Pharmacology of HTN Flashcards
hypertension - general treatment concepts
- reducing cardiac output: decrease blood volume/stroke volume, heart rate, and contractility
- reducing systemic vascular resistance: vasodilation
recall: MAP = CO x SVR
pharmacologic treatment of HTN - classes
ABCDs:
1. ACE inhibitors / ARBs
2. beta blockers (BBs)
3. calcium channel blockers (CCBs)
4. diuretics
other:
-direct acting vasodilators
-alpha1 receptor blockers
-centrally acting alpha2 agonists
angiotensin converting enzyme inhibitors (ACEi) - MOA
*inhibit ACE (in the lungs; inhibits conversion of Ang I to Ang II) → decreased Ang II → decreased GFR by dilating (preventing constriction of) efferent arterioles
*note - ACEi dilate both afferent and efferent arterioles, but predominantly the efferent arteriole
*increased renin due to loss of negative feedback
*prevents inactivation of bradykinin → buildup of bradykinin → vasodilation
angiotensin converting enzyme inhibitors (ACEi) - cardiorenal effects
*vasodilation that results in reduced arterial and venous pressure and a reduction in ventricular afterload & preload
*natriuretic and diuretic
*depresses sympathetic activity
*inhibit cardiac and vascular hypertrophy
angiotensin converting enzyme inhibitors (ACEi) - uses
*HYPERTENSION
*HEART FAILURE
*proteinuria
*diabetic nephropathy
angiotensin converting enzyme inhibitors (ACEi) - examples
“-prils”:
*lisinopril
*captopril
*enalapril
*ramipril
angiotensin converting enzyme inhibitors (ACEi) - ADEs
*COUGH
*ANGIOEDEMA
*HYPERKALEMIA
*renal injury / increased serum creatinine
*contraindicated in pregnancy
angiotensin II receptor blockers (ARBs) - MOA
*selectively block binding of Ang II to AT1 receptor → inhibits vasoconstriction and prevents release of aldosterone
*net effect: decrease in fluid volume + peripheral vasodilation
angiotensin II receptor blockers (ARBs) - examples
“-sartans”
*losartan
*candesartan
*valsartan
angiotensin II receptor blockers (ARBs) - ADEs
*HYPERKALEMIA
*ANGIOEDEMA
*increased serum creatinine
beta blockers - MOA in HTN tx
*block beta 1 adrenergic receptors to lower BP via several mechanisms:
-blockade of cardiac beta1 receptors → decreased HR and decreased contractility → decreased cardiac output
-blockade of beta1 receptors in juxtaglomerular cells → blocks renin secretion
beta blockers - uses
*hypertension
*heart failure
metoprolol - receptor selectivity
beta1 selective beta blocker (cardioselective)
labetalol - receptor selectivity
blocks alpha1, beta1, and beta2
carvedilol - receptor selectivity
blocks alpha1, beta1, and beta2
beta blockers - ADEs
*drowsiness
*lethargy
*erectile dysfunction
*confusion
*AV nodal blockade → bradycardia → shock
*CAN MASK HYPOGLYCEMIA SYMPTOMS
*beta blockers that block beta2 (labetalol, carvedilol) can cause bronchoreactive events (exacerbate asthma & COPD)
calcium channel blockers - MOA
*inhibit L-type calcium channels on vascular smooth muscle, cardiac myocytes, and nodal cells (SA and AV), inhibiting influx of calcium and resulting in:
1. reduced peripheral vascular resistance & reduced BP (vasodilation)
2. decreased contractility (negative inotropy) and decreased HR (negative chronotropy)
dihydropyridine calcium channel blockers (DHP CCBs) - MOA
*inhibit L-type calcium channels, mainly in vascular smooth muscle
*predominantly vasodilators → main effect is to lower SVR
examples: amlodipine, nifedipine
non-dihydropyridine calcium channel blockers (NDHP CCBs) - MOA
*inhibit L-type calcium channels, mainly in SA & AV nodes
*predominantly slow cardiac contractility & conduction → main effect is to lower HR
examples: verapamil, diltiazem
dihydropyridine calcium channel blockers - examples
*amlodipine
*nifedipine
dihydropyridine calcium channel blockers - uses
*more selective as vasodilators
*used for HTN
examples: amlodipine, nifedipine
dihydropyridine calcium channel blockers - ADEs
*flushing
*headache
*EDEMA
*gingival hyperplasia
examples: amlodipine, nifedipine
what causes the edema ADE associated with DHP CCBs?
*edema is due to increased capillary hydrostatic pressure from preferential pre-capillary arteriolar vasodilation
non-dihydropyridine calcium channel blockers - examples
*verapamil
*diltiazem
non-dihydropyridine calcium channel blockers - uses
*predominantly used for lowering heart rate and contractility
*AV nodal blocking activity → used for tachyarrhythmias and stable angina
examples: verapamil, diltiazem
non-dihydropyridine calcium channel blockers - ADEs
*bradycardia
*can precipitate heart failure (avoid starting if in acute heart failure)
*gingival hyperplasia
*constipation
examples: verapamil, diltiazem
hydralazine - drug class & MOA
*direct-acting vasodilator
*relaxes arterioles → decreased systemic vascular resistance → decreased BP
compensatory changes: tachycardia
hydralazine - ADEs
*headaches
*flushing
*tachycardia
*LUPUS-LIKE SYNDROME (erythematous rash)
note - tachycardia may precipitate angina in pts with coronary artery disease
minoxidil - drug class & MOA
*direct-acting vasodilator
*relaxes arterioles → decreased systemic vascular resistance → decreased BP
minoxidil - ADEs
*fluid retention
peripheral alpha1 receptor blockers - examples
“-zosins”
*prazosin
*doxazosin
*terazosin
peripheral alpha1 receptor blockers (“-zosins”) - MOA
*stimulation of alpha1 receptors in periphery → vasoconstriction
*BLOCK ALPHA1 RECEPTORS (with this drugs) → VASODILATION → decreased SVR → decreased BP
peripheral alpha1 receptor blockers (“-zosins”) - ADEs
*postural hypotension
*watch for first-dose syncope, dizziness, lethargy
alpha2 receptor agonists - examples
*clonidine
*methyldopa
alpha2 receptor agonists - MOA
*alpha2 are presynaptic receptors located on neurons that release NE
*NE activates alpha2 receptors → DECREASED NE RELEASE BY THE NEURON
*alpha2 receptor agonists → lower NE release → less smooth muscle contraction → lower BP
clonidine - drug class, MOA, ADEs
*drug class: alpha2 receptor agonist
*MOA: act within the CNS on alpha2 receptors to decrease sympathetic outflow to CV system → decreased BP
*ADEs: sedation, dry mouth, decreased HR
*rebound hypertension if abrupt cessation
methyldopa - drug class, MOA, ADEs
*alpha2 receptor agonist → less NE release → less smooth muscle contraction → decreased BP
*ADE: hemolytic anemia
*note - often used for HTN in pregnancy
what medication should you give to a patient with CKD (chronic kidney disease) or proteinuria?
ACEi or ARB
