PH4.5 | PH4.5 | Diuretics and Antidiuretic Drugs — Summary & Reflection

KEY TAKEAWAYS

Diuretics act at five distinct nephron sites, and the site determines both potency and electrolyte consequences. Loop diuretics (furosemide) are the most potent and remain effective in CKD — they are first-line in acute pulmonary oedema and severe fluid overload; they cause hypocalcaemia. Thiazides are moderate-potency, preferred for hypertension, and cause hypercalcaemia (useful in calcium stone disease; contraindicated in hypercalcaemia). Potassium-sparing agents (spironolactone, amiloride) prevent hypokalaemia and are essential in HFrEF (RALES/EMPHASIS-HF) and cirrhosis — monitor for hyperkalaemia. Carbonic anhydrase inhibitors (acetazolamide) are used for glaucoma and altitude sickness. Osmotic diuretics (mannitol) treat cerebral oedema. On the antidiuretic side, desmopressin (V2-selective) treats central diabetes insipidus and nocturnal enuresis; terlipressin (V1a) controls variceal bleeding; vaptans (tolvaptan, V2 antagonist) treat SIADH by aquaresis — always correct hyponatraemia no faster than 6–8 mEq/L per 24 hours to avoid osmotic demyelination.

REFLECT

Return to the opening patient: the 68-year-old man with HFrEF in acute pulmonary oedema whose potassium dropped to 2.9 mEq/L after IV furosemide 80 mg.

1. Why did the oral furosemide 40 mg at home fail to prevent decompensation, while the IV 80 mg worked?
2. What mechanism explains the hypokalaemia — and what monitoring would you institute?
3. He is on enalapril (an ACEi). Would you add spironolactone now? What would you watch for?
4. His admission blood gas shows metabolic alkalosis (pH 7.52, HCO₃ 32). How does furosemide cause this, and which electrolyte replacement is the priority?
5. Three weeks later, he is compensated and clinically dry. Would you continue the loop diuretic, reduce it, or switch to a thiazide?

Reflect on how nephron-site pharmacology translates directly into the bedside management decisions you made through this case.