Loop Diuretics — MOA & Use
Furosemide can pull liters of fluid off a patient in hours — but that power comes from blocking a transporter most students can't name. Know where it acts and why it's first-line.
Core Concept
Loop diuretics (furosemide, bumetanide, torsemide) block the sodium-potassium-2 chloride (Na+/K+/2Cl−) cotransporter in the thick ascending limb of the loop of Henle — the segment responsible for reabsorbing roughly 25% of filtered sodium. By shutting this transporter down, loops produce the most potent diuresis of any diuretic class. This makes them first-line for acute decompensated heart failure, pulmonary edema, and fluid overload refractory to other agents. IV furosemide begins working within 5 minutes; oral onset is about 30–60 minutes. The typical starting IV dose is 20–40 mg. Because the ascending limb also drives the kidney's concentrating mechanism, loops impair the medullary gradient, producing dilute urine in high volume. They also increase calcium and magnesium excretion — a distinction from thiazides, which retain calcium. Furosemide is the most commonly tested loop diuretic on NCLEX.
Watch Out For
Don't confuse loops with thiazides: loops waste calcium while thiazides spare it — this matters for a client with osteoporosis. Students mix up site of action: loops act on the ascending limb of the loop of Henle, not the distal tubule (that's thiazides). Unlike potassium-sparing diuretics, loops cause significant potassium and magnesium loss, not retention.
Clinical Pearl
Think "Loops Lose it all" — sodium, potassium, calcium, magnesium, and water. If it's an electrolyte, a loop diuretic is probably wasting it.
Test Your Knowledge
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