Class: Thiazide Diuretics
VA Class: CV701
CAS Number: 58-94-6
Brands: Diuril
Introduction
Chlorothiazide is a thiazide diuretic and antihypertensive agent.
Uses for Chlorothiazide Sodium
Hypertension
Used alone or in combination with other antihypertensive agents for all stages of hypertension.b f 110
Thiazides have well-established benefits, can be useful in achieving goal blood pressure alone or combined with other antihypertensive drugs, enhance the antihypertensive efficacy of multidrug regimens, and are more affordable than other agents.b f
JNC 7 recommends that thiazides be used as initial therapy for the treatment of uncomplicated hypertension in most patients, either alone or combined with other classes of antihypertensive drugs with demonstrated benefit (e.g., ACE inhibitors, angiotensin II receptor antagonists, β-blockers, calcium-channel blockers).f
Most hypertension outcome studies have involved thiazides, which generally have been unsurpassed in preventing cardiovascular complications of hypertension and are relatively inexpensive and well tolerated.f
The principal goal of preventing and treating hypertension is to reduce the risk of cardiovascular and renal morbidity and mortality, including target organ damage.f The higher the baseline blood pressure, the more likely the development of myocardial infarction, heart failure, stroke, and renal disease.f
Effective antihypertensive therapy reduces the risk of stroke by about 34–40%, MI by about 20–25%, and heart failure by more than 50%.f
Antihypertensive drug therapy is recommended for all patients with systolic/diastolic blood pressure ≥140/90 mm Hg who fail to respond to lifestyle/behavioral modifications.f
Initial antihypertensive therapy with drugs generally is recommended for anyone with diabetes mellitus, chronic renal impairment, or heart failure having systolic blood pressure ≥130 mm Hg or diastolic blood pressure ≥80 mm Hg.f
Black hypertensive patients generally tend to respond better to monotherapy with diuretics or calcium-channel blockers than to monotherapy with ACE inhibitors, angiotensin II receptor antagonists, or β-blockers.f
Diuretics largely eliminate the diminished response in blacks to ACE inhibitors, angiotensin II receptor antagonists, or β-blockers.f
Thiazides preferred in hypertensive patients with osteoporosis. Secondary beneficial effect in hypertensive geriatric patients of reducing the risk of osteoporosis due to effect on calcium homeostasis and bone mineralization.
Preeclampsia and Eclampsia
Although hypertension during pregnancy responds well to thiazides, and the drugs had been used widely in the past for preeclampsia and eclampsia,b g such use no longer is recommended and other antihypertensives (e.g., methyldopa, hydralazine, labetalol) currently are preferred.f
Although rarely induces acute gout, generally avoid or use with caution in hypertensive patients with a history of gout or elevated uric acid concentrations.f
Edema (General)
Management of edema resulting from various causes; diagnose etiology before use.b 110 111
Edema caused by renal disease or by corticosteroids or estrogens may be relatively resistant to treatment.b
Ineffective in patients with serum creatinine or BUN concentrations > twice normal.b
May be ineffective in patients with a GFR of <15–25 mL/minute; even when GFR is 25–50 mL/minute, more potent (e.g., loop) diuretics may be indicated.b
No substantial difference in clinical effects or toxicity of comparable thiazide or thiazide-like diuretics except metolazone may be more effective in edema with renal impairment.b
Edema in CHF
Management of edema associated with CHF.b c
Used in conjunction with moderate sodium restriction (3 g or less of sodium daily), an ACE inhibitor, and usually a β-adrenergic blocking agent, with or without a cardiac glycoside.c d
Beneficial effects are additive with those of cardiac glycosides and/or ACE inhibitors.c
Unless contraindicated or not tolerated, all patients with mild to severe CHF secondary to left ventricular systolic dysfunction (ejection fraction less than 35–40%) generally should receive therapy with a diuretic in conjunction with an ACE inhibitor with or without a cardiac glycoside or a β-adrenergic blocking agent.d
Diuretic therapy and sodium restriction are not routinely necessary in patients with left ventricular systolic dysfunction and no or minimal overt signs or symptoms of heart failure (NYHA functional class I heart failure);d diuretics should be added to ACE inhibitor therapy if volume overload develops or if symptoms of heart failure continue.
Concomitant diuretic therapy usually is indicated in patients with symptomatic heart failure (NYHA class II or greater) because of the llikelihood of sodium and fluid retention.d
Do not use diuretics as monotherapy in CHF even if symptoms (e.g., peripheral edema, pulmonary congestion) are well controlled; diuretics alone do not prevent progression of heart failure.
Diuretics produce rapid symptomatic benefits, relieving pulmonary and peripheral edema more rapidly (within hours or days) than cardiac glycosides, ACE inhibitors, or β-blockers (in weeks or months).
Once fluid retention has resolved in CHF, diuretic therapy should be maintained to prevent recurrence of fluid retention. Ideally, diuretic therapy should be adjusted according to changes in body weight (as an indicator of fluid retention) rather than maintained at a fixed dosage.
Diuretics should be continued in CHF and comorbid conditions (e.g., hypertension) where ongoing therapy with the drugs are indicated.
Edema Secondary to Nephrotic Syndrome
May be useful if the patient fails to respond to corticosteroid therapy.b
More likely to become refractory to thiazides than edema associated with congestive heart failure, and more potent diuretics may be required.b
Edema in Pregnancy
Generally responds well to thiazides except when caused by renal disease.b
Thiazides should not be used for routine therapy in pregnant women with mild edema who are otherwise healthy.b
Chlorothiazide Sodium Dosage and Administration
Administration
Administer orally or IV.a 110 111
The injection must not be administered subcutaneously or IM, and extravasation of the alkaline solution must be avoided.a 111
Oral Administration
Administer chlorothiazide tablets and suspension orally.a 110
IV Administration
Administer chlorothiazide sodium by slow IV injection or by IV infusion; however, the IV route should be used only when patients are unable to take the drug orally or in emergency situations.a 111
Extravasation of the alkaline solution must be avoided.a 111
Reconstitution
Reconstitute only with sterile water for injection.a
Addition of 18 mL of sterile water for injection to 500-mg vial provides a solution containing about 28 (27.8) mg/mL.a 111 No less than 18 mL of diluent should be used for initial reconstitution.a 111
Dilution
The injection may be administered undiluted or may be further diluted with sodium chloride, dextrose, or other compatible infusion fluids before administration.a 111
Rate of Administration
Slowly by direct IV injection or by IV infusion.a 111
Dosage
Dosage of chlorothiazide sodium is expressed in terms of chlorothiazide.a 111
IV and oral dosage are the same.a 111
Individualize according to requirements and response.a
If added to potent hypotensive agent regimen, initially reduce hypotensive dosage to avoid the possibility of severe hypotension.a
Pediatric Patients
Usual Dosage
Oral
Infants <6 Months of Age: Up to 30 mg/kg daily given in 2 divided doses.110
Children 6 Months to 12 Years of Age: 10–20 mg/kg daily in 1 or 2 divided doses.110
IV
Experience in infants and children is limited, and IV use in this age group generally is not recomended.a 111
Adults
Hypertension
Blood Pressure Monitoring and Treatment Goals
Carefully monitor blood pressure during initial titration or subsequent upward adjustment in dosage.d
Avoid large or abrupt reductions in blood pressure.d
Adjusted dosage at approximately monthly intervals (more aggressively in high-risk patients [stage 2 hypertension, comorbid conditions]) if blood pressure control is inadequate at a given dosage; it may take months to control hypertension adequately while avoiding adverse effects of therapy.d
Systolic blood pressure is the principal clinical end point, especially in middle-aged and geriatric patients.d Once the goal systolic blood pressure is attained, the goal diastolic blood pressure usually is achieved.
The goal is to achieve and maintain a lifelong systolic blood pressure <140 mm Hg and a diastolic blood pressure<90 mm Hg if tolerated.d
The goal in hypertensive patients with diabetes mellitus or renal impairment is to achieve and maintain a systolic blood pressure <130 mm Hg and a diastolic blood pressure <80 mm Hg.d
Monotherapy
Oral
Initially, 125–250 mg daily.101 102
Gradually increase until the desired therapeutic response is achieved or adverse effects become intolerable, up to 500 mg daily.a
If adequate response is not achieved at maximum dosage, add or substitute another hypotensive agent.101 102 103 110
Maintenance
Usually, 125–500 mg daily in 1 or 2 divided doses.102 109 110
IV
Not indicated for hypertension.111
Edema
Oral
Usually, 500 mg to 1 g daily in 1 or 2 doses.110 Occasionally, up to 2 g daily in 1 or 2 doses.a
After several days or when nonedematous weight is attained, dosage reduction to a lower maintenance level may be possible.a
With an intermittent schedule, excessive response and the resulting undesirable electrolyte imbalance are less likely to occur.a
IV
Usually, 500 mg to 1 g daily in 1 or 2 doses.110 Occasionally, up to 2 g daily in 1 or 2 doses.a
After several days or when nonedematous weight is attained, dosage reduction to a lower maintenance level may be possible.a
With an intermittent schedule, excessive response and the resulting undesirable electrolyte imbalance are less likely to occur.a 111
Prescribing Limits
Pediatric Patients
Oral
Infants <2 Years of Age: Maximum of 375 mg daily.a 110
Children ≥2 Years of Age: 1 g daily.a 110
Adults
Hypertension
Oral
Maximum before switching/adding alternative drug is 500 mg daily.a 101 102 103
Higher dosages had been used (up to 2 g daily in divided doses)e but no longer are recommended.101 Instead, switch to or add alternative drug.f
Edema
Oral
Maximum of 2 daily in divided doses.a 110
IV
Maximum of 2 daily in divided doses.a 111
Special Populations
Hepatic Impairment
No specific dosage recommendations for hepatic impairment; caution because of risk of precipitating hepatic coma.a 110 111
Renal Impairment
No specific dosage recommendations for renal impairment; caution because of risk of precipitating azotemia.a 110 111
Geriatric Patients
No specific geriatric dosage recommendations.a 110 111
Cautions for Chlorothiazide Sodium
Contraindications
Anuria.b 110 111
Known hypersensitivity to hydrochlorothiazide, other thiazides, or any ingredient in the formulation.b
Although manufacturers state allergy to other sulfonamide derivatives is a contraindication,110 111 evidence to support cross-sensitivity is limited, and history of sensitivity to sulfonamide anti-infectives (“sulfa sensitivity”) should not be considered an absolute contraindication.
Warnings/Precautions
Warnings
Severe Renal Impairment
Use with caution; thiazides decrease GFR and may precipitate azotemia.b 110 111
Effects may be cumulative in impaired renal function.b 110 111
Hepatic Impairment
Use with caution in patients with hepatic impairment or progressive liver disease (particularly with associated potassium deficiency); electrolyte imbalance may precipitate hepatic coma.b 110 111
Discontinue immediately if signs of impending hepatic coma appear.b
Hypotensive Agents
May potentiate effects of other hypotensive agents.110 111 Although additive or potentiated antihypertensive effect usually is used to therapeutic advantage,f hypotension could occur.110 111 b (See Interactions.)
Lupus Erythematosus
Possible exacerbation or activation of systemic lupus erythematosus.110 111
Lithium
Generally, do not use with lithium salts.110 111 (See Interactions.)
Sensitivity Reactions
Hypersensitivity
May occur with or without history of allergy or bronchial asthma.110 111
Sulfonamide cross-sensitivity unlikely. (See Contraindications under Cautions.)
General Precautions
Electrolyte Imbalance
Monitor for fluid or electrolyte imbalance (hyponatremia, hypochloremic alkalosis, hypokalemia).b 110 111
Observe for signs of electrolyte imbalance (e.g., dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, confusion, seizures, oliguria, muscle pains, cramps, muscular fatigue, hypotension, tachycardia, nausea, vomiting).110 111
Perform periodic serum electrolyte determinations (particularly of potassium, sodium, chloride, and bicarbonate); institute measures to maintain normal serum concentrations if necessary.b
Serum and urinary electrolyte measurements are especially important with diabetes mellitus, vomiting, diarrhea, parenteral fluid therapy, or expectations of excessive diuresis.b
Weekly (or more frequent) electrolyte measurement early in treatment; possible to extend interval between measurements to ≥3 months when electrolyte response has stabilized.b
Hypokalemia
May occur after brisk diuresis, when cirrhosis is present, or with prolonged therapy; inadequate oral electrolyte intake may contribute.110 111
May cause cardiac arrhythmis, exaggerate cardiac response to cardiac glycoside toxicity (increase ventricular irritability).110 111
Use potassium-sparing diuretics and/or potassium supplementation to avoid or treat hypokalemia.110 111
Hypochloremia
Generally mild, usually does not require specific treatment except in renal or hepatic impairment.110 111
Chloride replacement may be required for metabolic acidosis.109
Hyponatremia
Dilutional hyponatremia may occur in edematous patients in hot weather; appropriate treatment usually is water restriction rather than salt administration except when hyponatremia is life-threatening.110 111
In actual salt depletion, appropriate replacement is treatment of choice.110 111
Gout
Hyperuricemia or precipitation of gout may occur.110 111
Hyperglycemia
In diabetic patients, dosage adjustment of insulin or oral hypoglycemics may be required; hyperglycemia may occur and latent diabetes mellitus may become evident.110 111
Sympathectomy
Antihypertensive effect may be enhanced after sympathectomy.110 111
Hypomagnesemia
May increase magnesium urinary excretion, resulting in hypomagnesemia.110 111
Hypercalcemia
May decrease calcium urinary excretion, cause slight intermittent serum calcium increase in absence of known calcium metabolism disorder; marked hypercalcemia may indicate hyperparathyroidism.110 111
Discontinue parathyroid tests.110 111
Hyperlipidemia
May increase cholesterol and triglyceride concentrations.110 111 109
Clinical importance of these changes is unknown.b Diet low in saturated fat and cholesterol usually compensates.b
Hypotensive Effects
Orthostatic hypotension rarely occurs.b
Specific Populations
Pregnancy
Category C.110 111
Although hypertension during pregnancy responds well to thiazides, and the drugs had been used widely in the past for preeclampsia and eclampsia,b g such use no longer is recommended and other antihypertensives (e.g., methyldopa, hydralazine, labetolol) currently are preferred.f
Diuretics are not recommended for pregnancy-induced hypertension because of the maternal hypovolemia associated with this form of hypertension; decreased placental perfusion is possible.g
Diuretics are considered second-line agents for control of chronic hypertension in pregnant women.f
Thiazides should not be used as routine therapy in pregnant women with mild edema who are otherwise healthy.b 110 111
Edema associated with pregnancy generally responds well to thiazides except when caused by renal disease.b
Lactation
Distributed into milk.g h 110 111 Discontinue nursing or the drug.110 111
Although hydrochlorothiazide use generally is considered compatible with breast-feeding,g h thiazides can can reduce milk volume and thus suppress lactation.f g
Pediatric Use
No controlled studies in children; use is supported by experience and published literature about hypertension treatment in children.110
Experience with IV chlorothiazide sodium in infants and children is limited, and IV use in this age group generally is not recommended.a 111
Geriatric Use
Elderly may be at increased risk of dilutional hyponatremia, especially underweight females with poor oral fluid and electrolyte intake or excessive low-sodium nutritional supplement intake.b (See Hyponatremia under Warnings/Precautions.)
Hepatic Impairment
Use caution.b (See Hepatic Impairment under Warnings.)
Renal Impairment
Use caution.b (See Severe Renal Impairment under Warnings.)
Consider interruption or discontinuance if progressive renal impairment (rising nonprotein nitrogen, BUN, or serum creatinine) occurs.110 111
Common Adverse Effects
Potassium depletion, hyperuricemia (usually asymptomatic; rarely leading to gout).b Hypochloremic alkalosis in patients at risk (e.g., hypokalemic patients).b Hyperglycemia and glycosuria in diabetics.b
Interactions for Chlorothiazide Sodium
Specific Drugs and Laboratory Tests
Drug or Test
|
Interaction
|
Comments
|
|---|
Alcohol
|
Increased risk of postural hypotensionb
|
|
Amphetamine
|
Thiazides may cause slightly more alkaline urinary pH; may decrease urinary excretion of some amines (e.g., amphetamine) with concurrent useb
|
Urine pH change is not great during thiazide use and, toxic blood concentrations of amines usually do not occurb
Monitor for signs of toxicity after initiation of thiazides in patients receiving amphetamineb
|
Amphotericin B
|
Additive/potentiated potassium lossb
|
Severe potassium depletion may occur when used concomitantlyb
|
Anticoagulants, oral
|
Postulated that may antagonize oral anticoagulant effectsb
|
Confirmatory evidence is lackingb
|
Antidiabetic agents (sulfonylureas)
|
Thiazide hyperglycemic effect may exacerbate diabetes mellitus, increase antidiabetic agent requirements, and/or cause temporary loss of diabetic control or secondary failure to antidiabetic agentb
|
|
Barbiturates
|
Increased risk of postural hypotension with thiazidesb
|
|
Cholestyramine or colestipol
|
May bind thiazides, reduce their GI absorption, with cholestyramine reportedly producing greater binding in vitrob
|
Administer thiazides ≥2 hours before cholestyramine or colestipol when used concomitantlyb
|
Corticosteroids
|
Additive/potentiated potassium lossb
|
Severe potassium depletion may occur when used concomitantlyb
|
Corticotropin
|
Additive/potentiated potassium lossb
|
Severe potassium depletion may occur when used concomitantlyb
|
Diazoxide
|
May potentiate diazoxide hyperglycemic, hypotensive, and hyperuricemic effectsb
|
Use concomitantly with cautionb
|
Digitalis glycosides
|
Thiazide-induced electrolyte disturbances (principally hypokalemia, but also hypomagnesemia and hypercalcemia) may increase digitalis toxicity riskb
|
Perform periodic electrolyte determinations with concomitant use; correct hypokalemia if warrantedb
|
Hypotensive agents
|
Increased hypotensive effects of most other hypotensive agents b
Addition of thiazide to stabilized regimen with potent hypotensive agent (e.g., guanethidine sulfate, methyldopa, ganglionic blocking agent) may cause severe postural hypotensionb
|
Usually used to therapeutic advantageb
|
Insulin
|
May exacerbate diabetes mellitus, increase insulin requirements, cause temporary loss of diabetic control, or secondary failure to insulinb
|
|
Lithium
|
Thiazides (sometimes used with lithium to reduce lithium-induced polyuria), Reduced renal lithium clearance within several daysb
Can increase serum lithium concentrations and the risk of lithium intoxicationb
|
Occasionally, used to therapeutic advantage to reduce lithium-induced polyuria, but reduce lithium dosage by about 50% and monitor serum lithium carefullyb
Generally, avoid concomitant use because of increased lithium toxicity riskb
|
Methenamine
|
Urinary alkalinization may decrease the effectiveness of methenamine compounds which require a urinary pH of ≤5.5 for optimal activityb
|
Monitor urine pH during concurrent therapyb
|
NSAIAs
|
Increased risk of NSAIA-induced renal failure secondary to prostaglandin inhibition and decreased renal blood flowb
NSAIAs may interfere with the natriuretic, diuretic, and antihypertensive response to diureticsb
|
Monitor closely for possible adverse effects and/or attenuation of diuretic-induced therapeutic effects during concomitant useb
|
Neuromuscular blocking agents (e.g., tubocurarine chloride or gallamine triethiodide [both no longer commercially available in the US])
|
May cause prolonged neuromuscular blockadeb
|
Confirmatory evidence lackingb
|
Opiates
|
Increased risk of postural hypotension with thiazidesb
|
|
Probenecid
|
Blocks thiazide-induced uric acid retentionb
Also blocks renal tubular secretion of thiazide, but effect on thiazide duration of action apparently not studiedb
Apparently enhances excretion of calcium, magnesium, and citrate during thiazide therapy, but urinary calcium concentrations remain below normalb
Sodium, potassium, ammonia, chloride, bicarbonate, phosphate, and titratable acid excretion apparently not affected by concomitant probenecid and thiazide therapyb
|
Used to therapeutic advantageb
|
Quinidine
|
Thiazides may cause slightly more alkaline urinary pH; may decrease urinary excretion of some amines (e.g., quinidine) with concurrent useb
|
Urine pH change is not great during thiazide use and toxic blood concentrations of amines usually do not occurb
Monitor for signs of toxicity after initiation of thiazideb
|
Test, Amylase (serum)
|
Values may be increased substantially in both asymptomatic patients and in patients developing acute pancreatitis who are receiving thiazidesb
|
|
Test, Corticosteroids (urinary)(Glenn-Nelson technique)
|
Decreased values by interfering in vitro with the absorbance in the modified Glenn-Nelson technique for urinary 17-hydroxycorticosteroids; may also decrease urinary cortisol excretionb
|
Importance of effect on urinary corticosteroids is unclearb
|
Test, Estrogens (spectrophotometric assay of total urinary estrogen; assay of estradiol)
|
Although hydrochlorothiazide causes falsely decreased values, similar interference does not occur with chlorothiazideb
|
|
Test, Histamine for pheochromocytoma
|
False-negative resultsb
|
|
Test, Parathyroid function tests
|
May elevate serum calcium in the absence of known disorders of calcium metabolismb
|
Discontinue thiazides prior to performing parathyroid function testsb
|
Test, Phenolsulfonphthalein (PSP)
|
Thiazides compete with phenolsulfonphthalein (PSP) for secretion by the proximal renal tubulesb
|
Importance unknownb
|
Test, Phentolamine
|
False-negative resultsb
|
|
Test, Protein-bound iodine (PBI)
|
Values may be decreased, although usually not to subnormalb
|
|
Test, Triiodothyronine resin uptake
|
Decreased slightly, but 24-hour I 131 uptake is not affectedb
|
|
Test, Tyramine
|
False-negative resultsb
|
|
Vasopressors (e.g., norepinephrine)
|
Possible decreased arterial responsiveness to vasopressor amines b
|
Clinical importance not established;b decrease in pressor response not sufficient to preclude vasopressor use109
|
Chlorothiazide Sodium Pharmacokinetics
Absorption
Bioavailability
Incompletely and variably absorbed from the GI tract.a
Absorption from the GI tract appears to be site specific and saturable.a Several studies indicate that about 50 mg is absorbed following oral administration of a single 250-mg tablet, a single 500-mg tablet, or two 250-mg tablets to fasting healthy individuals.a
Onset
Diuretic effect (oral): within 2 hours; peak effect in 3–6 hours.b 109
Diuretic effect (IV): within 15 minutes; peak effect in 30 minutes.b
Hypotensive effect (oral): generally 3–4 days.b
Duration
Diuretic effect: 6–12 hours.b
Food
Concomitant administration with food appears to increase the extent of absorption.a
Distribution
Extent
Distributed in the extracellular space.a b
Readily crosses the placenta.a b g
Distributed into breast milk.a g h
Elimination
Metabolism
Not metabolized.a
Elimination Route
Excreted unchanged in urine;a about 95% of an IV dose is eliminated in 5 hours and about 20 or 10% of a 250- or 500-mg oral dose, respectively, is eliminated in 48–72 hours.a
Half-life
45–120 minutes.a
Stability
Storage
Oral
Tablets
Tight containers at 15–30°C; avoid freezing.100
Suspension
Tight containers at 15–30°C; avoid freezing.100
Parenteral
Powder for Injection
2–25°C.111
Compatibility
For information on systemic interactions resulting from concomitant use, see Interactions.
Parenteral
Solution CompatibilityHID
Compatible
|
|---|
Dextran 6% in dextrose 5%
|
Dextran 6% in sodium chloride 0.9%
|
Dextrose–Ringer’s injection combinations
|
Dextrose–Ringer’s injection, lactated, combinations
|
Dextrose–saline combinations
|
Dextrose 5% in sodium chloride 0.9%
|
Dextrose 2½% in water
|
Dextrose 5% in water
|
Dextrose 10% in water
|
Fructose 10% in sodium chloride 0.9%
|
Fructose 10% in water
|
Invert sugar 5 and 10% in sodium chloride 0.9%
|
Invert sugar 5 and 10% in water
|
Ionosol MB with dextrose 5%
|
Ionosol T with dextrose 5%
|
Ringer’s injection
|
Ringer’s injection, lactated
|
Sodium chloride 0.45%
|
Sodium chloride 0.9%
|
Sodium lactate (1/6) M
|
Incompatible
|
|---|
Ionosol B with dextrose 5%
|
Normosol M in dextrose 5%
|
Normosol M, 900 cal
|
Normosol R in dextrose 5%
|
Drug CompatibilityHID
Admixture Compatibility
Compatible
|
|---|
Cimetidine HCl
|
Lidocaine HCl
|
Nafcillin sodium
|
Ranitidine HCl
|
Incompatible
|
|---|
Amikacin sulfate
|
Chlorpromazine HCl
|
Hydralazine HCl
|
Morphine sulfate
|
Norepinephrine bitartrate
|
Polymyxin B sulfate
|
Procaine HCl
|
Prochlorperazine edisylate
|
Prochlorperazine mesylate
|
Promazine HCl
|
Promethazine HCl
|
Streptomycin sulfate
|
Triflupromazine HCl
|
Vancomycin HCl
|
ActionsActions
Exact mechanism of diuretic action is unclear; may act by altering metabolism of the tubular cells.b
Enhances excretion of sodium, chloride, and water by interfering with the transport of sodium ions across the renal tubular epithelium.b
Primary site of diuretic action appears to be the cortical diluting segment of the nephron.b
GFR decreases, but inclear whether secondary to a direct effect on renal vasculature or to the decrease in intravascular fluid volume or an increase in tubular pressure caused by the inhibition of sodium and water reabsorption.b The fall in GFR is not important in the mechanism of action.b
Enhances urinary excretion of potassium secondary to increased amount of sodium at distal tubular site of sodium-potassium exchnage.b
Increases urinary bicarbonate excretion (although to a lesser extent than chloride excretion) but change in urinary pH is usually minimal; diuretic efficacy is not affected by the acid-base balance of the patient.b
Hypocalciuric effect is thought to result from a decrease in extracellular fluid (ECF) volume, although calcium reabsorption in the nephron may be increased; also, slight or intermittent elevations in serum calcium concentration.b
Rate of uric acid excretion is decreased, probably because of competitive inhibition of uric acid secretion or a decrease in ECF volume and a secondary increase in uric acid reabsorption.b
Hypotensive activity in hypertensive patients; also augments the action of other hypotensive agents.b Precise mechanism of hypotensive action has not been determined, but postulated that part of this effect is caused by direct arteriolar dilation.b
Advice to Patients
Advise patient of signs of electrolyte imbalance (e.g., dryness of the mouth, thirst, weakness, lethargy, drowsiness, restlessness, confusion, seizures, oliguria, or muscle pains or cramps, muscular fatigue, hypotension, tachycardia, GI disturbances such as nausea and vomiting).b
Advise patients of importance of compliance with scheduled determinations of serum electrolyte concentrations (particularly potassium, sodium, chloride, and bicarbonate).b
Advise hypertensive patients of importance of continuing lifestyle/behavioral modifications that include weight reduction (for those who are overweight or obese), dietary changes to include foods that are rich in potassium and calcium and moderately restricted in sodium (adoption of the Dietary Approaches to Stop Hypertension [DASH] eating plan), increased physical activity, smoking cessation, and moderation of alcohol intake.
Advise that lifestyle/behavioral modifications reduce blood pressure, enhance antihypertensive drug efficacy, and decrease cardiovascular risk and remain an indispensable part of the management of hypertension.
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs as well as any concomitant illnesses.
Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.
Importance of informing patients of other important precautionary information. (See Cautions.)
Preparations
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Chlorothiazide
Routes
|
Dosage Forms
|
Strengths
|
Brand Names
|
Manufacturer
|
|---|
Oral
|
Suspension
|
250 mg/5 mL
|
Diuril (with alcohol 0.5%, benzoic acid, and parabens)
|
Merck
|
|
Tablets
|
250 mg*
|
Chlorothiazide Tablets
|
Mylan, UDL, West-Ward
|
|
|
500 mg*
|
Chlorothiazide Tablets
|
Mylan, UDL, West-Ward
|
Chlorothiazide Sodium
Routes
|
Dosage Forms
|
Strengths
|
Brand Names
|
Manufacturer
|
|---|
Parenteral
|
For injection, for IV use only
|
500 mg (of chlorothiazide)
|
Diuril Sodium Intravenous
|
Ovation
|
Comparative Pricing
This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 03/2011. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.
Chlorothiazide 250MG Tablets (MYLAN): 30/$13.99 or 90/$24.97
Chlorothiazide 500MG Tablets (MYLAN): 30/$14.99 or 60/$20.97
Diuril 250MG/5ML Suspension (SALIX PHARMACEUTICALS INC.): 237/$29.99 or 711/$75.97
Disclaimer
This report on medications is for your information only, and is not considered individual patient advice. Because of the changing nature of drug information, please consult your physician or pharmacist about specific clinical use.
The American Society of Health-System Pharmacists, Inc. and Drugs.com represent that the information provided hereunder was formulated with a reasonable standard of care, and in conformity with professional standards in the field. The American Society of Health-System Pharmacists, Inc. and Drugs.com make no representations or warranties, express or implied, including, but not limited to, any implied warranty of merchantability and/or fitness for a particular purpose, with respect to such information and specifically disclaims all such warranties. Users are advised that decisions regarding drug therapy are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and the information is provided for informational purposes only. The entire monograph for a drug should be reviewed for a thorough understanding of the drug's actions, uses and side effects. The American Society of Health-System Pharmacists, Inc. and Drugs.com do not endorse or recommend the use of any drug. The information is not a substitute for medical care.
AHFS Drug Information. © Copyright, 1959-2011, Selected Revisions August 2007. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.
References
Only references cited for selected revisions after 1984 are available electronically.
100. Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. The 1984 report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med. 1984; 144:1045-57. [IDIS 184763] [PubMed
