Antihypertensives and Diuretics
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| 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.
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| 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
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| 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
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| 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.
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| 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
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| 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)
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| 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 |
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| 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) |
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| 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
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| Sympatholytics (Antiadrenergic Drugs): Generally | SNS | Primarily exert their effect by suppressing the influence of the SNS on the heart and blood vessels | varies |
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| 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
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| 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 |
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| 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) |
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| 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: |
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| 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) |
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| 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
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| hydralazine (direct acting vasodilator) | C | sys lupus erythematosus-like syndrome |
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| minoxidil (Direct acting vasodilator) | C | pericardial effusion (fluid buildup); cardiac taponade (heart compress. r/t flud); hypertrichosis (excessive hair growth->active ingred. In rogaine) |
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| 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 |
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| 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)
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| 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
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