x | x |
Only parenteral thiazide available | |
MOA: Physical osmotic effect on tissue water distribution because it is retained in the vascular compartment | |
Toxicity: Nausea, vomiting, headache. May enhance congestive heart failure or cause pulmonary edema. | |
Inhibition of Na/K/Cl transporter in the ascending limb of Henle's loop | |
Used for peripheral edema, hypertension, acute hypercalcemia, hyperkalemia, acute renal failure, anion overdose | |
Mechanism like amiloride, much less potent, more toxic | |
Pharmacologic antagonist of aldosterone | |
Toxicity: Hyperkalemic metabolic acidosis | |
MOA: Blocks epithelial sodium channels in collecting tubules | |
Toxicity: Infusion site reactions | |
Antagonist at V1a and V2 ADH receptors. Reduces water reabsorption and increases plasma Na concentration | |
Not a sulfonamide but has typical loop activity and some uricosuric action loop diuretic | |
| x | x |
Like spironolactone, more selective for aldosterone receptor | |
MOA: Inhibition of NaCl transporter in the distal convoluted tubule | |
Toxicities: Ototoxicity, hypovolemia, K wasting, hyperuricemia, hypomagnesemia | |
Sulfonamide similar to thiazide | |
Toxicities: metabolic acidosis, renal stones, hyperammonemia in cirrhotics | |
Popular for use with loop agents for synergistic effects | |
Clinical applications: glaucoma, mountain sickness, edema with alkalosis | |
Toxicities: Hypokalemic metabolic alkalosis, hyperuricemia, hyperglycemia, hyponatremia | |
Reduces reabsorption of HCO3- in the kidney causing self limited diuresis | |
Toxicity: Hyperkalemia, gynecomastia | |
Used for hypertension, mild heart failure, nephrolithiasis, nephrogenic diabetes insipidus | |
MOA: Inhibition of the enzyme prevents dehydration of H2CO3 and hydration of CO2 | |
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