Pharm Flashcards
(31 cards)
lower intravascular volume (so lower BP)
diuretics
loop diuretics
very potent
good for heart issues (CHF)
BAD for chronic HTN
cause hypOkalemia, hypOchloremia, met alkalosis
thiazide diuretics
lower potency
good for essential HTN
K sparing diuretics
block Aldo receptors
lower potency
good for combo
which drugs cause risk of gout
thiazide diuretics
loop diuretics
(both inc reabsorption of uric acid)
venous tone reducers
nitric oxide derivatives
dihydropyridine CCB
dilate veins, inc venous capacitance, reduce pre-load
HR reducers
B-blockers
non-dihydropyridine CCB
which meds MUST be started after MI
B-blocker (suppresses lethal arythmias)
drugs influencing SVR (affecting SNS)
- alpha-2 agonists (central)
- alpha-1 blockers (peripheral)
drugs disrupting humoral vasoconstricors
- direct renin inhibitors
- ACE inhib
- ARB blockers
all will dec GFR and dec K+ secretion (hypERkalemia)
direct vasodilators
reduce venous tone AND dilate arterioles
nitric oxide derivatives
dihydropyridine CCB
proteinuria
indication for RAAS blockers + lowering BP to <130/80 to slow CKD progression
drugs interfering with RAAS
inc K+
which two drugs have greater bp lowering effect in Afr Amer
Ca blockers
diuretics
dilate arterioles CENTRALLY and dec SVR
alpha 2 agonists
nitrates
inc venous capacitance and cardiac filling
first line anti hypertensive in uncomplicated HTN
thiazide diuretics
second line in uncomplicated HTN
ACEi and ARB
mortality advantage in post-MI
beta blockers and ACEi
profound benefitt in patients w/ systolic dysfunction
blockade of RAAS
tx of diastolic dysfunciton
Ca chan blocckers
Nitrates MOA
increase [cGMP] promoting smooth muscle relaxation
Ca blocker MOA
block Ca entry into cell → MLCK not activated → prevent contraction
CO=HR * SV
fx of SV
SV is affected by pre-load (cardiac filling) and myocardial contractility (strength)