Active Substance: Amiloride HCl, Hydrochlorothiazide.
Overview
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This medicine contains an important and useful components, as it consists of
Amiloride HCl, Hydrochlorothiazideis available in the market in concentration
Amiloride Hydrochloride + Hydrochlorothiazide
Renal impairment; BUN >10 mmol/L, serum creatinine >130 mmol/L. Monitor serum electrolytes and blood urea levels in seriously ill patients e.g. those with hepatic cirrhosis with ascites and metabolic alkalosis, or those with resistant oedema. Pre-existing severe liver disease. May affect parathyroid function. Hyperuricaemia or gout may occur. Cholesterol and triglyceride levels may be increased. Thiazides may impair glucose tolerance. DM may be precipitated or aggravated. May activate or exacerbate SLE. Elderly. Hyponatraemia. Pregnancy. Lactation: Excretion in breast milk is unknown. Because of the potential for serious adverse reactions in nursing infants, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
Hypertension, Congestive heart failure, Hepatic cirrhosis with ascites and oedema
Hyperkalaemia; anuria; acute renal failure, severe progressive renal disease; severe hepatic failure, precoma associated with hepatic cirrhosis; Addison's disease; hypercalcaemia; diabetic neuropathy; DM. Child <18 yr. Lactation.
1-10% Amiloride Hyperkalemia (10%),Anorexia (3-8%),Diarrhea (3-8%),Headache (3-8%),Nausea (3-8%),Vomiting (3-8%),Abdominal pain (<3%),Appetite changes (<3%), Constipation (<3%), Cough (<3%), Dizziness (<3%), Dyspnea (<3%), Encephalopathy (<3%), Fatigue (<3%), Gas pain (<3%), Impotence (<3%), Muscle cramps (<3%), Weakness (<3%) Hydrochlorothiazide Hypotension,Anorexia,Epigastric distress,Hypokalemia,Phototoxicity
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Amiloride is an antikaliuretic with weak natriuretic, diuretic and antihypertensive effects. Some clinical studies found these effects to be partially additive to the effects of thiazide diuretics. Amiloride exerts its potassium-sparing effect by inhibiting Na reabsorption at the distal renal tubules; this decreases the net -ve potential of the tubular lumen and reduces both K and hydrogen secretion and their subsequent excretion. Hydrochlorothiazide is a diuretic and antihypertensive. It reduces electrolyte reabsorption from the renal tubules. Hydrochlorothiazide increases excretion of Na and chloride in approx equiv amounts. Natriuresis may be accompanied by some loss of K and bicarbonate. It exerts its hypotensive effect partly by reducing peripheral resistance.
Additive effects with other antihypertensives. May increase the responsiveness to tubocurarine. May reduce arterial responsiveness to pressor amines e.g. norepinephrine. Orthostatic hypotension may occur with alcohol, barbiturates and narcotics. Discontinue diuretics 2-3 days before initiation of an ACE inhibitor to reduce the likelihood of 1st dose hypotension. Increased hypokalaemia with corticosteroids or ACTH. Attenuation of diuretic, natriuretic and antihypertensive effects of diuretics with NSAIDs. Increased hyponatraemia with chlorpropamide. Increased hyperkalaemia with ciclosporin, tacrolimus, indometacin and angiotensin II receptor antagonists. Potentially Fatal: Increases risk of hyperkalaemia with other potassium-sparing diuretics (spironolactone or triamterene). Increases risk of lithium toxicity.
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