Anti-HTN drugs Flashcards
3 factors that determine BP
CO, SVR, blood volume
overall diuretic mech
inhibit reuptake of Na+ and thus water- water follows sodium
targets for the three main diuretics
loop- loop of henle
thiazides- distal tubule
K+ sparing- collecting duct
loop diuretics moa
inhibit Na/K/2Cl transporter in loop of henle, reduce Na reuptake (also K+ reuptake)
loop examples
furosemide, torsemide
loop adverse effects
hypokalemia and alkalosis- extracellular Na+ is traded for intracellular H+ downstream of targeted transporter, more Na+ w/ diuretic effect
thiazide moa
inhibit Na/Cl symporter in DCT
thiazide examples and adverse effects
hydrochlorothiazide, chlortalidone
hypokalemia and alkalois (same mech as loop)
K+ sparing moa
inhibit ENaC (epithelial Na channel) in collecting duct either directly (triamterene) or indirectly thru antagonizing aldosterone receptor (spironolacotne and eplerenone) which normally upregulates ENaC
K+ sparing adverse effects
gynecomastia- male breast enlargement in spironolactone (similar to estradiol) but not with eplerenone
interaction of diuretics and NSAIDs
NSAIDs inhibit glucoronidation of aldosterone (more ENaC) and thus more water retention, and inhibit PGE2 vasodilation
NSAIDs raise blood pressure, can blunt the effects of diuretics
why hypokalemia in loop/thiazide diuretics?
increased extracellular Na+from upstream drives loss of K+ in collecting duct
hypokalemia CV relevance
can cause hyperpolarization and delayed repolarization (long QT) which can cause arrhythmias
types of vasodilator drugs
hydralazine, K+ channel opening (diazoxide), Ca++ blockers (amlodipine, etc)
differentiate DHP and non-DHP Ca++ blockers
DHP (amlodipine and nifedipine) act mainly on vascular smooth muscle (SVR) while non DHP act on both vascular SM and cardiac tissue (verapamil and diltiazem)
Ca blockers moa
inhibit Ca influx channels, reduce strength of SM contraciton