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Sodium Diuril

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Overview

What is Sodium Diuril?

Intravenous Sodium DIURIL (chlorothiazide sodium) is a diuretic and antihypertensive. It is 6-chloro-2-1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide monosodium salt and its molecular weight is 317.71.

Its empirical formula is CHClNNaOS and its structural formula is:

Intravenous Sodium DIURIL is a sterile lyophilized white powder and is supplied in a vial containing:

Chlorothiazide sodium equivalent to chlorothiazide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0.5 g

Inactive ingredients: Mannitol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0.25 g

Sodium hydroxide to adjust pH.

DIURIL (chlorothiazide) is a diuretic and antihypertensive. It is 6-chloro-2-1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide. Its empirical formula is CHClNOS and its structural formula is:

It is a white, or practically white, crystalline powder with a molecular weight of 295.72, which is very slightly soluble in water, but readily soluble in dilute aqueous sodium hydroxide. It is soluble in urine to the extent of about 150 mg per 100 mL at pH 7.



What does Sodium Diuril look like?



What are the available doses of Sodium Diuril?

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What should I talk to my health care provider before I take Sodium Diuril?

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How should I use Sodium Diuril?

Intravenous Sodium DIURIL is indicated as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy.

Intravenous Sodium DIURIL has also been found useful in edema due to various forms of renal dysfunction such as nephrotic syndrome, acute glomerulonephritis, and chronic renal failure.

Intravenous Sodium DIURIL should be reserved for patients unable to take oral medication or for emergency situations.

Therapy should be individualized according to patient response. Use the smallest dosage necessary to achieve the required response.

Intravenous use in infants and children has been limited and is not generally recommended.

When medication can be taken orally, therapy with DIURIL tablets or oral suspension may be substituted for intravenous therapy, using the same dosage schedule as for the parenteral route.

Intravenous Sodium DIURIL may be given slowly by direct intravenous injection or by intravenous infusion.

Extravasation must be rigidly avoided. Do not give subcutaneously or intramuscularly.

The usual adult dosage is 0.5 to 1 g once or twice a day. Many patients with edema respond to intermittent therapy, i.e., administration on alternate days or on three to five days each week. With an intermittent schedule, excessive response and the resulting undesirable electrolyte imbalance are less likely to occur.


What interacts with Sodium Diuril?

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What are the warnings of Sodium Diuril?

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What are the precautions of Sodium Diuril?

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What are the side effects of Sodium Diuril?

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What should I look out for while using Sodium Diuril?

Anuria.

Hypersensitivity to any component of this product or to other sulfonamide-derived drugs.

Intravenous use in infants and children has been limited and is not generally recommended.

Use with caution in severe renal disease. In patients with renal disease, thiazides may precipitate azotemia. Cumulative effects of the drug may develop in patients with impaired renal function.

Thiazides should be used with caution in patients with impaired hepatic function or progressive liver disease, since minor alterations of fluid and electrolyte balance may precipitate hepatic coma.

Thiazides may add to or potentiate the action of other antihypertensive drugs.

Sensitivity reactions may occur in patients with or without a history of allergy or bronchial asthma.

The possibility of exacerbation or activation of systemic lupus erythematosus has been reported.

Lithium generally should not be given with diuretics (see ).


What might happen if I take too much Sodium Diuril?

The most common signs and symptoms observed are those caused by electrolyte depletion (hypokalemia, hypochloremia, hyponatremia) and dehydration resulting from excessive diuresis. If digitalis has also been administered, hypokalemia may accentuate cardiac arrhythmias.

In the event of overdosage, symptomatic and supportive measures should be employed. Correct dehydration, electrolyte imbalance, hepatic coma and hypotension by established procedures. If required, give oxygen or artificial respiration for respiratory impairment.

The degree to which chlorothiazide sodium is removed by hemodialysis has not been established.

The intravenous LD of chlorothiazide in the mouse is 1.1 g/kg.


How should I store and handle Sodium Diuril?

Intravenous Sodium DIURIL is a dry, sterile lyophilized white powder usually in plug form, supplied in vials containing chlorothiazide sodium equivalent to 0.5 g of chlorothiazide. NDC 76478-711-40. Intravenous Sodium DIURIL is a dry, sterile lyophilized white powder usually in plug form, supplied in vials containing chlorothiazide sodium equivalent to 0.5 g of chlorothiazide. NDC 76478-711-40.


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Clinical Information

Chemical Structure

No Image found
Clinical Pharmacology

The mechanism of the antihypertensive effect of thiazides is unknown. DIURIL (chlorothiazide) does not usually affect normal blood pressure.

DIURIL (chlorothiazide) affects the distal renal tubular mechanism of electrolyte reabsorption. At maximal therapeutic dosage all thiazides are approximately equal in their diuretic efficacy.

DIURIL (chlorothiazide) increases excretion of sodium and chloride in approximately equivalent amounts. Natriuresis may be accompanied by some loss of potassium and bicarbonate.

After oral use diuresis begins within 2 hours, peaks in about 4 hours and lasts about 6 to 12 hours. Following intravenous use of Sodium DIURIL, onset of the diuretic action occurs in 15 minutes and the maximal action in 30 minutes.

Non-Clinical Toxicology
Anuria.

Hypersensitivity to any component of this product or to other sulfonamide-derived drugs.

Intravenous use in infants and children has been limited and is not generally recommended.

Use with caution in severe renal disease. In patients with renal disease, thiazides may precipitate azotemia. Cumulative effects of the drug may develop in patients with impaired renal function.

Thiazides should be used with caution in patients with impaired hepatic function or progressive liver disease, since minor alterations of fluid and electrolyte balance may precipitate hepatic coma.

Thiazides may add to or potentiate the action of other antihypertensive drugs.

Sensitivity reactions may occur in patients with or without a history of allergy or bronchial asthma.

The possibility of exacerbation or activation of systemic lupus erythematosus has been reported.

Lithium generally should not be given with diuretics (see ).

When given concurrently the following drugs may interact with thiazide diuretics.

All patients receiving diuretic therapy should be observed for evidence of fluid or electrolyte imbalance: namely, hyponatremia, hypochloremic alkalosis, and hypokalemia. Serum and urine electrolyte determinations are particularly important when the patient is vomiting excessively or receiving parenteral fluids. Warning signs or symptoms of fluid and electrolyte imbalance, irrespective of cause, include dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, confusion, seizures, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, and gastrointestinal disturbances such as nausea and vomiting.

Hypokalemia may develop especially with brisk diuresis, when severe cirrhosis is present or after prolonged therapy.

Interference with adequate oral electrolyte intake will also contribute to hypokalemia. Hypokalemia may cause cardiac arrhythmias and may also sensitize or exaggerate the response of the heart to the toxic effects of digitalis (e.g., increased ventricular irritability). Hypokalemia may be avoided or treated by use of potassium-sparing diuretics or potassium supplements such as foods with a high potassium content.

Although any chloride deficit is generally mild and usually does not require specific treatment except under extraordinary circumstances (as in liver disease or renal disease), chloride replacement may be required in the treatment of metabolic alkalosis.

Dilutional hyponatremia may occur in edematous patients in hot weather; appropriate therapy is water restriction, rather than administration of salt, except in rare instances when the hyponatremia is life-threatening. In actual salt depletion, appropriate replacement is the therapy of choice.

Hyperuricemia may occur or acute gout may be precipitated in certain patients receiving thiazides.

In diabetic patients dosage adjustments of insulin or oral hypoglycemic agents may be required. Hyperglycemia may occur with thiazide diuretics. Thus latent diabetes mellitus may become manifest during thiazide therapy.

The antihypertensive effects of the drug may be enhanced in the postsympathectomy patient.

If progressive renal impairment becomes evident, consider withholding or discontinuing diuretic therapy.

Thiazides have been shown to increase the urinary excretion of magnesium; this may result in hypo-magnesemia.

Thiazides may decrease urinary calcium excretion. Thiazides may cause intermittent and slight elevation of serum calcium in the absence of known disorders of calcium metabolism. Marked hypercalcemia may be evidence of hidden hyperparathyroidism. Thiazides should be discontinued before carrying out tests for parathyroid function.

Increases in cholesterol and triglyceride levels may be associated with thiazide diuretic therapy.

The following adverse reactions have been reported and, within each category, are listed in order of decreasing severity.

Whenever adverse reactions are moderate or severe, thiazide dosage should be reduced or therapy withdrawn.

To report SUSPECTED ADVERSE REACTIONS, contact Oak Pharmaceuticals, Inc. at 1-800-932-5676 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

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Reference

This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
"https://dailymed.nlm.nih.gov/dailymed/"

While we update our database periodically, we cannot guarantee it is always updated to the latest version.

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Professional

Clonazepam Description Each single-scored tablet, for oral administration, contains 0.5 mg, 1 mg, or 2 mg Clonazepam, USP, a benzodiazepine. Each tablet also contains corn starch, lactose monohydrate, magnesium stearate, microcrystalline cellulose, and povidone. Clonazepam tablets USP 0.5 mg contain Yellow D&C No. 10 Aluminum Lake. Clonazepam tablets USP 1 mg contain Yellow D&C No. 10 Aluminum Lake, as well as FD&C Blue No. 1 Aluminum Lake. Chemically, Clonazepam, USP is 5-(o-chlorophenyl)-1,3-dihydro-7-nitro-2H-1,4-benzodiazepin-2-one. It is a light yellow crystalline powder. It has the following structural formula: C15H10ClN3O3 M.W. 315.72
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Tips

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Interactions

Interactions

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