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30 Cards in this Set
- Front
- Back
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types of hypertension
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primary hypertension: no known cause, 92%, 90% 55+ age
secondary: known cause, include: kidney disease hyperthyroidism pregnancy erythropoietin pheochromacytoma sleep apnea contraceptive use |
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how to measure blood pressure
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blood pressure=cardiac output x peripheral resistance
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baroreceptor
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sens BP at aortic arch and carotid sinus, sympathetic pathway, instantly
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RAAS
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protein hormones in kidney, take hours
angiotensinogn->antiotensin 1->2->ADH and aldosterone -cause vasoconstriction and renal retention of sodium/water vasoconstriction increase BP retention of water increase blood volume/increase cardiac output |
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renin
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catalyze formation of angiotensionogen to angiotensin I
-made by juxtaglomerular function: |
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Angiotensin converting enzymes (ACE)
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convert angio I->II
angio II: produce vasoconstriction in posterior pituitary releasing ADH， causing water retention under hypotention, kidney retains water |
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obese and sodium impact and potassium
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obesity increase insulin secretion, cause reabsorption of NA and water, having higher blood volume
high NA cause reabsorption of blood potassium is negative |
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DASH
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dietary approaches to stop hypertension
best to do in prehypertension |
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Diuretics 3 classes
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loop diuretics
thiazide diuretics potassium sparing diuretics/aldosterone antagonists |
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function of diuretics
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block Na and Cl reabsorption from nephron, making tubule attracts water prevent reabsorption.
retention of water promote excretion of water and sodium/chloride ions |
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Loop diuretics
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block NACL reabsorption in ascending loop
cause hypokalemia (K+), due to transportion of K+ into blood |
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Thiazide Diuretics
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block at distal tube NACL
decrease vascular resistance less effective than loop diuretics |
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Potassum sparing diuretics/aldosterone antagonist
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minimal among 3, block aldosterone receptor in collecting duct.
aldesterone cause NA reuptake and K secretion, blocking cause NA excretion and K retention, (potassium sparing) this is used to counter hypokalemia side effect, can cause hyperkalemia tho |
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beta blocker treat hypertension by 2 mechanisms
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1. block cardiac beta 1 receptor
2. block beta 1 receptor on juxtaglomerular cells |
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blocking cardiac beta 1 receptor
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binding catecholamines (Epi or NoEpi) to beta receptor = increase cardiac output, block beta receptor=decrease cardiac output
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blocking beta 1 receptor on jux cells
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jux=release renin=activate RAAS=vasoconstriction
-beta blocker decrease renin, decrease RAAS and decrease peripheral resistance |
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suffix for beta blocker
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olol
eg propanolo |
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type of beta blockers
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antagonists, since they block receptors
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first gen vs 2nd gen in beta blockers
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1st gen: nonselective, block both beta 1 and beta 2(in lung)
2nd gen: only block beta 1 |
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ACEI
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1. -decrease angiotensin II production (II = vasoconstrictor)
-also decrease total blood volume, reduce both cardiac output and peripheral resistance 2. inhibit breakdown of bradykinin (this cause vasodilation) or making more bradykinin |
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suffix for ACEI
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pril.
captopril ramipril. |
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angiotensin receptor blockers ARBs
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similar to ACEI, decrease angiotensin II.
block binding of angio II to receptor AT1. DONOT affect synthesis vasodilation. also cause decrease aldosterone=increase sodium and water excretion. |
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suffix for ARBs
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sartan
losartan valsartan |
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direct renin inhibitors DRIs
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bind renin and block conversion from angiotensinogen to angiotensin I.
cause hyperkalemia |
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calcium channel blockers
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Ca channel is essential for contraction
blocker decrease contraction. |
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2 categories of calcium channel blockers
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1. dihydropyridine calcium channel blockers
2. non-dihydropyridine calcium channel blockers |
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dihydropyridine calcium channel blockers
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block calcium influx in SM, cause relaxation and vasodilation.
DO NOT act on the heart, |
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suffix for dihydropyridine calcium channel blockers
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dipine
nifedipine felodipine |
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non-dihydropyridine calcium channel blockers
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block heart and SM in arteries.
vasodilation and decrease cardiac output |
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centrally acting alpha 2 agonist
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activate alpha 2 receptor in brainstem
-decrease sympathetic outflow to heart and BV. -activation of alpha 2 receptor=inhibition of sympathetic=decrease cardiac output and peripheral resistance |
