Furosemide (Frusemide)

• It is a high ceiling/loop diuretic.
• Oral diuretic, Fast acting and highly efficaceous.
• The primary site of action for loop diuretics lies in the thick ascending limb of the loop of Henle.
• It inhibits Na⁺ - K⁺- 2Cl^- cotransport.
• Furosemide, a diuretic, has a weak inhibitory effect on carbonic anhydrase. It increases the concentration of bicarbonate in the blood, leading to increased excretion of bicarbonate and water. As a result, the pH of the urine may rise, but the predominant anion in the urine is chloride, which prevents the development of acidosis.
• Intravenous Furosemide increases systemic venous capacitance, decreasing left ventricular filling pressure and providing quick relief in LVF and pulmonary edema.
• Effects on Electrolyte Excretion: Furosemide increases calcium and magnesium excretion by abolishing the lumen positive transepithelial potential difference in the thick ascending loop of Henle.
• Impact on Uric Acid and Blood Sugar: Furosemide tends to raise blood uric acid levels and may cause a small rise in blood sugar levels, but to a lesser extent than thiazides.

• Loop diuretics act on the thick ascending limb of Henle’s loop, blocking Na⁺-K⁺-2Cl^- cotransporter and increasing Na⁺ and Cl^- excretion. They also lead to K⁺ loss due to increased exchange of Na⁺ with K⁺ in DCT as tubuar fluid contains more Na⁺ and increased HCO3^-, Mg²⁺ Ca²⁺ excretion.

• The loop diuretics are rapidly absorbed through the GI tract.
• It can be given by oral (onset of action (osa): 30-40 min), Intravenous (i.v.) (osa: 2-5 min), intramuscular (i.m) (osa: 10-20 min).
• Duration of action: Short (2-4 hours)
• Lipid solubility is low and highly bound to plasma proteins.
• It is partly conjugated with glucuronic acid.
• It is excreted unchaged by glomerular filtration and tubular secretion. It is also excreted in bile and directly in intestine also
• Plasma half life avarages 1-2 hour.

• Furosemide is usually prescribed at a dose of 20-80 mg once daily in the morning.
• In cases of renal insufficiency, the dose may be increased to 200 mg 6 hourly, administered by i.m./i.v. route.
• In pulmonary edema, a dose of 40-80 mg may be injected i.v.
• LASIX is available in the following forms: 40 mg tab., 20 mg/2 ml inj., LASIX HIGH DOSE 500 mg tab, 250 mg/25 ml inj.
• SALINEX and FRUSENEX are also available in 40 mg tab. and 100 mg tab. forms, respectively.
• LASIX and SALINEX are available in tablet form, while FRUSENEX is available in tablet and injection form.
• LASIX and SALINEX are used to treat fluid retention, while FRUSENEX is used to treat high blood pressure.

• Loop diuretics are preferred during initial stages of renal and cardiac edema.
• Used to treat acute pulmonary oedema.
• I.v. Furosemide alomg with isotonic saline is used to treat hypercalcaemia.
• Furosemide is not preferred in primary hypertension due to its short duration of action. Other loop diuretics can be used to treat hypertension.
• It is used to prevent overload during blood transfusion.

1. Electrolyte disturbances: Hypokalaemia, Hypoatraemia, Hypocalcaemia and Hypomagnesaemia
2. Metabolic affects: Hyperglycaemia, Hyperlipidaemia, Hyperuricaemia
3. Diarrhea, constipation, loss of appetite, numbness or tingling, headache, dizziness or blurred vision
4. Ototoxicity: It is due to damage in inner ear and the symptoms are vertigo, deafness and tinnitus which are reversible on stoppage of therapy.
5. Hypersensitivity: Skin rashes, eosinophilia,photosensitivity, etc.

1. Digoxin: These diuretics increases the binding of digoxin to Na- K⁺ ATPase leading to digoxin toxicity and hypokalaemia.
2. Aminoglycosides: Cause severe ototoxicity as both are ototoxic drugs.
3. Non steroidal anti-inflammatory drugs (NSAIDs): NSAIDs inhibit prostaglandin synthesis and block the hemodynamic changes mediated by prostaglandins caused by loop diuretics. Chronic use of NSAIDs results in sodium and water retention, thereby diminishing the antihypertensive effect of loop diuretics and thiazides.
4. Lthium: Diuretics cause hyponatraemia, leading to compensatory sodium and lithium reabsorption in the PCT, causing lithium toxicity.
5. Amiloride: Furosemide/chlorthalidone causes hypokalemia, while amiloride conserves potassium. Combining these diuretics improves diuretic response without altering potassium levels.