Hytaz

Hydrochlorothiazide.

Diuretic/Antihypertensive.
Pharmacology: Pharmacodynamics: Thiazide diuretics increase the excretion of water by inhibiting the reabsorption of sodium and chloride ions at the distal renal tubule. The natriuretic effects are accompanied by a secondary loss of potassium and bicarbonate which can cause a mild hypokalemic, hypochloremic, metabolic alkalosis. Thiazides also decrease the elimination of calcium and uric acid. Thiazide diuretics usually do not affect normal blood pressure. When chronically administered, thiazide diuretics decrease peripheral vascular resistance. The exact mechanism responsible for lowered peripheral resistance is not known. However, excretion of urinary sodium by the kidneys is required to achieve blood pressure reduction.
Pharmacokinetics: Hydrochlorothiazide (HCTZ) is absorbed from the GIT. HCTZ crosses the placental but not the blood-brain barrier and is distributed into breast milk. Based on determination of plasma-drug concentrations over a period of at least 24 hrs, the plasma t_½ of HCTZ reportedly ranges from 5.6-14.8 hrs.
HCTZ is apparently metabolized and excreted unchanged in urine. At least 61% of the drug is reportedly eliminated from the body within 24 hrs.

Edema associated with congestive heart failure, hepatic cirrhosis, corticosteroid and estrogen therapy.
Edema due to various forms of renal dysfunction (eg, nephritic syndrome, acute glomerulonephritis and chronic renal failure).
Control of essential hypertension.

Dosage: Edema: Usual Initial Dose: 25-200 mg daily in 1-3 divided doses.
Maintenance Dose: 25-100 mg daily as single or divided doses.
Hypertension: Adults: Usual Initial Dose: 12.5-50 mg once daily.
Maintenance Dose: 25-100 mg once daily.
Administration: Hydrochlorothiazide is administered orally.
Individualize therapy according to patient response. Use the smallest dosage necessary to achieve the required response.

Sulfonamide allergy, anuria and renal impairment.

Patients with renal disease resulting in severe renal impairment because HCTZ decreases the glomerular filtration rate and may precipitate azotemia in these patients.
Patients with hepatic disease since minor alterations of fluid and electrolyte balance may precipitate hepatic coma.
Patients with gout or hyperuricemia since thiazide diuretics eg, HCTZ have been reported to reduce the clearance of uric acid.
Patients with history of pancreatitis since thiazide diuretics have been reported to cause pancreatitis.

The following adverse reactions have been reported and within each category are listed in order of decreasing severity.
Body as a Whole: Weakness.
Cardiovascular: Hypotension including orthostatic hypotension (may be aggravated by alcohol, barbiturates, narcotics or antihypertensive drugs).
Digestive: Pancreatitis, jaundice (intrahepatic cholestatic jaundice), diarrhea, vomiting, sialadenitis, cramping, constipation, gastric irritation, nausea, anorexia.
Hematologic: Aplastic anemia, agranulocytosis, leukopenia, hemolytic anemia, thrombocytopenia.
Hypersensitivity: Anaphylactic reactions, necrotizing angiitis (vasculitis and cutaneous vasculitis), respiratory distress including pneumonitis and pulmonary edema, photosensitivity, fever, urticaria, rash, purpura.
Metabolic: Electrolyte imbalance, hyperglycemia, glycosuria, hyperuricemia.
Musculoskeletal: Muscle spasm.
Nervous System/Psychiatric: Vertigo, paresthesias, dizziness, headache, restlessness.
Renal: Renal failure, renal dysfunction, interstitial nephritis.
Skin: Erythema multiforme including Stevens-Johnson syndrome, exfoliative dermatitis including toxic epidermal necrolysis, alopecia.
Urogenital: Impotence.

Lithium: Volume depletion increases lithium absorption and may cause lithium toxicity, unless levels are closely monitored and dosage reduced accordingly. Conversely, sudden stopping of diuretic treatment may result in sub-therapeutic levels of circulating lithium.
Anticancer Drugs: Thiazide diuretics may potentiate the bone marrow suppression caused by cancer chemotherapy.
Aminoglycoside Antibiotics: Diuretic-induced volume depletion can potentiate aminoglycoside nephrotoxicity.
Diabetic Therapy: Thiazides can impair control of diabetes mellitus by diet and oral hypoglycemic agents.
Cardiac Glycosides: Digitalis toxicity caused by hypokalemia may be precipitated.
Corticosteroids: There is an increased risk of hypokalemia when the drugs are given concurrently.
Tubocurarine: Prolonged paralysis may occur due to hypokalemia.

Store at temperatures not exceeding 30°C.

Diuretics

C03AA03 - hydrochlorothiazide ; Belongs to the class of low-ceiling thiazide diuretics.

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