Renal Drugs Flashcards
Mechanism of mannitol
osmotic diuretic
increases tubular osmolarity –> increased urine flow, decreased intracranial/intraocular pressure
Use of mannitol
drug overdose, elevated intracranial/intraocular pressure
Toxicity of mannitol
pulmonary edema, dehydration
contraindicated in anuria, HF
Mechanism of acetazolamide
carbonic anhydrase inhibitor - prevents brush border conversion of HCO3- + H+ to CO2 and H2O
causes a self-limited NaHCO3 diuresis and decrease total body HCO3- stores
Use of acetazolamide
glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor
Toxicity of acetazolamide
hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy
Name the loops diuretics
furosemide, bumetanide, torsemide
Mechanism of the loop diuretics
sulfonamide loop diruetics inhibit cotransport of Na/K/2Cl in thick ascending limb of loop of henle
abolish hypertonicity of medulla, preventing concentration of urine
stimulate PGE release (vasodilatory effect on afferent arteriole) - inhibited by NSAIDs
Use of loop diuretics
edemtatous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia
Toxicity of loop diurietics
hypercalciuria, ototoxicity, hypokalemia, dehydration, allergy (sulfa), nephritis (interstitial), gout
Mechanism of ethacrynic acid
phenoxyacetic acid derivative (not a sulfa drug) with same mech as furosemide
Use of ethacrynic acid
as diuretic for pts with sulfa allergy
Toxicity of ethacrynic acid
similar to furosemide; can cause hyperuricemia so never used to treat gout
Name the thiazide diuretics
chlorthalidone, hydrochlorothiazide
Mechanism of thiazide diruetics
inhibit NaCl reabsorption in DCT –> decreased diluting capacity of nephron
Use of thiazide diruetics
hypertension, HF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis (bc increases calcium)
Toxicity of thiazides
hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia
sulfa allergy
Name the K+ sparing diruetics
spironolactone and eplerenone; trimaterene and amiloride
Mechanism of spironolactone and eplerenone
competitive aldosterone antagonists in cortical collecting tubule
Mechanism of triamterene and amiloride
act in cortical collecting tubule to inhibit ENAC channels
Use of K+ sparing diuretics
hyperaldosteronism, K+ depletion, HF
Toxicity of K+ sparing diuretics
hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (gynecomastia and antiandrogen effects)
Urine NaCl changes
increases with all diuretics except acetazolamide
Urine K+ changes
increases with loop and thiazides
Blood pH
acidemia:
- carbonic anhydrase inhibitors
- K+ sparing
alkalemia:
- loops
- thiazides
How do CA inhibitors cause acidemia?
decrease HCO3- reabsorption in the pCT
How do K+ sparing cause acidemia?
aldosterone blockade prevents K+ secretion and H+ secretion
hyperkalemia –> K+ entering the cells in exchange for H+ leaving the calls contributing further to the acidemia
How do loops and thiazides cause alkalosis?
- volume contraction –> increased AT II –> increased Na+/H+ exchange in PT –> increased HCO3- reabsorption (“contraction alkalosis”)
- K+ loss leading to K+ exiting the cells and H+ entering the cells
- in low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule –> alkalosis and “paradoxical aciduria”
Name the ACE inhibitors
captopril, enalapril, lisinopril, ramipril
Mechanism of ACE inhibitors
inhibit ACE –> decreased AT II –> decreased GFR by preventing constriction of efferent arteriole
increase renin levels
inhibition of ACE also leads to decreased bradykinin breakdown –> vasodilation
Use of ACE inhibitors
hypertension, HF, proteinuria, diabetic nephropathy
prevent unfavorable heart remodeling in chronic hypertension
How do ACE inhibitors work in diabetic nephropathy?
decrease intraglomerular pressure, slowing GBM thickening
Toxicity of ACE inhibitors
dry cough, angioedema, teratogen, increased creatinine, hyperkalemia, and hypotension
Contraindications to ACE inhibitors
C1 esterase inhibitor deficiency
bilateral renal artery stenosis because will further decrease GFR –> renal failure
Name the angiotensin II receptor blockers
losartan, candesartan, valsartan
Mechanism of ARBs
selectively block binding of angiotensin II to AT1 receptors
effects similar to ACE inhibitors, but no bradykinin increase
Use of ARBs
hypertension, HF, proteinuria, or diabetic nephropathy with intolerance to ACE inhibitors (e.g. cough, angioedema)
Toxicity of ARBs
hyperkalemia, decreased renal function, hypotension; teratogen
Mechanism of aliskiren
direct renin inhibitor, blocks conversion of angiotensinogen to angiotensin I
Use of aliskiren
hypertension
Toxicity of aliskiren
hyperkalemia, decreased renal function, hypotension
Contraindication of aliskiren
diabetics taking ACE inhibitors or ARBs
