14. Renal Pharm
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Created by:
francyface on May 30, 2012
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29 terms
Terms | Definitions |
|---|---|
Drugs/Exposures that cause transitional cell carcinoma | phenacetin (aspirin derivative)smoking aniline dyes cyclophosphamide |
Mannitol--Mechanism | PCTosmotic diuretic, inc tubular fluid osmolarity = inc urine flow gets filtered but can't be absorbed, leads to dec Na+ and H20 reabsorbtion |
Mannitol--Use | shockdrug overdose inc intracranial/intraocular pressure |
Mannitol--Toxicity | pulmonary edemadehydration contraindicated in anuria, CHF |
Acetazolamide--Mechanism | PCTcarbonic anydrase inhibitor = self-limited NaHCO3 diuresis and dec in HCO3- stores |
Acetazolamide--Use | glaucomaurinary alkalinization metabolic alkalosis altitude sickness |
Acetazolamide--Toxicity | hyperchloremic metabolic acidosisneuropathy NH3 toxicity sulfa allergy |
Furosemide--Mechanism | sulfonamide loop diureticinhibits Na+, K+, Cl- cotransport of thick ascending limb stops hypertonicity of medulla preventing concentration of urine inc Ca2+ excretion |
Furosemide--Use | edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema)HTN hyperCa2+ |
Furosemide--Toxicity | "OH DANG"ototoxicity hypoK+ deH20 Allergy (sulfa) Nephritis (interstitial) Gout |
Ethacrynic acid--Mechanism and Use | same action as furosemide (NOT sulfa)phenoxyacetic acid derivative diuresis in patients with sulfa allergy |
Ethacrynic acid--Toxicity | same as furosemide BUT can be used in hyperuricemia/acute gout |
Hydrochlorothiazide--Mechanism | thiazide diureticinhibits NaCL reabsorption in DCT dec Ca2+ excretion |
Hydrochlorothiazide--Use | HTNCHF idiopathic hypercalciuria nephrogenic diabetes insipidus |
Hydrochlorothiazide--Toxicity | hypoK+metabolic alkalosishypoNa+ hyperglycemia hyperlipidemia hyperuricemia hyperCa2+ sulfa allergy |
K+ sparing diuretics--List | spironolactonetriamterene amiloride eplerenone |
K+ sparing diuretics--Mechanism | spironolactone = competitive aldosterone receptor antagonist in collecting tubuletriamterene and amiloride = block Na+ channels on CCT |
K+ sparing diuretics--Use | hyperaldosteronismK+ depletion CHF |
K+ sparing diuretics--Toxicity | hyperK+endocrine effects with aldosterone antagonists (ex: spironolactone causes gynecomastia, antiandrogen effects) |
Diuretic Effects on Urine NaCL | Increasedserum NaCL may dec |
Diuretic Effects on Urine K+ | Increased in all except K+ sparingserum K+ may dec |
Diuretics that cause dec pH (acidemia) | Carbonic anhydrase inhibitorsK+ sparing (aldosterone block prevents K+ and H+ secretion) also..hyperK+ causes K+ to enter and H+ to leave (K+/H+ transporter) |
Diuretics that cause inc pH (alkalosis) | Loop diuretics and thiazides1) Volume contraction: inc ATII = inc Na+/H+ exchange in proximal tubule = inc HCO3- 2) K+ loss leads to K+ exiting cells and H+ entering cells 3) In low K+ state, H+ is exchanged for Na+ leading to "paradoxical aciduria) |
Effect of loop diuretics on urine Ca2+ | Increasedabolish lumen-positive potential in thick ascending limb = dec paracellular Ca2+ reabsorption = hypoCa2+ = inc urinary Ca2+ |
Effects of thiazides on urine Ca2+ | Decreasedvolume depletion = upregulation of Na+ reabsorption = enhanced paracellular Ca2+ reabsorption in PCT and loop of Henle also block luminal Na+/Cl- cotransport in DCT = inc Na+ gradient = increased Na+/Ca2+ exchange |
ACE Inhibitors--List | captoprilenalapril lisinopril |
ACE Inhibitors--Mechanism | inhibit angiotensin converting enzyme and prevent inactivation of bradykinin (vasodilator)renin release is increased d/t loss of feedback inhibition |
ACE Inhibitors--Use | HTNCHF diabetic renal disease |
ACE Inhibitors--Toxicity | "CAPTOPRIL"cough angioedema proteinuria taste changes hypOtn pregnancy problems (fetal renal damage) rash increased renin lower angiotensin II AND hyperK+ avoid with bilateral renal artery stenosis because ACE inhibitors dec GFR by preventing constriction of efferent arterioles |
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