Product Overview
[Drug Name]
Generic Name: Furosemide Tablets
Trade Name: Jintan Furosemide Tablets 20mg x 100 Tablets
[Main Ingredient]
The main ingredient of this product is furosemide, whose chemical name is 2-[(2-furylmethyl)amino]-5-(sulfamoyl)-4-chlorobenzoic acid.
[Properties]
This product is white tablets.
[Indications/Main Functions]
1. Edema disorders, including congestive heart failure, cirrhosis, and renal disease (nephritis, nephropathy, and acute and chronic renal failure due to various causes). This class of drugs may still be effective, especially when other diuretics are ineffective. It can also be used in combination with other drugs to treat acute pulmonary edema and acute cerebral edema. 2. Hypertension. While generally not the first choice for the treatment of essential hypertension, this class of drugs is particularly suitable when thiazides are ineffective, especially when accompanied by renal insufficiency or hypertensive crisis. 3. Prevention of acute renal failure. It is used for various reasons leading to insufficient renal blood perfusion, such as dehydration, shock, poisoning, anesthesia accidents and circulatory insufficiency. Timely application while correcting insufficient blood volume can reduce the chance of acute tubular necrosis. 4. Hyperkalemia and hypercalcemia. 5. Dilutional hyponatremia, especially when the blood sodium concentration is lower than 120mmol/L. 6. Syndrome of excessive secretion of antidiuretic hormone (SIADH). 7. Acute drug poisoning, such as barbiturate poisoning.
[Specification]
20mg*100 tablets
[Usage and Dosage]
Adults (1) Treatment of edematous diseases. The starting dose is 20~40mg (1-2 tablets) orally once a day. If necessary, add 20~40mg (1-2 tablets) after 6~8 hours until a satisfactory diuretic effect is achieved. Although the maximum dose can reach 600 mg (30 tablets) per day, it should generally be controlled within 100 mg (5 tablets) and taken in 2 to 3 divided doses to prevent excessive diuresis and adverse reactions. For some patients, the dose can be reduced to 2040 mg (1-2 tablets), once every other day, or taken continuously for 2 to 4 days per week, 20 to 40 mg (1-2 tablets) per day. (2) Treatment of hypertension. Start with 40 to 80 mg (2-4 tablets) per day, taken in 2 divided doses, and adjust the dose as appropriate. (3) Treatment of hypercalcemia. Take 80 to 120 mg (4-6 tablets) orally daily, taken in 1 to 3 divided doses. 2. Children: For the treatment of edematous diseases, start with 2 mg/kg of body weight, orally, and if necessary, add 1 to 2 mg/kg every 4 to 6 hours. The dosing interval should be extended for newborns. Adverse Reactions: Common adverse reactions are related to fluid and electrolyte imbalances, especially with high doses or prolonged use. These include orthostatic hypotension, shock, hypokalemia, hypochloremia, hypochloremic alkalosis, hyponatremia, hypocalcemia, and associated thirst, fatigue, muscle aches, and arrhythmias. Less common adverse reactions include allergic reactions (including rash, interstitial nephritis, and even cardiac arrest), blurred vision, xanthophthalmia, photosensitivity, dizziness, headache, sodium deficit, nausea, vomiting, abdominal pain, diarrhea, pancreatitis, muscle rigidity, bone marrow suppression leading to granulocytopenia, thrombocytopenic purpura, and aplastic anemia, liver damage, paresthesias of the digits, hyperglycemia, positive urine glucose, exacerbation of pre-existing diabetes, and hyperuricemia. Tinnitus and hearing impairment are more common with high-dose rapid intravenous injection (greater than 4-15 mg per minute). They are usually transient, but a few are irreversible, especially when used concurrently with other ototoxic drugs. Hypercalcemia can cause kidney stones. There are also reports that this drug can aggravate idiopathic edema.
[Drug Interactions]
(1) Adrenal glucose, mineralocorticoids, adrenocorticotropic hormone and estrogen can reduce the diuretic effect of this drug and increase the chance of electrolyte imbalance, especially hypokalemia. (2) Non-steroidal anti-inflammatory analgesics can reduce the diuretic effect of this drug and increase the chance of renal damage. This is related to the former inhibiting prostaglandin synthesis and reducing renal blood flow. (3) When used in combination with sympathomimetic drugs and anticonvulsants, the diuretic effect is weakened. (4) When used in combination with clofibrate (clofibrate), the effects of both drugs are enhanced, and muscle soreness and stiffness may occur. (5) When used in combination with dopamine, the diuretic effect is enhanced. (6) Alcohol, alcohol-containing preparations and drugs that can cause a decrease in blood pressure can enhance the diuretic and antihypertensive effects of this drug; when used in combination with barbiturates and anesthetics, it is easy to cause orthostatic hypotension. (7) This drug can reduce uric acid excretion and increase blood uric acid. Therefore, when used in combination with drugs for the treatment of gout, the latter's dosage should be appropriately adjusted. (8) It reduces the efficacy of hypoglycemic drugs. (9) It reduces the effects of anticoagulants and antifibrinolytic drugs, mainly due to the decrease in blood volume after diuresis, which leads to an increase in the concentration of coagulation factors in the blood, and the improvement of liver blood supply and increased synthesis of coagulation factors by diuresis. (10) This drug enhances the effects of non-depolarizing muscle relaxants and is related to a decrease in blood potassium. (11) When used in combination with antibiotics such as amphotericin, cephalosporin, and aminoglycosides, nephrotoxicity and ototoxicity increase, especially in patients with pre-existing renal damage. (12) When used in combination with antihistamines, ototoxicity increases, and tinnitus, dizziness, and vertigo are more likely to occur. (13) When used in combination with lithium, nephrotoxicity increases significantly and should be avoided as much as possible. (14) Intravenous injection of this drug after taking chloral hydrate may cause sweating, facial flushing and increased blood pressure. This is related to the increase in the conversion of thyroid hormone from bound to free state, leading to enhanced decomposition. (15) The chance of hypochloremic alkalosis increases when used in combination with sodium bicarbonate.
[Precautions]
(1) Cross-allergy. Patients who are allergic to sulfonamides and thiazide diuretics may also be allergic to this drug. (2) Interference with diagnosis: It may cause increased blood sugar and positive urine sugar, especially in patients with diabetes or prediabetes. Excessive dehydration may temporarily increase blood uric acid and urea nitrogen levels. The concentrations of blood Na+, Cl-, K+, Ca2+ and Mg2+ decrease. (3) Use with caution in the following situations: ① Patients with anuria or severe renal impairment, in which case the dosage should be increased, so the dosing interval should be extended to avoid adverse reactions such as ototoxicity; ② Diabetes; ③ Hyperuricemia or a history of gout; ④ Severe liver impairment, as water and electrolyte imbalance may induce hepatic coma; Acute myocardial infarction, excessive diuresis may precipitate shock; Pancreatitis or a history of this condition; Patients with a tendency to hypokalemia, especially those taking digitalis or ventricular arrhythmias; Lupus erythematosus, as this drug may aggravate the condition or induce activity; Prostatic hyperplasia. (4) Follow-up examinations: Blood electrolytes, especially those taking digitalis or corticosteroids, and those with liver and kidney impairment; ② Blood pressure, especially for antihypertensive use, high-dose use, or use in the elderly; ③ Renal function; ④ Liver function; Blood sugar; Blood uric acid; Acid-base balance; ® Hearing. (5) The drug dosage should start from the minimum effective dose and then be adjusted according to the diuretic response to reduce the occurrence of side effects such as water and electrolyte imbalance. (6) When hypokalemia or hypokalemia tendency exists, potassium salt supplementation should be noted. (7) When used in combination with antihypertensive drugs, the latter's dose should be adjusted as appropriate. (8) If the patient with oliguria or anuria still has no effect after 24 hours of using the maximum dose, the drug should be discontinued. (9) Athletes should use with caution.
[Drug use in children]
The half-life of this drug is significantly prolonged in newborns, so the dosing interval for newborns should be extended.
[Drug use in elderly patients]
The elderly are more likely to develop hypotension, electrolyte imbalance, thrombosis and renal damage when using this drug.
[Pharmacology and toxicology]
(1) Effect on water and electrolyte excretion. It can increase the excretion of water, sodium, chloride, potassium, calcium, magnesium, phosphorus, etc. Unlike thiazide diuretics, furosemide and other diuretics have a clear dose-effect relationship. As the dose increases, the diuretic effect is significantly enhanced, and the drug dosage range is wide. This type of drug mainly inhibits the active reabsorption of NaCl by the thick-walled segment of the renal tubular medullary tube. As a result, the concentrations of Na+ and Cl- in the tubular fluid increase, while the concentrations of Na+ and Cl- in the interstitial fluid decrease. This reduces the osmotic pressure gradient and the concentrating function of the renal tubules, thereby increasing the excretion of water, Na+, and Cl-. Due to the reduced reabsorption of Na[sup]+[/sup], the concentration of Na[sup]+[V/sup] in the distal tubule increases, which promotes the increase of Na[sup]+[/sup]-K[sup]+[/sup] and Na[sup]+[/sup]-H[sup]+[/sup] exchange, and increases the excretion of K[sup]+[/sup] and H[sup]+[/sup]. As for the mechanism by which furosemide inhibits Cl- reabsorption in the thick-walled segment of the ascending medullary limb of the renal tubule, it was previously believed that a chloride pump existed in this area. Current studies have shown that a Na+ and Cl- paired transport system, associated with the Na+-K+ ATPase, exists on the lateral side of the basement membrane of this area. Furosemide reduces Na+ and Cl- reabsorption by inhibiting this system. Furthermore, furosemide may also inhibit Na+ and Cl- reabsorption in the proximal and distal tubules, promoting K+ secretion in the distal tubule. Furosemide increases the excretion of Ca2+ and Mg2+ by inhibiting the reabsorption of Ca2+ and Mg2+ by Henkel. Short-term use can increase uric acid excretion, while long-term use can cause hyperuricemia. (2) Effects on hemodynamics. Furosemide can inhibit the activity of prostaglandin degrading enzymes, increase the content of prostaglandin E2, and thus have a vasodilatory effect. Dilation of renal blood vessels, reduction of renal vascular resistance, and increase of renal blood flow, especially deep renal cortical blood flow, are of great significance in the diuretic effect of furosemide and are also the theoretical basis for its use in preventing acute renal failure. In addition, unlike other diuretics, furosemide does not decrease the glomerular filtration rate while increasing the renal tubular fluid flow, which may be related to the reduction of chloride flowing through the macula densa, thereby weakening or blocking the glomerular-tubular balance. Furosemide can dilate pulmonary capacitance veins and reduce pulmonary capillary permeability. Combined with its diuretic effect, this reduces venous return and lowers left ventricular end-diastolic pressure, aiding in the treatment of acute left heart failure. Because furosemide can reduce pulmonary capillary permeability, it provides a theoretical basis for its treatment of adult respiratory distress syndrome.
