Pharm - HTN Flashcards
(15 cards)
Thiazides
Type, Mechanism, Effect, Side Effect, Use
T: Hydroclorothiazide (HCTZ), Chlorothalidone, Metolazone
DCT Diuretic
M: Inhibit Na-Cl symporter in nephron DCT
E: 1. trap more Na+ in urine = lower BVol = lower BP; 2. increase Ca2+ resorption (charge balance) = hypercalcemia (BAD side effect, but good for treating kidney stones)
SE: Impotence, Fluid/Electrolyte Imbalances (Hypo-K/Na, Hyper-Ca)
U: First Line HTN Tx, edema
Loop of Henle Diuretics
types, Mechanism, Effect, Side Effect, Use
T: “-emides” (Furosemide, Bumetanide)
M: Inhibit NKCC symporter in TALH, more effect than thiazides because TALH 30% Na resorption (DCT 7%)
E: 1. Na & K loss = lower BV = lower BP - very powerful due to blocking 30% resorption
SE: Electrolyte Imbalance (Hypo-K/Ca/Mg), Volume depletion, Ototoxicity, Hyperuricemia (can lead to gout)
U: volume overload (rapid diuresis), HTN - esp in CKD, use when thiazides not effective
K+ Sparing Diuretics
Types, Mechanism, Side Effects, Use
Spironolactone (+ epleronone), Amiloride
spir: blocks Aldo-Receptor: 1. traps Na in urine = lower BV = lower BP; 2. spares K+ secretion = hyperkalemia
ami: blocks Na Channels in late DT/CD for same effects
SE: hyperkalemia (ami: nausea, vomiting) (spir: gynecomastia b/c hormonal agent - Epleronone - less hormonal agent)
U: Add-on Tx in HTN on diuretic of another class (thiazide + spironolactone = K balance)
What is the main effect of diuretics on lowering BP?
- MAIN: decrease PVR due to changing ion concentrations to promote VD
- MINOR: decreasing intravascular volume, body will compensate with VC after 5% BV loss
ACE Inhibitors (Mechanism, Effect, Types, Side Effects, Use)
M: block conversion of AngI to AngII
E: less sympathetic activation, less SMC VC (MAIN EFFECT: lower PVR), more bradykinin (more VD), less Aldosterone (less Na/H20 retention = less BV)
T: “-prils”
SE: cough/angioedema (bradykinins), hyper-K, renal failure, TERATOGENIC
U: HTN patients, esp with HF/DM/CAD as adjunctive agent with 1st line diuretics
Angiotensin Receptor Blockers
Mechanism, Effect, Types, Side Effects, Use
M: block AT1 receptor for AngII
E: less sympathetic, less SMC VC (MAIN EFFECT: lower PVR), less Na/H20 Retention (less BV), decreased bradykinin (not blocked, lower VD, but washed out effect)
T: “-artans”
SE: hyperkalemia, renal failure, TERAToGENIC
U: HTN pts, esp w/HF/DM/CAD/post-MI as adjunctive agent with 1st line diuretics
Methyldopa
type, mechanism, side effects, use
T: Centrally acting sympatholytic
M: replaces NE, still causes VC but performs more negative feedback, increasing VD and lowering BP (Major: decrease PVR)
SE: (centrally acting) sedation, dry mouth, fatigue, depression, hepatotoxicity
U: well-established, use adjunctively due to side effects
Clonidine
type, mechanism, side effects, use
T: centrally acting sympatholytic
M: activates presynaptic alpha-2 receptor- prevents NE release - no VC, more VD, lower BP (Major: decrease PVR)
SE: sedation, dry mouth, depression, bradycardia, withdrawal
U: use adjunctively due to SE, good add-on b/c minimal drug-drug interaction
Prazosin, Terazosin, Doxazosin (‘-zosin’)
type, mechanism, side effect
T: peripherally acting sympatholytic (ALPHA-1 BLOCKER)
M: blocks post-synaptic alpha-1 receptor to prevent NE binding = less VC (lower PVR) = lower BP
SE: Orthostatic Hypotension (peripherally acting)
Beta Blockers ('-lols')
(Mechanism, Side Effect, Use, Types)M: blocking B1 (lower HR, Contractility, Renin Release = lower CO), blocking B2 (causes VC in muscle but minor)
SE: if block B2 (cold fingers - peripheral VC, and ashtma - bronchoconstriction), else (bradycardia, hyperkalemia, fatigue)
U: CAD, HTN, HF, good adjunctive with drugs that would increase symp stim (peripheral VDs, diruetics)
T: Labetalol/Carvedilol - also block alpha-1 receptors (block VC = lower PVR) - good for HF pts
Nebivolol: blocks primarily B-1 receptors PLUS VD properties via NO (beta-3 effect)
Nifedipine, Amlodipine (‘-ipines’)
Type, Mechanism, Side Effects, Interactions
T: CCB, dihydropyridine
M: CCB in Vascular Smooth Muscle
SE: headaches, flushing, dizziness, GERD/constipation (GI relaxation), PERIPHERAL EDEMA
I: CYP450 metabolism (grapefruit juice)
Diltiazem
Type, Mechanism, Side Effects, Interactions
T: CCB, benzothiazipine
M: CCB in BOTH Vascular smooth muscle + heart
SE: less than dihydropyridines/verapamil - edema, headache, nausea, dizziness, constipation, diarrhea, bradycardia
I: CYP450 metabolism (can inhibit benzodiazepines, statins, cyclosporin)
Verapamil
Type, Mechanism, Side Effects, Interactions
T: CCB, phenylalkylamine
M: CCB in predominantly HEART
SE: BRADYCARDIA, constipation, dizziness, nausea
I: CYP450 Metabolism
Tx Population for CCBs
Pts with DM/renal or lipid problems/asthma
Don’t use if they have conduction abnormalities
Synergistic with other agents - good add-on with ACE-Is, diruetics, b-blockers
Can be first line with B-blocker 2nd line
Peripheral Vasodilators (Hydralazine, Minoxidil, Nitroprusside) (Mechanisms, SE, Use)
M: H - lower BP thru relaxing arteriolar SMC; Mi - activates K-ATP Channels in vascular SMC = hyperpolarize membrane = smooth muscle relaxation; Ni - metabolized by blood vessels to NO - activates cGMP - more VD (ALL LOWER PVR)
SE: H (headache, nausea, flushing, dizziness, angina, edema/HF, drug-induced lupus), Mi (Na/H20 retention, tachycardia, angina, HF, hypertrichosis - treats hair loss, effusions), Ni (hypotension, cyanide toxicity - lactic acidosis, anorexia, fatigue, confusion, psychosis)
U: Pt’s w/hard to control HTN on multiple agents, which will help control these SEs
(Ni only available IV)
