Patients allergic to sulfonamides may also be allergic to FUROSEMIDE TABLET. Increases in blood glucose and alterations in glucose tolerance tests (with abnormalities of the fasting and 2-hour postprandial sugar) have been observed, and rarely, precipitation of diabetes mellitus has been reported.Īsymptomatic hyperuricemia can occur and gout may rarely be precipitated. Digitalis therapy may exaggerate metabolic effects of hypokalemia, especially myocardial effects.Īll patients receiving FUROSEMIDE TABLET therapy should be observed for these signs or symptoms of fluid or electrolyte imbalance (hyponatremia, hypochloremic alkalosis, hypokalemia, hypomagnesemia or hypocalcemia): dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, arrhythmia, or gastrointestinal disturbances such as nausea and vomiting. Hypokalemia may develop with FUROSEMIDE TABLET, especially with brisk diuresis, inadequate oral electrolyte intake, when cirrhosis is present, or during concomitant use of corticosteroids or ACTH. As with any effective diuretic, electrolyte depletion may occur during FUROSEMIDE TABLET therapy, especially in patients receiving higher doses and a restricted salt intake. If the physician elects to use high dose parenteral therapy, controlled intravenous infusion is advisable (for adults, an infusion rate not exceeding 4 mg FUROSEMIDE TABLET per minute has been used).Įxcessive diuresis may cause dehydration and blood volume reduction with circulatory collapse and possibly vascular thrombosis and embolism, particularly in elderly patients. Usually, reports indicate that FUROSEMIDE TABLET ototoxicity is associated with rapid injection, severe renal impairment, doses exceeding several times the usual recommended dose, or concomitant therapy with aminoglycoside antibiotics, ethacrynic acid, or other ototoxic drugs. If increasing azotemia and oliguria occur during treatment of severe progressive renal disease, FUROSEMIDE TABLET should be discontinued.Ĭases of tinnitus and reversible or irreversible hearing impairment have been reported. Supplemental potassium chloride and, if required, an aldosterone antagonist are helpful in preventing hypokalemia and metabolic alkalosis. Sudden alterations of fluid and electrolyte balance in patients with cirrhosis may precipitate hepatic coma therefore, strict observation is necessary during the period of diuresis. In hepatic coma and in states of electrolyte depletion, therapy should not be instituted until the basic condition is improved. In patients with hepatic cirrhosis and ascites, FUROSEMIDE TABLET therapy is best initiated in the hospital. There are no significant differences between the two oral formulations in the amount of unchanged drug excreted in urine. Significantly more furosemide is excreted in urine following the IV injection than after the tablet or oral solution. The terminal half-life of furosemide is approximately 2 hours. Peak plasma concentrations increase with increasing dose but times-to-peak do not differ among doses. ![]() Although furosemide is more rapidly absorbed from the oral solution (50 minutes) than from the tablet (87 minutes), peak plasma levels and area under the plasma concentration-time curves do not differ significantly. In fasted normal men, the mean bioavailability of furosemide from FUROSEMIDE TABLET and FUROSEMIDE ORAL SOLUTION is 64% and 60%, respectively, of that from an intravenous injection of the drug. The duration of diuretic effect is 6 to 8 hours. The peak effect occurs within the first or second hour. The onset of diuresis following oral administration is within 1 hour. The unbound fraction averages 2.3 to 4.1% at therapeutic concentrations. Plasma concentrations ranging from 1 to 400 µg/ml are 91 to 99% bound in healthy individuals. Furosemide is extensively bound to plasma proteins, mainly to albumin. Recent evidence suggests that furosemide glucuronide is the only or at least the major biotransformation product of furosemide in man. The action on the distal tubule is independent of any inhibitory effect on carbonic anhydrase and aldosterone. The high degree of efficacy is largely due to the unique site of action. ![]() It has been demonstrated that FUROSEMIDE TABLET inhibits primarily the absorption of sodium and chloride not only in the proximal and distal tubules but also in the loop of Henle. ![]() Investigations into the mode of action of FUROSEMIDE TABLET have utilized micropuncture studies in rats, stop flow experiments in dogs and various clearance studies in both humans and experimental animals.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |