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proximal tubule (urine alkalinizing) MOA: reversible inhibition of carbonic anhydrase PD: inhibits reabsorption of HCO3- in proximal tubule PK: well absorbed orally; effect beings within 30 min and is maximal within 2 hrs; duration=12 hrs; renal secretion via organic acid transporter AE: metabolic acidosis, hypokalemia, calcium phosphate stones, drowsiness, parethesias and hypersensitivity rxns ConIn: cirrhosis (impairs NH4+ excretion) CI: diuretic agent (weak), glaucoma, urinary alkalinization (drug overdose/stones), acute mountain sickness |
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loop diuretic MOA: inhibits Na+/K+/Cl- cotransporter, vasodilation PD: reduce reabsorption of Na+, K+, Cl-, also Ca2+ and Mg2+; renal vasodilation improves renal blood flow PK: oral absorption rapid but variable, ½ life short=1.5-2hrs, duration=2-3hrs, renal secretion, oral acid transporter AE: hyponatremia, hypokalemia, hypomagnesia, dehydration, metabolic alkalosis, hyperuricemia, ototoxicity, hypersensitivity rxns CI: acute pulmonary edema, edema associated w/ CHF, acute hypercalcemia, acute hyperkalemia, acute renal failure? |
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loop diuretic 40x more potent than furosemide shorter ½ life than furosemide (~1hr) 50% metabolized by liver |
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loop diuretic longer ½ life than furosemide (~3hrs) longer duration of action (~5-6hrs) better oral absorption than furosemide 80% metabolized by liver |
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loop diuretic last resort-used only when others exhibit sulfur hypersensitivity nephrotoxic and ototoxic |
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potassium-sparing MOA: competitive inhibitor of aldosterone; anti-andronergic effects (decrease testosterone synthesis, competitive inhibition of DHT receptor) PD: mild diuresis due to decreased Na+ reabsorption secondary to aldosterone inhibition, sparing of K+ and H+ also secondary to aldosterone inhibition PK: slow onset of action-days to take effect, liver metabolism to several active metabolites AE: hyperkalemia, metabolic acidosis, gynecomastia, impotence, decreased libido, GI upset (peptic ulcers), CNS effects-headache, fatigue, confusion CI: liver cirrhosis, primary and secondary hyperaldosteronism, hypertension |
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potassium-sparing brand new (expensive) alternative to spironolactone but without the SEs same action as spironolactone |
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potassium-sparing MOA: blocks Na+ channels in principal cells PD: blocking Na+ influx decrases driving force for K+ efflux so K+ is “spared” PK: 1/2 life=21 hrs, secreted into tubule via organic base transporter, excreted unchanged by kidney AE: hyperkalemia (NSAIDs can exacerbate), GI upset (nausea, vomiting, diarrhea), muscle cramps, CNS effects (headache, dizziness) CI: edema, hypertension, combo with other diuretics to reduce K+ loss, adjunct for lithium Tx (mania) to decrease diabetes insipidus |
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potassium-sparing MOA: blocks Na+ channels in the principal cells PD: blocking Na+ influx decrases driving force for K+ efflux so K+ is “spared”; active form can precipitate in the tubules and obstruct flow PK: ½ life=4hrs, 10x less potent than amiloride, liver metabolizes drug to active form -> secreted using the organic base transporter |
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thiazide MOA: inhibition of Na+/Cl- cotransporter in distal tubule PD: relatively mild diuresis, increased Ca2+ reabsorption PK: good oral absorption and renal elimination; ½ life=2.5hrs AE: hyponatremia and hypokalemia, dehydration, metabolic alkalosis, hyperuricemia, hyperglycemia, hyperlipidemia (increased LDL), weakness, fatigue, paresthesias and hypersensitivity rxns CI: hypertension, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus |
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thiazide 10x more potent than hydrochlorothiazide ½ life=4-5hrs |
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thiazide 20x more potent than hydrochlorothiazide ½ life=10-22hrs, metabolized extensively by liver |
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thiazide same potency as hydrochlorothiazide ½ life=44hrs |
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osmotic agent MOA: major osmotic effects in proximal tubule and loop of Henle PD: IV admin causes expansion of intravascular volume, powerful diuretic effect once it reaches kidney PK: not orally absorbed-must be injected IV to reach kidney, bolus excreted within 30-60min AE: acute pulmonary edema, dehydration, hypernatremia, headache, nausea, and vomiting ConIn: CHF, pulmonary edem CI: increased intracranial pressure, renal excretion of toxic substances (contrast dye, myoglobinemia) |
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vasopressin (ADH) antagonist selective V2 receptor antagonist-renal ADH receptors |
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vasopressin (ADH) antagonist V1A and V2 receptor antagonist-vasodilator and ADH antagonist |
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renin inhibitor lower elevated blood pressure, combo w/ ACE inhibitors, ARBs, aldosterone antagonists -> synergistic effects |
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