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Antihypertensives

Antihypertensives and Diuretics

Drug ClassSite of ActionMechanism of ActionPregnancy CategoryAdverse EffectsDrug InteractionsImportant Notes
Loop Diuretics (furosemide/Lasix) Ascending loop of Henle blocks reabsorption of water C orthostatic hypotension; hypokalemia, hyponatremia, hypochloremia, hyperglycemia, hyperuricemia, dehydration; ototoxicity! increased LDL, TG; Decreased HDL, decreased magnesium, *decreased calcium other diuretics (hypovelemia, -lyte imbalance, hypotension), digoxin (toxicity), ototoxic drugs (increse risk of ototoxicity), lithium, antihypertensives (accentuate BP lowering effect), NSAIDS (reduce intensity of furosemide's diuretic effects) Produce much greater diuresis than thiazides. Can cause up to 20% of filtered load excreted. Not used routinely for HTN.
K+ Sparing Diuretics (Non-Aldosterone antagonists: Amiloride, Triamterene) Blocks Na/K exchange in the distal nephron Modest increase in urine production, but substantial decrease in K excretion (retention of K and increased excretion of Na); Some heart failure pts. may use this to decrease risk of hypokalemia Amiloride: B Triamterene:D hyperkalemia (immediately discontinue drugs), photosensitivity (triamterene) other diuretics (hypovolemia, -lyte imbalance, hypotension); lithium; antihypertensives (accentuate BP lowering affect); K supplements (hyperkalemia), ACE/ARBs (raise K levels) can help play a role in combination therapy by reducing the risk of hypokalemia
K+ Sparing and Aldosterone Antagonist (Spironolactone) Blocks Na/K exchange in the distal nephron Modest increase in urine production, but substantial decrease in K excretion (retention of K and increased excretion of Na); Some heart failure pts. may use this to decrease risk of hypokalemia. Provides additional level of regulation for pts. with more c D- Absolutely contraindicated (amniotic fluid loss) benign and malignant tumors, endocrine effects: gynecomastia, menstrual irregularities, impotence, hirstutism, deepening of the voice other diuretics (hypovolemia, -lyte imbalance, hypotension); lithium; antihypertensives (accentuate BP lowering affect); K supplements (hyperkalemia), ACE/ARBs (raise K levels) drug is a steroid derivative
Renin Inhibitors (Aliskiren) Direct renin inhibitor decreases plasma's renin activity interfering with conversion of angiotensinogen to angiotensin I C/D, depending on trimester (contraindicated) -angioedema (rapid edema of skin, mucosa, and submucsal tissues in head and neck) -Hyperkalemia (esp. when used w/ other drugs that cause hyperk) -severe hypotension -fetal harm/abnormalities -GI symptoms -Increased BUN/Cr -Rash -Increased uric ac -Aliskiren is a substrate of 3A4 (goes through 3A4 pathway to be metabolized), so inhibitors (-azole antifungals) may increase serum levels of the drug, increasing adverse effects such as hyperk -drugs that increase K-additive effects -reduces [furosemi has not yet been evaluated in pts with significantly impaired renal fxn, so should be avoided in this population of pts.
Angiotensin-Converting Enzyme Inhibitors (ACE-I); catopril, ramipril Inhibits angiotensin converting enzyme Inhibits angiotensin converting enzyme, which decreases the formation of ANG-II and thereby preventing vasoconstriction and aldosterone mediated volume expansion C/D/D, therefore should not be used. Contraindicated. -first dose hypotension -fetal injury -cough (accumulation of bradykinin increase) -angioedema -hyperkalemia -renal failure -diuretics (d/c i wk prior to start of tx) -antihtn agents (drop BP too much) -drugs that raise K levels (by suppression aldosterone and there4 excretion of K) -lithium (toxic accumulation) -NSAIDS (reduce antihtn effects and increase renal failure ri All ACE-I are excreted by the kidneys, so nearly all can accumulate to dangerous levels in patients with kidney disease and hence dosages MUST BE REDUCED in these patients (**only fosinopril does not require dosage reduction) Adjust dose according to a pa
Angiotensin II Receptor Blockers (ARBS); losartan, valsartan blocks angiotensin II receptors prevents angiotensin II mediated vasoconstriction and aldosterone mediated volume expansion C/D/D. contraindicated -hypotension (primarily in FVD pts and those rx diuretics) -angioedema -fetal harm -renal failure (like ACEI, can cause RF in pts with bilat. renal artery stenosis or stenosis in the artery of a single remaining kidney. So contraindicated in these pts -Diuretics (intensity effects of hypotension) Antihtn agents Drugs that raise K levels -Lithium (toxicity) -NSAIDS (reduce antihtn effects, increase risk of RF) ARBs do not inhibit kinase II and do not increase levels of bradykinin, so can be used as an alternative to ACEI if a pt. develops a cough caused by accum. of bradykinin 2/2 inhibition of kinase II/ACE)
Aldosterone Antagonists; spioronolactone, eplerenone Blocks aldosterone receptors Promotes renal excretion of Na and water, reducing blood volume and BP spironolactone: D. contraindicated eplerenone: B (no adequate study in humans, not recommended) hyperkalemia (both promote renal retention of K so should not be combined with K-sparing diuretic or K supp. as well as use caution w/ ACEI/ARB
Spironolactone -blocks aldosteron in the distal nephron -retention of K, increased excretion of Na+ -binds with receptors of other steroid hormones -binds with receptors of other steroid hormones D -hyperkalemia -benign and malignant tumors -endocrine effects -diuretics agents that raise K levels (i.e. Aliskiren)
Eplerenone aldosterone receptors selective blockade of aldosterone receptors B (not studied or recommended) hyperkalemia -potent inhibitors of 3A4 (antifungals, macrolide antibiotics) can increase levels of elplerenone and therefore cardiovascular risks of hyperk -drugs that raise K levels -caution when combined with lithium -ACEI/ARB pharmacokinetics: absorption is not effected by food, hepatically metabolized (use with caution in patients with hepatic dysfunction due to increased leveld of ADRs and Rx interaction) 3A4 substrate
Sympatholytics (Antiadrenergic Drugs): Generally SNS Primarily exert their effect by suppressing the influence of the SNS on the heart and blood vessels varies
Beta Blockers: propranolol, metoprolol 1-blockade of cardiac B-1 receptors (dec. HR and contractility=dec. CO) 2-suppres reflex tachycardia caused by vasodilators 3- blockade of B1 receptors on JG cells, dec. renin=reduction in ANGII-med. vasoconstriction & aldosterone-med. volume expansion 3- blockade of B1 receptors on JG cells, dec. renin=reduction in ANGII-med. vasoconstriction & aldosterone-med. volume expansion varies -bradycardia (dec AV conduction and reduced contractility->should not be used in pts with sick sinus synd. or 2nd or 3rd deg. AV block;use w/ care w/ HF pts) -Dec. AV conduction -Reduced contractility -Mask hypoglycemic Sx; B2 blockade can inhibit glyc other hypotensives (exacerbated effect); CCBs (cardiosuppression); digoxin (bradycardia); bupropion with metoprolol (combo may inc. BB levels->monitor BP and SE); Sitagliptin (combo may alter glucose metab and prolong hypoglycemia) B1: stim. by epinephrine induces a +chronotropic and inotropic effect on hear and increases cardiac conduction velocity and automaticity. Stim in kidney causes renin release. B2: induces smooth muscle relaxation in lungs=bronchodilation. use B1 selective
A1 Blockers; doxazosin, terazosin 1st dose orthostatic hypotension (v. exag. In older men); reflex tachycardia (increase HR by triggering baroreceptor reflex->can be suppressed by BB); impotence; nasal congestion PDE-5 inhibitors (eg. Viagara, levitra, cialis) can cause an increase in hypotension; other hypotensives
A/B Blockers; carvedilol, labetalol A1 blockage (dilation of arteries and veins); B1 blockade (reduces HR and contractility); B1 block of JG cells (reduce renin release) A1 blockage (dilation of arteries and veins); B1 blockade (reduces HR and contractility); B1 block of JG cells (reduce renin release) C see A and B Blocker interactions: Bradycardia; orthostatic hypotension; AV block; asthma exacerbation other hypotensives (exacerbated effect)+ PDE inhibitors; CCBs (cardiosuppression); digoxin (bradycardia); bupropion with metoprolol (combo may inc. BB levels->monitor BP and SE); Sitagliptin (combo may alter glucose metab and prolong hypoglycemia)
Centrally acting A2 Agonists (Rare); clonidine, methyldopa Act within the brainstem to suppress sympathetic outflow to the heart and blood vessels Vasodilation and reduced CO (both of which help to lower BP) clonidine: C/D, methyldopa: B (may see this rx in pregnancy-induced htn) Dry mouth; sedation; severe rebound htn if tx is abruptly d/c; hepatotoxicity (rare)/hemolytic anemia (methyldopa) other hypotensive agents, MAOI: contraindicated for use w/in 14 days of an MAOI. Combo may decrease antihtn response or result in htn crisis upon d/c of A2 agonist:
Adregernic Neuron Blockers (V. Rare); Reserpine Decrease BP through actions in the terminals of postganglionic sym. Neurons Vasodilation and reduced CO (both of which help to lower BP) C Depression (depleting monoamide neutotrans in synapses. Can be devastating->suicide); nasal congestion, nausea, vomiting, bradycardia, o.hypotn, GI distress, ED Levodopa (decrease levodopa effect); digoxin (increase risk of arrythmia); other hypotn agents (severely dec. BP)
Direct Acting Vasodilators (rare, but effective); hydralazine, minoxidil promotes dilation of arterioles (not veins, so very little orthostatic hypotn) promotes dilation of arterioles (not veins, so very little orthostatic hypotn) C (po preps) postural hypotn; reflex tachycardia (and renin release, so add B Blocker); Expansion of blood volume (Na and H2O retention, so add diuretic); other hypotensive agents Rarely used d/t SE
hydralazine (direct acting vasodilator) C sys lupus erythematosus-like syndrome
minoxidil (Direct acting vasodilator) C pericardial effusion (fluid buildup); cardiac taponade (heart compress. r/t flud); hypertrichosis (excessive hair growth->active ingred. In rogaine)
Calcium Channel Blockers: Dyhydropyridines; nifedipine, amlodipine arterioles relaxation of smooth muscle->vasodilation by preventing Ca++ from entering cells C dizziness, facial flushing, headache; peripheral edema; gingival hyperplasia' *reflex tachycardia (b/c CC of heart are not blocked at regular dose, do not supp. Automaticity, AV conduction or contractility) NB:*B blockers cab prevent reflex tachy. (diff. from non-dihydropyridines); dogoxin and antidysrhythmics
Calcium Channel Blockers: Non-Dihydropyridines (verapamil-phenylalkylamine and diltiazem-benzothiazepine) arterioles directly in heart resulting in vasodilation, reduced arterial pressure and inc. coronary perfusion. Direct suppressant effect on heart relaxation of smooth muscle->vasodilation by preventing Ca++ from entering cells C dizziness, facial flushing, headache; peripheral edema; *constipation(verapamil); gingival hyperplasia; reflex tachycardia (minimal r/t cardiosuppression); cardiac supp./heart block *B blockers (risk of excessive cardiosupp); digoxin and antidysrhythmics (supp of impule through AV node, so monitor closely); Ranolazine (verapamil and diltiazem inhibit CYP3A4 metabolization and P-glycoprotein, so toxicity of ranolazine->fatal dysrh) Toxicity: CCB lose selectivity, causing severe hypotn, bradycardia, AV block, v tach)
Thiazides (hydrochlorothiazide) Early distal convoluted tubule 1)Reduction of blood volume 2)Reduction of arterial resistance B/C, enters breast milk orthostatic hypotension, hypokalemia, hyponatremia, hypochloremia, dehydration, hyperglycemia, hyperuricemia; increased LDL, TC, TG, increased calcium, decreased magnesium, photosensitivity other diuretics (hypovolemia, -lyte imbalance, hypotension; digoxin (toxicity); lithium (toxicity); antihypertensives (excessive BP drop) The ability of thiazides to promote diuresis is adequate kidney function. Ineffective when GFR is low
Created by: jellyfishh on 2008-10-03



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