Loop Diuretics

Loop Diuretics


  • Inhibitors of Na+ & Cl- reabsorption.
  • By inhibiting Na+ K+ 2Cl- cotransporter on thick ascending limb.
  • Hence, excreting Na2+.
  • Na2+ excretion continues even if ECF is less & hence causes dehydration & hypotension. 
  • Na2+ excretion accompanies increased H+ & K+ loss. 
  • May cause metabolic alkalosis.
Image result for loop diuretics
  • Produces vasodilator action, directly or indirectly by releasing renal factor.
  • Potentiates thiazides action.


Diuretic actions:

  • Reduces edema due to cardiac failure, hepatic disease, nephrotic syndrome.
  • Eg: Acute pulmonary edema, cerebral edema, acute chronic renal failure, pregnancy & idiopathic edema.
  • Drug of choice for acute left ventricular failure is I/V Furosemide.
  • Useful in Barbiturate poisoning, salicylate poisoning.

Nondiuretic action of Loop Diuretics:

  • As an antihypertensive.
  • Idiopathic calcium urolithiasis.
  • Hyponatremic states due to water retention.
  • Glaucoma.


  • Hypokalemia – Combined with potassium-sparing diuretics.
  • Hyponatremia, dehydration & metabolic acidosis.
  • Hyperglycemiahyperuricemia, Hypomagnesemia .
  • Weakness, fatigue, dizziness, cramps & myalgia.
  • Prostatic hypertrophy, ototoxicity, cardiac arrest after IV injection.
  • Hepatic insufficiency, gastric upset.
  • Orthostatic hypotension.


  • Potent oral diuretic.
  • Has halogenated sulfamoyl benzene ring common to Thiazide diuretics.
  • Acts on thick ascending loop of Henle, blocking Na+-K+ 2Cl symport.
  • Furosemide attaches to Cl- binding site of protein (Na+ K+ 2Cl-) inhibiting its transport function.
  • 160 mg furosemide – Cirrhosis & portal hypertension.



  • Excretion of Na+, K+, Cl-, PO4.
  • IV administration increases renal blood flow.
  • Increases PGE2 synthesis in kidneys – Has locally protective & vasodilator effect.
  • In physiological or pharmacological stress – Counteracts intrarenal vasoconstriction.
  • Excessive chloride loss →hypochloremic alkalosis.
  • K+ loss→ Hypokalemia. (Less marked with Furosemide than Thiazides).
  • Little change in Urine pH. Potent renin releasers.

Blood vessels & BP:- 

  • IV furosemide dilates peripheral vasculature.
  • Lowers the arterial BP.
  • Rapid venous pooling of blood.
  • Reducing cardiac preload & afterload.

Metabolic actions:- 

  • ↑ blood uric acid, ↑ blood urea & disturbances of glucose tolerance.
  • ↑  Ca++ & Mg++ excretion.


  • Absorbed orally.
  • Bioavailability 60-100%.
  • Food reduces bioavailability.
  • Onset of action is quick & short.
  • Low lipid solubility.
  • Excreted within 4 hours.
  • 50% excreted unchanged, rest conjugated with glucuronide in kidney.


  • 3 times more potent than furosemide.
  • Oral absorption more rapid & complete. 
  • 80% metabolized in liver.
  • t1/2= 3.5 hrs. 
  • Duration of action= 4-8 hrs.
  • Used in hypertension & edema.


  • 40 times more potent than furosemide.
  • Onset & duration and its effect on electrolyte excretion are similar to furosemide.
  • 80% absorption. 
  • Metabolized in liver & its half-life is not prolonged in renal insufficiency.


  • Max. diuresis within 2-3 hrs after giving orally.
  • Used in edematous states, especially in patients allergic to sulphonamides.
  • Less used because prone to cause adverse effects (Ototoxicity mainly)similar to those of furosemide.


  • Potentiate all other antihypertensives. 

Hypokalaemia induced by these diuretics:

  • Enhances digitalis toxicity.
  • Produces polymorphic ventricular tachycardia with quinidine and other antiarrhythmics.
  • Potentiates competitive neuromuscular blockers and reduces sulfonylurea action.
  • Loop diuretics + aminoglycoside antibiotics – both ototoxic and nephrotoxic → additive toxicity.
  • Cotrimoxazole + loop diuretics- thrombocytopenia.
  • Indomethacin/ NSAIDs + Loop diuretics- diminishes diuretic and antihypertensive effect of loop diuretics.
  • Probenecid + furosemide and thiazides competitively inhibit tubular secretion of furosemide and thiazides.
  • Serum lithium level rises when diuretic therapy 
  • Furosemide and warfarin/ Clofibrates: Displacement of plasma protein binding of warfarin
Exam Question
  • Hyperglycemia, Hypomagnesemia, acidosis, Hypokalemia, Ototoxicity & Hyperuricemia  are adverse effects can be caused by Loop Diuretics
  • The usual maximum dose of furosemide and spironolactone in patients with cirrhosis and portal hypertension is Furosemide 160 mg and spironolactone 400 mg
  • Loop diuretic is the mechanism of action of bumetanide
  • Loop diuretics are most likely to result in contraction alkalosis
  • Loop diuretics act on Thick ascending limb
  • Ethacrynic acid causes increased concentration of Na’ & Cl in urine with normal bicarbonate
  • Furosemide  is used in pulmonary edema
  • Ethacrynic acid is not used due to Ototoxicity
  • Loop diuretics interact with cefotaxime 
  • IV fluid with furosemide is given in Hypercalcemia
  • Drug of choice for acute left ventricular failure is I/V Furosemide
  • Furosemide is excreted unchanged in urine
  • Diuretics of choice for acute pulmonary edema is Loop diuretics
  • The site of action of the loop diuretic furosemide is Thick ascending limb of loop of Henle
Don’t Forget to Solve all the previous Year Question asked on Loop Diuretics

Leave a Reply

Free Mini Course on Stomach

Mini Course – Stomach

22 High Yield Topics in Stomach

in Just 2 Hours

Submission received, thank you!

Close Window
%d bloggers like this:
Malcare WordPress Security