Kenzamide

Furosemide.

Tablet: Each uncoated tablet contains: Furosemide BP 40 mg.
Injection: Each mL contains: Furosemide 10 mg.

Pharmacology: Injection: Action: Furosemide (Kenzamide) is a potent diuretic with a rapid action. It inhibits the reabsorption of electrolytes in the ascending limb of the loop of Henle and also in the distal renal tubules. It may also have a direct effect in the proximal tubules. Excretion of sodium, potassium and chloride ions is increased and water excretion enhanced. It has no clinically significant effect on carbonic anhydrase. Used similarly to chlorothiazide and may be effective in patients unresponsive to thiazide diuretic. It is also used in the treatment of renal insufficiency unlike the thiazide diuretics were owing to their flat dose-response curve, very little is gained by increasing the dose, Furosemide (Kenzamide) has a steep dose-response curve, which gives it a wide therapeutic range.
Pharmacokinetics: Tablet: Furosemide is fairly rapidly absorbed from the gastrointestinal tract; bioavailability has been reported to be about 60 to 70% but absorption is variable and erratic. The half-life of Furosemide is up to about 2 hours although it is prolonged in neonates and in patients with renal and hepatic insufficiency. It is up to 99% bound to plasma albumin, and is mainly excreted in the urine, largely unchanged. There is also some excretion via the bile and non-renal elimination is considerably increased in renal impairment. Furosemide crosses the placental barrier and is distributed into breast milk. The clearance of Furosemide is not increased by haemodialysis.
Injection: Absorption: Furosemide (Kenzamide) is readily absorbed from injection site. The onset of diuresis following intravenous administration is within 5 minutes and somewhat later intramuscular administration.
Blood concentration: The peak effect occurs within the first half hour. The duration of diuretic effect is approximately 2 hours.
Half-life: Peak plasma concentrations increase with increasing dose but times-to-peak do not differ among doses. The terminal half-life of is approximately 2 hours.
Protein binding: Plasma concentrations ranging from 1 to 400 mcg/ml are 91 to 99% bound in healthy individuals. The unbound fraction averages 2.3 to 4.1% at therapeutic concentration.
Excretion: It is mainly excreted in the urine; largely unchanged variable amounts are also excreted in the bile, non-renal elimination being considerably increased in renal failure.

Tablet: Furosemide is a potent diuretic with a rapid action. Like the other loop or high-ceiling diuretics, it is used in the treatment of oedema associated with heart failure, including pulmonary oedema and with renal and hepatic disorders and may be effective in patients unresponsive to thiazide diuretics. It is also used in high doses in the management of oliguria due to renal failure or insufficiency. Furosemide is also used in the treatment of hypertension either alone or together with other antihypertensives.
Furosemide inhibits the reabsorption of electrolytes primarily in the thick ascending limb of the loop of Henle and also in the distal renal tubules. Excretion of sodium, potassium, calcium and chloride ions is increased and water excretion enhanced. It has no clinical significant effect on carbonic anhydrase.
Injection: For the treatment of oedema associated with heart failure, pulmonary oedema, and with renal & hepatic disorders. For patients unresponsive to thiazide diuretics and management of oliguria due to renal failure or insufficiency & for hypertension.

Tablet: Furosemide's effects are evident within 30 minutes to 1 hour after a dose by mouth, peak at 1 to 2 hours, and last for about 4 to 6 hours; after intravenous injection its effects are evident in about 5 minutes and last for about 2 hours. It is given by mouth, usually in the morning. Alternatively it may be administered intramuscularly or intravenously as the sodium salt; doses are expressed in terms of furosemide base. 10.7 mg of furosemide sodium is approximately equivalent to 10 mg of furosemide base. The manufacturers recommend that whether by direct intravenous injection or by infusion the rate of intravenous administration should not exceed 4 mg/minute although the British National Formulary advises that a single dose of up to 80 mg may be given more rapidly.
Unlike the thiazide diuretics where, owing to their flat dose-response curve, very little is gained by increasing the dose, furosemide has a steep dose-response curve, which gives it a wide therapeutic range.
In the treatment of oedema, the usual initial dose is 40 mg once daily by mouth, adjusted as necessary according to response. Mild cases may respond to 20 mg daily or 40 mg on alternate days. Some patients may require doses of 80 mg or more daily given as one or two doses daily, or intermittently. Severe cases may require gradual titration of the furosemide dosage up to 600 mg daily. In an emergency or when oral therapy cannot be given, 20 to 50 mg of furosemide may be administered by slow intravenous injection; intramuscular injection may be given in exceptional cases but is not suitable for acute conditions. If necessary further doses may be given, increasing by 20-mg increments and not given more often than every 2 hours. If doses greater than 50 mg are required they should be given by slow intravenous infusion. For pulmonary oedema, if an initial slow intravenous injection of 40 mg does not produce a satisfactory response within one hour, a further 80 mg may be given slowly intravenously.
For children, the usual dose by mouth is 1 to 3 mg/kg daily up to a maximum of 40 mg daily; doses by injection are 0.5 to 1.5mg/kg daily up to a maximum of 20 mg daily.
In the treatment of hypertension, furosemide is given in doses of 40 to 80 mg daily by mouth, either alone, or with other antihypertensives.
Or as prescribed by a physician.
Injection: Adults: 20 to 50 mg by slow IV injection; IM may be given but not for acute conditions. Increase the dose by 20mg but not given more than every 2 hours. Increase initial dose to 80mg if not satisfactory.
Children: 0.5 to 1.5mg/kg daily up to a maximum of 20 mg daily or as prescribed by the physician.

Tablet: High doses of Furosemide therapy is contraindicated in renal failure caused by nephrotoxic or hepatotoxic drugs and in renal failure associated with hepatic coma.
Injection: Hypersensitivity, pregnant and lactating women.

Tablet: Although Furosemide is used in high doses for oliguria due to chronic or acute renal insufficiency it should not be given in anuria or in renal failure caused by nephrotoxic or hepatotoxic drugs nor in renal failure associated with hepatic coma. Furosemide should not be given in precomatoses states associated with hepatic cirrhosis. It should be used with care in patients with prostatic hyperplasia or impairment of micturition since it can precipitate acute urinary retention.
To reduce the risk of ototoxicity, the manufacturers recommend that Furosemide should not be injected intravenously at a rate exceeding 4 mg per minute although some authorities advise that a single dose of up to 50 mg may be given more rapidly.
Furosemide should be used with caution during pregnancy and breast feeding since it crosses the placenta and also appears in breast milk. Furosemide may compromise placental perfusion by reducing maternal blood volume; it may also inhibit lactation.
Use in Children: The half-life of Furosemide in term and preterm neonates is markedly prolonged compared with that in adults. Half lives of 4.5 to 46 hours have been reported and it has been suggested that the prolongation may be greater in preterm than in term neonates. These effects are due primarily to immature renal function and if repeated doses are necessary over a short period accumulation may occur.
Injection: If particularly higher doses are given over prolonged periods, serum electrolytes should be checked regularly. Potassium-rich diet or potassium drugs should be supplemented. The blood pressure and circulating blood volume of patients in shock should be normalized before treatment. Use with caution to patients with hypertrophy of the prostate and dysuria, as it may cause acute urine retention, elderly people, diabetic patients (increased insulin doses may be necessary), patients in liver cirrhosis associated with ascites, patients with disturbed uric acid metabolism.

Tablet: The most common side-effect associated with Furosemide therapy is fluid and electrolyte imbalance including hyponatraemia, hypokalaemia and hypochloraemic alkalosis, particularly after large doses or prolonged administration. Because of their shorter duration of action, the risk of hypokalaemia may be less with loop diuretics such as Furosemide than with thiazide diuretics. Unlike the thiazide diuretics, Furosemide increases the urinary excretion of calcium. Nephrocalcinosis has been reported when Furosemide has been used to treat preterm infants.
Furosemide may provoke hyperglycaemia and glycosuria, but probably to a lesser extent than the thiazide diuretics. It may cause hyperuricaemia and precipitate attacks of gout in some patients. Signs of electrolyte imbalance include headaches, hypotension, muscle cramps, dry mouth, thirst, weakness, lethargy, drowsiness, restlessness, oliguria, cardiac arrhythmias and gastrointestinal disturbances.
Other side-effects are relatively uncommon and include blurred vision, yellow vision, dizziness, headaches and orthostatic hypotension. Skin rashes and photosensitivity reactions, although rare, may be severe and hypersensitivity reactions including interstitials nephritis, vasculitis and fever occur rarely. Pancreatic is more common at high doses and cholestatic jaundice has been reported. Bone marrow depression may occur rarely: agranulocytosis, thrombocytopenia and leucopenia have been reported. Tinnitus and deafness may rarely occur in particular during rapid high-dose parenteral Furosemide therapy. Rarely, deafness may be permanent particularly if Furosemide has been given to patients taking other ototoxic.
Injection: Nausea, vomiting, diarrhea, indigestion, visual disturbance, tinnitus, transient hearing impairment, muscle spasm, paresthesia, orthostatic hypotension, pancreatitis, hepatic dysfunction, photosensitivity, dizziness, fatigue, muscular weakness, increased thirst and impulse to urinate, rarely skin rash, myelopathy (leukopenia, thrombocytopenia). Disturbance of electrolyte and fluid balance, particularly hypokalemia may occur.
Inform a doctor in case of any adverse reactions related to drug use.

Tablet: The interactions of furosemide that are due to its effects on fluid and electrolyte balance are similar to those of hydrochlorothiazide.
Many of the interactions of hydrochlorothiazide and other thiazides are due to their effects on fluid and electrolyte balance. Diuretic-induced hypokalaemia may enhance the toxicity of digitalis glycosides and may also increase the risk of arrhythmias with drugs that prolong the QT interval, such as astemizole, terfenadine, halofantrine, pimozide, and sotalol. Thiazides may enhance the neuromuscular blocking action of competitive neuromuscular blockers, such as atracurium, probably by their hypokalaemic effect. The potassium-depleting effect of diuretics may be enhanced by corticosteroids, corticotropin, beta2 agonists such as salbutamol, carbenoxolone, amphotericin B, or reboxetine.
Diuretics may enhance the effect of other antihypertensives, particularly the first-dose hypotension that occurs with alpha blockers or ACE inhibitors.
Orthostatic hypotension associated with diuretics may be enhanced by alcohol, barbiturates, or opioids. The antihypertensive effects of diuretics may be antagonised by drugs that cause fluid retention, such as corticosteroids, NSAIDs, or carbenoxolone; diuretics may enhance the nephrotoxicity of NSAIDs. Thiazides have been reported to diminish the response to pressor amines, such as noradrenaline, but the clinical significance of this effect is uncertain.
Thiazides should not usually be used with lithium since the association may lead to toxic blood concentrations of lithium. Other drugs for which increased toxicity has been reported when given with thiazides include allopurinol and tetracyclines. Thiazides may alter the requirements for hypoglycaemics in diabetic patients.
Furosemide may enhance the nephrotoxicity of cephalosporin antibacterials such as cefalotin and can enhance the ototoxicity of aminoglycoside antibacterials and other ototoxic drugs.
Injection: Concurrent use of Furosemide with the following drugs should be avoided: Alcohol, barbiturate and narcotics: may aggravate orthostatic hypotension.
Corticotropin or corticosteroid: may intensify electrolyte imbalance, particularly hypokalemia.
Aminoglycoside antibiotics: may increase the potential for ototoxicity and nephrotoxicity.
Cephaloridine or Cephalothin: may increase the potential for nephrotoxicity.
Lithium salts: may provoke lithium toxicity.

Store at temperatures not exceeding 30°C.

Diuretics

C03CA01 - furosemide ; Belongs to the class of high-ceiling sulfonamide diuretics.

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