Renal Pharm Flashcards
Osmotic diuretic, increased tubular fluid osmolarity, producing increased urine flow. Primary site of action at proximal convoluted tubule.
Mannitol mechanism of action?
Shock, drug overdose, decreases intracranial/intraocular pressure (glaucoma), decreases cyclosporine toxicity, oligouric states (statin induced rhabdomyolysis).
Mannitol uses?
Pulmonary edema, dehydration, headache, nausea, and vomiting.
- Contraindicated in anuria, and CHF.
Mannitol side effects?
Carbonic anhydrase inhibitor. Causes self-limited NaHCO3 diuresis and reduction in total-body HCO3- stores.
Acetazolamide, dorzolamide mechanism of action?
Glaucoma (dorzolamide), urinary alkalinization, metabolic alkalosis, altitude sickness.
Acetazolamide, dorzolamide uses?
Hyperchloremic metabolic acidosis, paresthesia, NH3 toxicity, sulfa allergy, hypokalemia, renal stones (struvite, due to increased urine pH).
Acetazolamide, dorzolamide (“ACID”azolamide causes ACIDosis)
Inhibits NaKCC of the TAL. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilation of afferent arteriole); inhibited by NSAIDs.
Furosemide, torsemide mechanism of action?
Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia.
Furosemide, torsemide uses?
Reversible Ototoxicity, Hypokalemic metabolic alkalosis, Dehydration, sulfa Allergy, interstitial Nephritis, hyperuricemia (Gout), hypocalcemia/hypomagnesemia. Increased toxicity with aminoglycosides, lithium, and digoxin.
Furosemide, torsemide (OH DANG!)
Inhibits NaKCC of the TAL. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilation of afferent arteriole); inhibited by NSAIDs.
Ethacrynic acid mechanism of action?
Diuresis in patients allergic to sulfa drugs.
Ethacrynic acid uses?
NO SULFA ALLERGY, can be used with gout. Irreversible otoxoticity (higher than furosemide), hypokalemic metabolic alkalosis, dehydration, nephritis, hypocalcemia/hypomagnesemia. Increased toxicity with aminoglycosides, lithium, an digoxin.
Ethacrynic acid side effects?
Inhibits NaCl reabsorption in the early distal tubule. Opens ATP-dependent K+ channel (beta islet cells, arterioles).
Hydrochlorothiazide, indapamide, metolazone mechanism of action?
Hypertension, CHF, idiopathic hypercalcinuria (nephrolithiasis), nephrogenic diabetes insipidus. DON’T USE IN PATIENTS WITH DIABETES MELLITUS TYPE 2.
Hydrochlorothiazide, indapamide, metolazone uses?
Hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia (inhibits insulin release), hyperLipidemia (LDL, cholesterol), hyperUricemia, and hyperCalcemia. Sulfa allergy. Increased toxicity with digoxin.
Hydrochlorothiazide, indapamide, metolazone (HyperGLUC)
Aldosterone antagonist on principle cells of the cortical collecting tubule. Potassium sparing diuretic.
Spironlactone mechanism of action?
Hyperaldosteronism (Conn’s syndrome), reverses hypokalemia, CHF. Slows cardiac remodeling. Anti-androgen (for acne, hirsutism).
Spironlactone uses?
Hyperkalemic metabolic acidosis. Gynectomastia (anti-androgen effects).
Spironlactone side effects?
Selective aldosterone antagonist on principle cells of the cortical collecting tubule. Potassium sparing diuretic.
Eplerenone mechanism of action?
Hyperaldosteronism (Conn’s syndrome), reverses hypokalemia, CHF. Slows cardiac remodeling.
Eplerenone uses?
Hyperkalemic metabolic acidosis. No anti-androgen effects.
Eplerenone side effects?
Block sodium channels in the cortical collecting tubule. Potassium sparing diuretic.
Triamterene mechanism of action?
Reverses hypokalemia, CHF, lithium-induced nephrogenic diabetes insipidus.
Triamterene uses?
Hyperkalemic metabolic acidosis.
Triamterene side effects?
Block sodium channels in the cortical collecting tubule. Potassium sparing diuretic.
Amiloride mechanism of action?
Reverses hypokalemia, CHF, lithium-induced nephrogenic diabetes insipidus.
Amiloride uses?
Hyperkalemic metabolic acidosis.
Amiloride side effects?
Mech: Inhibit angiotensin-converting enzyme (ACE) –> decreased angiotensin II –> decreased GFR by preventing efferent arteriole constriction.
- Renin increases.
- Inactivation of bradykinin (potent vasodilator)
Ace Inhibitors (PRILs) - Captopril, enalapril, lisinopril
Similar to ACE inhibitors but do not increase bradykinin –> no cough or angioedema.
Angiotensin II Receptor Blockers
Used for: Hypertension, CHF, proteinuria, diabetic renal disease.
- Also prevents unfavorable heart remodeling from chronic hypertension.
Ace Inhibitors (PRILs) - Captopril, enalapril, lisinopril
SE: Cough, Angioedema, Teratogen (fetal renal malformation), Creatinine increase (decreased GFR), Hyperkalemia, and Hypotension.
- Avoid in bilat renal artery stenosis because they will further decrease GFR –> renal failure.
Ace Inhibitors (PRILs)
- Captopril, enalapril, lisinopril
- Captopril’s CATCHH.