The page you were looking for was not found. Amiloride HCl, an antikaliuretic-amiloride (midamor) 5 mg tablet agent, is a pyrazine-carbonyl-guanidine that is unrelated chemically to other known antikaliuretic or diuretic agents. 5 mg of anhydrous amiloride HCl.
C Yellow 10, iron oxide, lactose, magnesium stearate and starch. Registered trademark of Paddock Laboratories, Inc. These effects have been partially additive to the effects of thiazide diuretics in some clinical studies. When administered with a thiazide or loop diuretic, Midamor has been shown to decrease the enhanced urinary excretion of magnesium which occurs when a thiazide or loop diuretic is used alone.
Midamor is not an aldosterone antagonist and its effects are seen even in the absence of aldosterone. This mechanism accounts in large part for the potassium sparing action of amiloride. Midamor usually begins to act within 2 hours after an oral dose. Its effect on electrolyte excretion reaches a peak between 6 and 10 hours and lasts about 24 hours. Peak plasma levels are obtained in 3 to 4 hours and the plasma half-life varies from 6 to 9 hours. Effects on electrolytes increase with single doses of amiloride HCl up to approximately 15 mg. Amiloride HCl is not metabolized by the liver but is excreted unchanged by the kidneys.
About 50 percent of a 20 mg dose of Midamor is excreted in the urine and 40 percent in the stool within 72 hours. Midamor has little effect on glomerular filtration rate or renal blood flow. Because amiloride HCl is not metabolized by the liver, drug accumulation is not anticipated in patients with hepatic dysfunction, but accumulation can occur if the hepatorenal syndrome develops. The use of potassium-conserving agents is often unnecessary in patients receiving diuretics for uncomplicated essential hypertension when such patients have a normal diet. Midamor has little additive diuretic or antihypertensive effect when added to a thiazide diuretic. Midamor should rarely be used alone. Midamor should be used alone only when persistent hypokalemia has been documented and only with careful titration of the dose and close monitoring of serum electrolytes.
Midamor should not be given to patients receiving other potassium-conserving agents, such as spironolactone or triamterene. Such concomitant therapy can be associated with rapid increases in serum potassium levels. Anuria, acute or chronic renal insufficiency, and evidence of diabetic nephropathy are contraindications to the use of Midamor. 30 mg per 100 mL or serum creatinine levels over 1. Midamor is contraindicated in patients who are hypersensitive to this product. The risk of hyperkalemia may be increased when potassium-conserving agents, including Midamor, are administered concomitantly with an angiotensin-converting enzyme inhibitor, an angiotensin II receptor antagonist, cyclosporine or tacrolimus. Warning signs or symptoms of hyperkalemia include paresthesias, muscular weakness, fatigue, flaccid paralysis of the extremities, bradycardia, shock, and ECG abnormalities.
Monitoring of the serum potassium level is essential because mild hyperkalemia is not usually associated with an abnormal ECG. When abnormal, the ECG in hyperkalemia is characterized primarily by tall, peaked T waves or elevations from previous tracings. There may also be lowering of the R wave and increased depth of the S wave, widening and even disappearance of the P wave, progressive widening of the QRS complex, prolongation of the PR interval, and ST depression. If hyperkalemia occurs in patients taking Midamor, the drug should be discontinued immediately. If the serum potassium level exceeds 6.
Such measures include the intravenous administration of sodium bicarbonate solution or oral or parenteral glucose with a rapid-acting insulin preparation. If needed, a cation exchange resin such as sodium polystyrene sulfonate may be given orally or by enema. In diabetic patients, hyperkalemia has been reported with the use of all potassium-conserving diuretics, including Midamor, even in patients without evidence of diabetic nephropathy. Therefore, Midamor should be avoided, if possible, in diabetic patients and, if it is used, serum electrolytes and renal function must be monitored frequently. Midamor should be discontinued at least three days before glucose tolerance testing.
Antikaliuretic therapy should be instituted only with caution in severely ill patients in whom respiratory or metabolic acidosis may occur, such as patients with cardiopulmonary disease or poorly controlled diabetes. If Midamor is given to these patients, frequent monitoring of acid-base balance is necessary. Hyponatremia and hypochloremia may occur when Midamor is used with other diuretics and increases in BUN levels have been reported. These increases usually have accompanied vigorous fluid elimination, especially when diuretic therapy was used in seriously ill patients, such as those who had hepatic cirrhosis with ascites and metabolic alkalosis, or those with resistant edema. When amiloride HCl is administered concomitantly with an angiotensin-converting enzyme inhibitor, an angiotensin II receptor antagonist, cyclosporine or tacrolimus, the risk of hyperkalemia may be increased.
Therefore, if concomitant use of these agents is indicated because of demonstrated hypokalemia, they should be used with caution and with frequent monitoring of serum potassium. Lithium generally should not be given with diuretics because they reduce its renal clearance and add a high risk of lithium toxicity. Read circulars for lithium preparations before use of such concomitant therapy. In some patients, the administration of a non-steroidal anti-inflammatory agent can reduce the diuretic, natriuretic, and antihypertensive effects of loop, potassium-sparing and thiazide diuretics. Therefore, when Midamor and non-steroidal anti-inflammatory agents are used concomitantly, the patient should be observed closely to determine if the desired effect of the diuretic is obtained.