clearance ? Calculation & what it means ? Explain CHF ? relation to OTC medications (NSAIDs) ____________________________________________________________ ____________ Renin-Angiotensin System ? Renin is serine acid protease protein enzyme released by kidneys when arterial pressure falls too low ? Renin synthesized and stored in inactive form (prorenin) in juxtaglomerular cells (JG cells) of kidneys ? JG cells are modified smooth muscle cells in walls of afferent arterioles immediately proximal to glomeruli ? Decreased arterial pressure ? intrinsic reactions in kidneys cause many prorenin molecules in JG cells to split and release renin ? Most renin enters renal blood and passes out of kidneys into circulation ? Small amts of renin remain in local fluids of kidney and initiate intrareneal functions ? Renin acts enzymatically on another plasma protein called angiotensinogen to release 10-aa peptide, angiotensin I ? Angiotensin I has mild vasoconstrictor properties but not enough to cause significant changes in circulatory function ? w/in few seconds to minutes after formation of angiotensin I, 2 more aa's are split off from angiotensin I to form 8-aa peptide, angiotensin II ? conversion to AII occurs in lungs while blood flows through small vessels of lungs, catalyzed by angiotensin converting enzyme that is present in endothelium of lung vessels ? AII is powerful vasoconstrictor, but only persists in blood for 1-2 mins b/c it's rapidly inactivated by multiple blood and tissue enzymes collectively called angiotensinases ? Angiotensin II has 2 main effects that can elevated arterial pressure 1) vasoconstriction in many areas of body occurs rapidly ? acute effect ? arterial vasoconstriction > venous vasoconstriction ? arteriole constriction increases total peripheral resistance ? raises arterial pressure ? mild venous constriction promotes increased venous return of blood to heart ? helps heart pump against increasing pressure 2) decreased excretion of both salt and water by kidneys ? long-term effect ? causes increase in extracellular fluid volume ? increased arterial pressure during subsequent hours and days ? renin-angiotensin vasoconstrictor system requires 20 min to become fully active ? thus: slower to act for pressure control than nervous reflexes and sympathetic norepinephrine-epinephrine system ? angiotensin II causes kidneys to retain both salt and water in 2 major ways: 1) AII acts directly on kidneys to cause salt and water retention ? Mechanisms of AII on kidneys: ? Constrict renal arterioles ? diminishes blood flow through kidneys ? less fluid filters through glomeruli into tubules ? Slows flow of blood through kidney ? reduces pressure in peritubular capillaries ? causes rapid reabsorption of fluid from tubules ? Direct effect on tubular cells ? increase tubular reabsorption of sodium and water 2) AII causes adrenal glands to secrete aldosterone ? aldosterone increases salt and water reabsorption by kidney tubules ? Activation of renin-angiotensin system causes rate of aldosterone secretion to also increase ? Function of aldosterone ? increase sodium reabsorption by kidney tubules ? increases total body extracellular fluid sodium ? increased Na causes water retention ? increases extracellular fluid volume ? long-term elevation of arterial pressure ? Direct effect of angiotensin on kidneys is perhaps 3 or more times as potent as indirect effect acting through aldosterone Role of Renin-Angiotensin system in maintaining normal arterial pressure despite salt intake ? Increased salt intake ? elevated extracellular fluid volume ? elevated arterial pressure ? increased blood flow through kidneys ? reduced rate of secretion of renin ? decreased renal retention of salt and water ? return of extracellular fluid volume almost to normal ? return of arterial pressure almost to normal ? Thus: renin-angiotensin system is automatic feedback mech...

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