RENAL Flashcards
Acetazolamide
MOA: Carbonic anhydrase inhibitor. specifically inhibits CA in proximal tubule cells–>causes self-limited NaHCO3 diuresis and decreased total body HCO3- stores
USES: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudomotor cerebri
SIDE EFFECTS: hyperchloremic metabolic acidosis, parasthesis, NH3 toxicity, sulfa allergy
Mannitol
MOA: Osmotic Diuretic. filtered at glomerulus but not reabsorbed, so draws water into lumen
USES: drug overdose, elevated ICP/intraocular pressure
SIDE EFFECTS: pulmonary edema, dehydration. Contraindicated in anuria, HF.
Furosemide
MOA: sulfonamide Loop diuretic. inhibits co transport of Na/K/2Cl of TAL. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs. Increases calcium.
USES: edematous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia
TOXICITY: ototoxicity, hypokalemia, dehydration, allergy (sulfa), nephritis (interstitial), gout.
Bumetanide
MOA: sulfonamide Loop diuretic. inhibits co transport of Na/K/2Cl of TAL. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs. Increases calcium.
USES: edematous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia
TOXICITY: ototoxicity, hypokalemia, dehydration, allergy (sulfa), nephritis (interstitial), gout.
Torsemide
MOA: sulfonamide Loop diuretic. inhibits co transport of Na/K/2Cl of TAL. Abolishes hypertonicity of medulla, preventing concentration of urine. Stimulates PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs. Increases calcium.
USES: edematous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema), HTN, hypercalcemia
TOXICITY: ototoxicity, hypokalemia, dehydration, allergy (sulfa), nephritis (interstitial), gout.
Ethacrynic acid
MOA: loop diuretic. Phenoxyacetic acid derivative (not a sulfonamide). Essentially same action a furosemide.
USES: diuresis in patients allergic to sulfa drugs.
TOXICITY: similar to furosemide; can cause hyperuricemia; never use to treat gout.
Hydrochlorothiazide
MOA: Thiazide diuretic. inhibits NaCl reabsorption in early distal convoluted tubule–>decreases diluting capacity of nephron. Decreases calcium excretion.
USES: HTN, CHF, idiopathic hypercalciuria (retain more calcium), nephrgenic DI, osteoporosis
OTOTOXICITY: hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, and hypercalcemia. Sulfa allergy.
Chlorthalidone
MOA: Thiazide diuretic. inhibits NaCl reabsorption in early distal convoluted tubule–>decreases diluting capacity of nephron. Decreases calcium excretion.
USES: HTN, CHF, idiopathic hypercalciuria (retain more calcium), nephrgenic DI, osteoporosis
OTOTOXICITY: hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, and hypercalcemia. Sulfa allergy.
Spironolactone
MOA: K+-sparing diuretic. competitive aldosterone antagonists in cortical collecting tubule–block ENaC channels–>reduce sodium reabsorption, which slows action of Na/K-ATPase, so less K excretion
USES: hyperaldosteronism, hypokalemia, CHF
TOXICITY: hyperkalemia (can lead to arrhythmias), gynecomastia, menstrual irregularities (anti-androgen effects)
Eplerenone
MOA: K+-sparing diuretic. competitive aldosterone antagonists in cortical collecting tubule–block ENaC channels–>reduce sodium reabsorption, which slows action of Na/K-ATPase, so less K excretion
USES: hyperaldosteronism, hypokalemia, CHF
TOXICITY: hyperkalemia (can lead to arrhythmias), gynecomastia, menstrual irregularities (anti-androgen effects)
Triamterene
MOA: K+ sparing diuretic. block ENaC channels located in CD and principal cells–>reduces Na reabsorption and thus the Na/k ATPase–>less k excretion
USES: hyperaldosteronism, hypokalemia, CHF
SIDE EFFECTS: hyperkalemia, anti-androgen effects
Amiloride
MOA: K+-sparing diuretic. competitive aldosterone antagonists in cortical collecting tubule–block ENaC channels–>reduce sodium reabsorption, which slows action of Na/K-ATPase, so less K excretion
USES: hyperaldosteronism, hypokalemia, CHF
TOXICITY: hyperkalemia (can lead to arrhythmias), gynecomastia, menstrual irregularities (anti-androgen effects)
Captopril
MOA: ACE inhibitor. Inhibits ACE–>decreases AT II–>decreases GFR by preventing constriction of efferent arterioles. Levels of renin increase as a result of loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator.
USES: HTN, CHF, Proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling. Prevent unfavorable heart remodeling as a result of chronic HTN.
TOXICITY: cough, angioedema (contraindicated in C1 esterase inhibitor deficiency), teratogen (fetal renal malformations), increased creatinine (decreased GFR), hyperkalemia, and hypotension. Avoid in bilateral renal artery stenosis, because ACE inhibitors will further decrease GFR leading to renal failure.
Enalapril
MOA: ACE inhibitor. Inhibits ACE–>decreases AT II–>decreases GFR by preventing constriction of efferent arterioles. Levels of renin increase as a result of loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator.
USES: HTN, CHF, Proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling. Prevent unfavorable heart remodeling as a result of chronic HTN.
TOXICITY: cough, angioedema (contraindicated in C1 esterase inhibitor deficiency), teratogen (fetal renal malformations), increased creatinine (decreased GFR), hyperkalemia, and hypotension. Avoid in bilateral renal artery stenosis, because ACE inhibitors will further decrease GFR leading to renal failure.
Lisinopril
MOA: ACE inhibitor. Inhibits ACE–>decreases AT II–>decreases GFR by preventing constriction of efferent arterioles. Levels of renin increase as a result of loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator.
USES: HTN, CHF, Proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling. Prevent unfavorable heart remodeling as a result of chronic HTN.
TOXICITY: cough, angioedema (contraindicated in C1 esterase inhibitor deficiency), teratogen (fetal renal malformations), increased creatinine (decreased GFR), hyperkalemia, and hypotension. Avoid in bilateral renal artery stenosis, because ACE inhibitors will further decrease GFR leading to renal failure.
