Active Substance: Hydrochlorothiazide.
Overview
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This medicine contains an important and useful components, as it consists of
Hydrochlorothiazideis available in the market in concentration
Hydrochlorothiazide
Patients w/ electrolyte disturbances, history of gout, allergy or bronchial asthma, DM, parathyroid disease, hypercholesterolaemia. May exacerbate SLE. Hepatic and mild to moderate renal impairment. Pregnancy and lactation. Monitoring Parameters Assess wt, input and output reports daily to determine fluid loss, BP, serum electrolytes, BUN, creatinine. Lactation: Drug excreted in breast milk; use with caution (American Academy of Pediatrics states that it is "compatible with nursing")
Hypertension, Congestive heart failure, Oedema, Diabetes insipidus, Renal tubular acidosis
Hypersensitivity to sulfonamide-derived drugs, anuria, severe renal impairment.
Electrolyte disturbances, weakness, hypotension, pancreatitis, jaundice, diarrhoea, vomiting, sialadenitis, cramping, constipation, gastric irritation, nausea, anorexia, aplastic anaemia, agranulocytosis, leukopenia, haemolytic anaemia, thrombocytopenia, anaphylactic reactions, necrotising angiitis, resp distress, photosensitivity, fever, urticaria, rash, purpura, hyperglycaemia, glycosuria, hyperuricaemia., muscle spasm, vertigo, paraesthesias, dizziness, headache, restlessness, renal failure, renal dysfunction, interstitial nephritis, erythema multiforme, exfoliative dermatitis, alopecia, transient blurred vision, xanthopsia, impotence. Potentially Fatal: Hypersensitivity reactions.
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Hydrochlorothiazide inhibits the reabsorption of Na and chloride in the distal tubules causing increased excretion of Na and water K and hydrogen ions.
Increases toxicity of lithium. May potentiate orthostatic hypotension w/ barbiturates and narcotics. Enhanced neuromuscular blocking action of competitive neuromuscular blockers (e.g. atracurium). Increased hypokalaemic effect w/ corticosteroids, corticotropin, beta2 agonists (e.g. salbutamol). Additive effect w/ other antihypertensives. Potentiation of orthostatic hypotension w/ barbiturates or opioids. Reduced antihypertensive effect by drugs that cause fluid retention (e.g. corticosteroids, NSAIDs, carbenoxolone). Enhanced nephrotoxicity of NSAIDs. Reduced therapeutic effect of antidiabetics.
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