antihypertensives Flashcards
(40 cards)
has C/I of
* Anuric pts (avoid in renal dysfxn– SCr >1.5 or CrCL < 30 ml/min bc they lose effectivenes)
* Sulfa allergy
* Gout
thiazide diuretics
has SE of
* Low Na,K, Mg. High Ca
* Hyperuricemia, hyperglycemia, hyperlipidemia
* Hypotension, impotence, azotemia
thiazide diuretics
which class has the Ceiling effect– increasing dose does not increase BP lowering effect
thiazide diuretics
which class should you use cautiously w/ NSAIDs, digoxin, lithium, antidiabetic meds
thiazide diuretics
which class should you monitor BUN/SCr and K levels after initiation and w/ dosage titrations
thiazide diuretics
which class of vasodilators has C/I of 2nd/3rd heart block, decompensated heart failure, asthma/COPD
beta blockers
which class causes hypo-kalemia vs hyper-kalemia
- thiazide diuretics= low K
- ARBs & ACEs= high K
which types of meds cause LE edema vs reflex tachy
- RAAS inhibitors– edema
- vasodilators (DHP-CCB, alpha blockser, centrals)– reflex tachy
MOA of thiazide diuretics
less blood volume by stopping Na/water reabsorption at DCT
lower Ca excretion
4 ways beta blockers work
- decrease CO
- inhibit NE to cause vasodilation
- Block renin release
- block alpha-1 receptors
4 ways beta blockers work
- decrease CO
- inhibit NE to cause vasodilation
- Block renin release
- block alpha-1 receptors
which class may mask tachy sx of hypoglycemia in DM by causing bradycardia
beta blockers
which 2 meds must be tapered inorder to prevent HYPERTENSIVE CRISIS?
- clonidine over 2-4 days
- beta blockers over 1-2 wks
inhibits AG II creation, aldosterone & has diuretic effect
increases bradykinin & decrease endothelin
ACEinhibitors
hx of what 4 conditions calls for use of ACEs
- DM
- old MI
- CHF
- nephropathy
which class should be avoided in bilateral renal stenosis because the increased creatinine doesnt return to normal after starting the med?
ACE
3 C/I of ACEs
- pregnancy
- bilateral renal stenosis
- h/o angioedema
SE of
* hypotension
* azotemia/renal insufficiency
* high K
* hyperuricemia
(not comprehensive list)
ACEs
ACEs have 2 important drug reactions. name them
NSAIDs and lithium
how do ARBS work
similar to ACEs but binds/blocks AG II receptors and does not increase bradykinin
how do CCBs work? DHP vs non-DHP
block L type Ca channels in vascular smooth muscle to block constriction
Non-DHP has negative inotropic & chronotropic effects
C/I of CHF, 2nd/3rd heard block
CCB
SE of
* peripheral edema
* hypotension, HA, dizziness
* constipation
& interacts with statins
CCBs
blocks renin release from JG cells of DCT
renin inhibitors