Renal drugs Flashcards
Mannitol
Osmotic diuretic, increase tubular fluid osmolarity -> increase urine flow, decrease ICP, decrease IOP
Use: Drug overdose, elevated ICP/IOP
Tox: Pulmonary edema, dehydration, CI in anuria, HF
Acetazolamide
Carbonic anhydrase inhibitor. Causes NaHCO3 diuresis -> Metabolic acidosis
Use: Glaucoma, urinary alkanilzation, metabolic alkalosis, respiratory alkalosis (altitude sickness), pseudomotor cerebri
Tox: hyperchloremic metabolic acidosis, sulfa allergy, NH3 toxicity
Furosemide, Torsemide, Bumetanide
Loop diuretics
Moa: Sulfonamide loop diuretic. Inhibit cotransport (Na/K/ 2Cl) in thick ascending limb -> destroy the hypertonicity of medulla -> prevent concentration of urine
Stimulate PGE release; inhbited by NSAIDs; increase Ca excretion
Use: Edematous states (HF, cirrhosis, nephrotic syndrome, PE, HTN, hypercalcemia
Tox: Ototoxicity, Hypokalemia, Dehydration, sulfa allergy , interstitial nephritis, Gout
Ethacrynic acid
NOT sulfonamide. Same action as furosemide
Use: diuresis in patients with sulfa drug allergy
Toxicity same as furosemide: Ototox, Hypokalemia, Dehydration, Hyperuricemia (Gout), no allergy to sulfa.
Thiazide diuretics
Chlorthalidone, hydrochlorothiazide
Inhibit NaCl reabsorption in early DCT -> can’t dilute urine;
decrease Ca excretion
Use:
HTN, HF, IDIOPATHIC hypercalciuria, nephrogenic DI, osteoporosis
Tox: hypokalemia, contraction metabolic alkalosis, hyponatremia, Hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia
Sulfa allergy
K sparing diuretics
Spironolactone and eplerenone, Triamterene, Amiloride
Spironolactone and eplerenone are Aldosterone receptor antagonists. Eplerenone no gynecomastia
Triamterene and Amiloride - ENac Channel inhibitor in CD
Use: SIADH (hyperaldosteronism), K depletion, HF, CHF, and ascites
Tox: Hyperkalemia -> arrhythmias; gynecomastia by Spironolactone
ACE inhibitors
-Prils, Lisinopril
Use: inhibit ACE-> decrease ATII-> decrease GFR
Renin level, AT1 level, Bradykinin increase (vasodilator)
USE: HTN, HF, Proteinuria (nephrotic syndrome), diabetic nephropathy. Prevent negative remodeling of heart in chronic HTN.
Tox: Cough, Angioedema, Teratogen (fetal renal malformation), increased Cr (decreased GFR), Hyperkalemia, and hypotension
CI in BILATERAL RENAL STENOSIS
ARBs
-sartans
Blocks AT2 binding to AT1 receptors; No increase in Bradykinin
Use: HTN, HF, Proteinuria, diabetic nephropathy,
Tox: Hyperkalemia, decreasd renal function, hypotension, teratogen
Aliskiren
Direct renin inhibitor, blocks Angiotensinogen to AT1
Use: HTN
Tox: Hyperkalemia, decreased renal function, hypotension
Diuretics electrolyte changes
Blood pH
Acetazolamide, K sparing diuretics -> decrease blood pH
Aldosterone blockers prevent K and H secretion at CD. Also, Hyperkalemia -> more H out of cell and K into cell
Loop and Thiazide diuretics increase blood pH.
Thiazides -> volume contraction -> Increased AT2 -> increase Na/H transporters at PCT -> H secreted and Bicarb reabsorbed = contraction alkalosis
Diuretics electrolyte changes
Urine NaCl
Loop diuretics, thiazides, K sparing diuretics increase urine NaCl
EXCEPT acetazolamide
Diuretics electrolyte changes
Urine K
Urine Ca
Urine K Increase with loop and thiazide diuretics
Urine Ca increase: loop diuretics
Urine Ca decrease: thiazide (enhanced Ca reabsorption at DCT)