Diuretics Pharmacology Flashcards
Mannitol MOA
Osmotic diuretic. Increase tubular fluid osmolarity–> increases urine flow, decreases intracranial/intraocular pressure. Acts primarily in proximal tubule.
Mannitol clinical use
Drug overdose, elevated intracranial/intraocular pressure
Mannitol toxicity
Pulmonary edema, dehydration, contraindicated in anuria, HF.
Acetazolamide MOA
Carbonic anyhydrase inhibitor. Causes self limited NaHCO3 diuresis and decreased total bicarb stores. Acts in proximal tubule. Reduces bicarb and Na+ reabsorption
Acetazolamide clinical use
Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, psuedotumor cerebri.
Acetazolamide toxicity
Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy.
Loop diuretics (3 names)
Furosemide, bumetanide, torsemide
Loop diuretic MOA
Sulfonamide loop diuretics. Inhibit cotransport system (Na+/K+/2Cl-) of thick ascending limb of loop of henle. Prevent concentration of urine by abolishing hypertonicity of medulla. Increases Na+, K+, H20 excretion. Stimulate PGE release (vasodilatory effect on afferent arteriole). Increase Ca++ excretion
Loop diuretic clinical uses
Edema (HF, cirrosis, nephrotic syndrome, pulmonary edema). HTN, hypercalcemia.
Loop diuretic toxicity
Ototoxicity, Hypokalemia, Dehydration, Allergy, Nephritis, Gout (OH DANG)
Ethacrynic acid MOA
Phenoxyacetic acid derivative. Same action as furosemide (but not sulfonamide)
Ethacrynic acid clinical use
Diuresis in patients with a sulfa allergy.
Ethacrynic acid toxicity
Similar to furosemide. Can cause hyperuricemia. Never use to treat gout.
Thiazide diuretics (3 names)
Chlorthalidone, hydrochlorothiazide, metaloxone
Thiazide MOA
Inhibit NaCl reabsorption in the early DCT. Decrease diluting capacity of nephron. Decrease Ca++ excretion. Opens K+ channels–> hyperpolarize vessels–>vasodilation
Thiazide clinical use
HTN, HF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis.
Thiazide toxicity
Hypokalemic metabolic acidosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sufla allergy.
How do thiazides cause hyperglycemia?
Bind to SUR on K+ channel controlling insulin release–> opens channel–> hyperpolarizes beta cell–> suppresses insulin release–> hyperglycemia
K+ sparing diuretics (4 drugs)
Spironolactone and eplernone, triamterene, amiloride
Spironolactone and eplernone MOA
Competitive aldosterone receptor antagonists in cortical collecting tubule.
Triamterene and amiloride MOA
Block ENaC–> block the Na+ exchange for K+ and H+ in cortical collecting tubule.
K+ sparing diuretic clinical use
Mild diuretics, hyperaldosteronism, K+ depletion, HF. Spironolactone used post-MI for cardiac remodeling
K+ sparing toxicity
Hyperkalemia (can cause arrhythmias), hypercholeremic metabolic acidosis, endocrine effects with spironolactone (gynecomastia, antiandrogen effects). Triamterene + indomethacin can cause ARF, kidney stones
ADH and congeners (Vasopressin and desmopressin) MOA
Stimulate GPCR–>Gs–>cAMP–>PKA–> increase aquaporins–> allows for concentration of urine. Act in the medullary collecting duct
