Learning Objective
Compare mechanisms, electrolyte effects, and acid-base consequences of major classes of diuretics.
Diuretics: Mechanisms and Effects
| Drug/Class | Mechanism of Action | Urinary Electrolytes | Blood pH / Acid-Base Effect |
|---|---|---|---|
| Acetazolamide | Carbonic anhydrase inhibitor (PCT) | ↑ Na⁺, ↑ K⁺, ↑ HCO₃⁻ | Metabolic acidosis |
| Loop diuretics (furosemide, torsemide, ethacrynic acid) | Na⁺/K⁺/2Cl⁻ cotransporter inhibitor (TAL) | ↑↑ Na⁺, ↑ K⁺, ↑ Ca²⁺, ↑ Mg²⁺, ↑ Cl⁻ | Metabolic alkalosis |
| Thiazides (HCTZ, chlorthalidone, indapamide) | Na⁺/Cl⁻ cotransporter inhibitor (DCT) | ↑ Na⁺, ↑ K⁺, ↑ Cl⁻, ↓ Ca²⁺ | Metabolic alkalosis |
| K⁺-sparing diuretics (amiloride, triamterene, spironolactone, eplerenone) | Block Na⁺ channels/aldosterone receptors (collecting tubule) | ↑ Na⁺ (small), ↓ K⁺ | Metabolic acidosis |
Activity
High-Yield Clinical Notes
- Acetazolamide → alkalinizes urine, causes systemic acidosis; used for glaucoma, altitude sickness, metabolic alkalosis.
- Loop diuretics → potent diuresis, risk of hypokalemia, hypomagnesemia, hypocalcemia, and alkalosis; used in edema/CHF.
- Thiazides → moderate diuresis, hypercalcemia risk, hypokalemia; used in hypertension, calcium stones.
- K⁺-sparing diuretics → weak diuretics, counteract K⁺ loss, may cause hyperkalemia; aldosterone blockers improve CHF survival.
- Site matters: Effects on electrolytes and acid-base depend on nephron segment: PCT → TAL → DCT → Collecting duct.
