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
Ca blockers adverse effects
drug-induced gingival enlargement
Ca blockers and pregnancy
nifedipine is drug of choice from this class
goal of anti-angiotensin drugs
reduce vasoconstriction and water retention
ACE inhib moa
inhibit ACE, conversion of angiotensin I to angiotensin II
ACE also breaks down bradykinin, these drugs cause accumulation
ARB inhib moa
inhibit angiotensin receptor at vessels and kidneys (prevent constriction and aldo release)
ACE inhib examples
captopril, lisinopril
ARB examples
losartan, valsartan
toxicities of ACEi and ARBs
dry cough, angioedema (from excess bradykinin causing endothelial leakage, worse in african americans)
hyperkalemia and risk of arrhythmias
ACEi and ARBs in pregnancy
teratogenic in first trimester, cause fetal hypotension and renal failure in second 2 trimesters
goal of sympatholytics
reduce BP by inhibiting SNS
why prefer B blockers to vasodilators?
B blockers less likely to induce reflex tachycardia
a2 agonist example and moa
clonidine and methyldopa- inhibit SNS from the CNS, reinforcing NE negative feedback loop on the presynaptic receptor
Beta blockers moa
inhibit B1 receptors- reduce HR and contractility
a1 inhibs moa
block a1 and inhibit VSM contraction
B blockers for HF?
yes, documented to decrease mortality
B blocker toxicities
can both raise and lower blood sugar (careful with diabetics)
exacerbate asthma/COPD (when non selective for B1)
a1 examples
prazosin, terazosin, doxazosin
a1 toxicities
fist dose causes orthostatic Hypotension (esp w/ prazosin)
HTN drug of choice during pregnancy?
methyldopa, a2 agonist
which drugs for HTN and angina?
B blockers and Ca blockers
drugs for HTN and diabetes/nephropathy?
ACEi or ARBs
drugs for HTN and HF
diuretics, ACEi/ARBs, B blockers, hydralazine and nitrates
drugs for HTN and BPH?
a1 antagonists
threshold for HTN tx?
greater than or equal to 140/90
or 130/80 and CVD, CKD, DM, high CVD risk
first line HTN agents
thiazides, Ca blockers, ARBs, ACEi
can combine any except ACEi and ARBs
