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Homatropine Hydrobromide
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Overview
What is HOMATROPINE HYDROBROMIDE OPHTHALMIC?
Homatropine hydrobromide is an anticholinergic prepared as a sterile topical ophthalmic solution.
What does HOMATROPINE HYDROBROMIDE OPHTHALMIC look like?
What are the available doses of HOMATROPINE HYDROBROMIDE OPHTHALMIC?
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What should I talk to my health care provider before I take HOMATROPINE HYDROBROMIDE OPHTHALMIC?
Sorry No records found
How should I use HOMATROPINE HYDROBROMIDE OPHTHALMIC?
A moderately long-acting mydriatic and cycloplegic for cycloplegic refraction and in the treatment of inflammatory conditions of the uveal tract. For pre and postoperative states when mydriasis is required. Use as an optical aid in some cases of axial lens opacities.
For refraction, instill one or two drops topically in the eye(s). May be repeated in five or ten minutes if necessary. For uveitis, instill one or two drops topically up to every three to four hours. Individuals with heavily pigmented irides may require larger doses.
What interacts with HOMATROPINE HYDROBROMIDE OPHTHALMIC?
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What are the warnings of HOMATROPINE HYDROBROMIDE OPHTHALMIC?
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What are the precautions of HOMATROPINE HYDROBROMIDE OPHTHALMIC?
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What are the side effects of HOMATROPINE HYDROBROMIDE OPHTHALMIC?
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What should I look out for while using HOMATROPINE HYDROBROMIDE OPHTHALMIC?
Contraindicated in persons with primary glaucoma or a tendency toward glaucoma, e.g. narrow anterior chamber angle, and in those persons showing hypersensitivity to any component of this preparation.
What might happen if I take too much HOMATROPINE HYDROBROMIDE OPHTHALMIC?
When signs and symptoms of homatropine toxicity develop (see ), physostigmine should be administered parenterally (for dosage refer to Goodman & Gilman or other pharmacology reference). In infants and pediatric patients, the body surface must be kept moist.
How should I store and handle HOMATROPINE HYDROBROMIDE OPHTHALMIC?
Store Temozolomide Capsules at 25°C (77°F); excursions permitted to 15°–30°C (59°–86°F) [see USP Controlled Room Temperature].5mL size in a white plastic bottle5mL - NDC 59390-192-05
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In view of the long and variable half-life of amiodarone, potential for drug interactions exists, not only with concomitant medication, but also with drugs administered after discontinuation of amiodarone.
Drugs inducing TdP or prolonging QT
Co-administration of amiodarone with drugs known to prolong the QT interval (such as class I and III antiarrhythmics, lithium, certain phenothiazines, tricyclic antidepressants, certain fluoroquinolone and macrolide antibiotics, IV pentamidine, and azole antifungals) increases the risk of Torsades de Points. Avoid concomitant use of drugs that prolong the QT interval.
Drugs lowering heart rate or causing automaticity or conduction disorders
Concomitant use of drugs with depressant effects on the sinus and AV node (e.g., digoxin, beta blockers, verapamil, diltiazem, clonidine) can potentiate the electrophysiologic and hemodynamic effects of amiodarone, resulting in bradycardia, sinus arrest, and AV block. Monitor heart rate in patients on amiodarone and concomitant drugs that slow heart rate.
Effects of other medicinal products on amiodarone
Since amiodarone is a substrate for CYP3A and CYP2C8, drugs/substances that inhibit CYP3A (e.g., certain protease inhibitors, loratadine, cimetidine, trazodone) may decrease the metabolism and increase serum concentrations of amiodarone. Concomitant use of CYP3A inducers (rifampin, St. John's Wort), may lead to decreased serum concentrations and loss of efficacy. Consider serial measurement of amiodarone serum concentration during concomitant use of drugs affecting CYP3A activity.
Grapefruit juice given to healthy volunteers increased amiodarone AUC by 50% and Cmax by 84%, and decreased DEA to unquantifiable concentrations. Grapefruit juice inhibits CYP3A-mediated metabolism of oral amiodarone in the intestinal mucosa, resulting in increased plasma levels of amiodarone; therefore, grapefruit juice should not be taken during treatment with oral amiodarone. This information should be considered when transitioning from intravenous to oral amiodarone. Cholestyramine reduces enterohepatic circulation of amiodarone thereby increasing its elimination. This results in reduced amiodarone serum levels and half-life.
Effects of amiodarone on other medicinal products
Amiodarone inhibits P-glycoprotein and certain CYP450 enzymes, including CYP1A2, CYP2C9, CYP2D6, and CYP3A. This inhibition can result in unexpectedly high plasma levels of other drugs which are metabolized by those CYP450 enzymes or are substrates of P-glycoprotein. Reported examples of this interaction include the following:
Cyclosporine
The use of HMG-CoA reductase inhibitors that are CYP3A substrates in combination with amiodarone has been associated with reports of myopathy/rhabdomyolysis.
Limit the dose of simvastatin in patients on amiodarone to 20 mg daily. Limit the daily dose of lovastatin to 40 mg. Lower starting and maintenance doses of other CYP3A substrates (e.g., atorvastatin) may be required as amiodarone may increase the plasma concentration of these drugs.
In patients receiving therapy, administration of oral amiodarone results in an increase in the serum digoxin concentration. Amiodarone taken concomitantly with digoxin increases the serum digoxin concentration by 70% after one day. If digitalis treatment is continued, serum levels should be closely monitored and patients observed for clinical evidence of toxicity.
The metabolism of quinidine, procainamide, flecainide can be inhibited by amiodarone. Amiodarone taken concomitantly with quinidine increases quinidine serum concentration by 33% after two days. Amiodarone taken concomitantly with procainamide for less than seven days increases plasma concentrations of procainamide and n-acetyl procainamide by 55% and 33%, respectively. In general, any added antiarrhythmic drug should be initiated at a lower than usual dose with careful monitoring.
Combination of amiodarone with other antiarrhythmic therapy should be reserved for patients with life-threatening ventricular arrhythmias who are incompletely responsive to a single agent or incompletely responsive to amiodarone. During transition to amiodarone the dose levels of previously administered agents should be reduced by 30 to 50% several days after the addition of amiodarone, when arrhythmia suppression should be beginning. The continued need for the other antiarrhythmic agent should be reviewed after the effects of amiodarone have been established, and discontinuation ordinarily should be attempted. If the treatment is continued, these patients should be particularly carefully monitored for adverse effects, especially conduction disturbances and exacerbation of tachyarrhythmias, as amiodarone is continued. In amiodarone-treated patients who require additional antiarrhythmic therapy, the initial dose of such agents should be approximately half of the usual recommended dose.
Metabolism of lidocaine (CYP3A substrate) can be inhibited by amiodarone resulting in increased lidocaine concentrations. Sinus bradycardia and seizure has been reported in patients receiving concomitant lidocaine and amiodarone.
Potentiation of warfarin-type (CYP2C9 and CYP3A substrate) anticoagulant response is almost always seen in patients receiving amiodarone and can result in serious or fatal bleeding. Since the concomitant administration of warfarin with amiodarone increases the prothrombin time by 100% after 3 to 4 days, the dose of the anticoagulant should be reduced by one-third to one-half, and prothrombin times should be monitored closely
A potential interaction between clopidogrel and amiodarone resulting in ineffective inhibition of platelet aggregation has been reported.
Dabigatran etexilate when taken concomitantly with amiodarone may result in elevated serum concentration of dabigatran.
Fentanyl
Increased steady-state levels of phenytoin during concomitant therapy with amiodarone have been reported. Monitor phenytoin levels in patients taking both drugs.
Dextromethorphan is a substrate for both CYP2D6 and CYP3A. Amiodarone inhibits CYP2D6 and CYP3A. Chronic (>2 weeks) amiodarone treatment impairs metabolism of dextromethorphan leading to increased serum concentration.
To avoid excessive systemic absorption, the lacrimal sac should be compressed by digital pressure for two to three minutes after installation. To avoid inducing angle closure glaucoma, an estimation of the depth of the angle of the anterior chamber should be made. Excessive topical use of this drug can potentially lead to a confusional state characterized by delirium, agitation, and rarely coma. This state is more apt to occur in the pediatric and geriatric age groups. The specific anti-dote for this systemic anticholinergic syndrome is injectable physostigmine salicylate.
Transient symptoms of stinging and burning may occur. Prolonged use may produce local irritation characterized by follicular conjunctivitis, vascular congestion, edema, exudates, and an eczematoid dermatitis. Thirst or dryness of mouth, eye irritation not present before therapy, or increased sensitivity of eyes to light may occur.
To report SUSPECTED ADVERSE REACTIONS, contact Altaire Pharmaceuticals, Inc. at (800)-258-2471.
Clinical Information
Chemical Structure
No Image foundClinical Pharmacology
This anticholinergic preparation blocks the responses of the sphincter muscle of the iris and the accommodative muscle of the ciliary body to cholinergic stimulation, producing pupillary dilation (mydriasis) and paralysis of accommodation (cycloplegia).
Non-Clinical Toxicology
Contraindicated in persons with primary glaucoma or a tendency toward glaucoma, e.g. narrow anterior chamber angle, and in those persons showing hypersensitivity to any component of this preparation.In view of the long and variable half-life of amiodarone, potential for drug interactions exists, not only with concomitant medication, but also with drugs administered after discontinuation of amiodarone.
Drugs inducing TdP or prolonging QT
Co-administration of amiodarone with drugs known to prolong the QT interval (such as class I and III antiarrhythmics, lithium, certain phenothiazines, tricyclic antidepressants, certain fluoroquinolone and macrolide antibiotics, IV pentamidine, and azole antifungals) increases the risk of Torsades de Points. Avoid concomitant use of drugs that prolong the QT interval.
Drugs lowering heart rate or causing automaticity or conduction disorders
Concomitant use of drugs with depressant effects on the sinus and AV node (e.g., digoxin, beta blockers, verapamil, diltiazem, clonidine) can potentiate the electrophysiologic and hemodynamic effects of amiodarone, resulting in bradycardia, sinus arrest, and AV block. Monitor heart rate in patients on amiodarone and concomitant drugs that slow heart rate.
Effects of other medicinal products on amiodarone
Since amiodarone is a substrate for CYP3A and CYP2C8, drugs/substances that inhibit CYP3A (e.g., certain protease inhibitors, loratadine, cimetidine, trazodone) may decrease the metabolism and increase serum concentrations of amiodarone. Concomitant use of CYP3A inducers (rifampin, St. John's Wort), may lead to decreased serum concentrations and loss of efficacy. Consider serial measurement of amiodarone serum concentration during concomitant use of drugs affecting CYP3A activity.
Grapefruit juice given to healthy volunteers increased amiodarone AUC by 50% and Cmax by 84%, and decreased DEA to unquantifiable concentrations. Grapefruit juice inhibits CYP3A-mediated metabolism of oral amiodarone in the intestinal mucosa, resulting in increased plasma levels of amiodarone; therefore, grapefruit juice should not be taken during treatment with oral amiodarone. This information should be considered when transitioning from intravenous to oral amiodarone. Cholestyramine reduces enterohepatic circulation of amiodarone thereby increasing its elimination. This results in reduced amiodarone serum levels and half-life.
Effects of amiodarone on other medicinal products
Amiodarone inhibits P-glycoprotein and certain CYP450 enzymes, including CYP1A2, CYP2C9, CYP2D6, and CYP3A. This inhibition can result in unexpectedly high plasma levels of other drugs which are metabolized by those CYP450 enzymes or are substrates of P-glycoprotein. Reported examples of this interaction include the following:
Cyclosporine
The use of HMG-CoA reductase inhibitors that are CYP3A substrates in combination with amiodarone has been associated with reports of myopathy/rhabdomyolysis.
Limit the dose of simvastatin in patients on amiodarone to 20 mg daily. Limit the daily dose of lovastatin to 40 mg. Lower starting and maintenance doses of other CYP3A substrates (e.g., atorvastatin) may be required as amiodarone may increase the plasma concentration of these drugs.
In patients receiving therapy, administration of oral amiodarone results in an increase in the serum digoxin concentration. Amiodarone taken concomitantly with digoxin increases the serum digoxin concentration by 70% after one day. If digitalis treatment is continued, serum levels should be closely monitored and patients observed for clinical evidence of toxicity.
The metabolism of quinidine, procainamide, flecainide can be inhibited by amiodarone. Amiodarone taken concomitantly with quinidine increases quinidine serum concentration by 33% after two days. Amiodarone taken concomitantly with procainamide for less than seven days increases plasma concentrations of procainamide and n-acetyl procainamide by 55% and 33%, respectively. In general, any added antiarrhythmic drug should be initiated at a lower than usual dose with careful monitoring.
Combination of amiodarone with other antiarrhythmic therapy should be reserved for patients with life-threatening ventricular arrhythmias who are incompletely responsive to a single agent or incompletely responsive to amiodarone. During transition to amiodarone the dose levels of previously administered agents should be reduced by 30 to 50% several days after the addition of amiodarone, when arrhythmia suppression should be beginning. The continued need for the other antiarrhythmic agent should be reviewed after the effects of amiodarone have been established, and discontinuation ordinarily should be attempted. If the treatment is continued, these patients should be particularly carefully monitored for adverse effects, especially conduction disturbances and exacerbation of tachyarrhythmias, as amiodarone is continued. In amiodarone-treated patients who require additional antiarrhythmic therapy, the initial dose of such agents should be approximately half of the usual recommended dose.
Metabolism of lidocaine (CYP3A substrate) can be inhibited by amiodarone resulting in increased lidocaine concentrations. Sinus bradycardia and seizure has been reported in patients receiving concomitant lidocaine and amiodarone.
Potentiation of warfarin-type (CYP2C9 and CYP3A substrate) anticoagulant response is almost always seen in patients receiving amiodarone and can result in serious or fatal bleeding. Since the concomitant administration of warfarin with amiodarone increases the prothrombin time by 100% after 3 to 4 days, the dose of the anticoagulant should be reduced by one-third to one-half, and prothrombin times should be monitored closely
A potential interaction between clopidogrel and amiodarone resulting in ineffective inhibition of platelet aggregation has been reported.
Dabigatran etexilate when taken concomitantly with amiodarone may result in elevated serum concentration of dabigatran.
Fentanyl
Increased steady-state levels of phenytoin during concomitant therapy with amiodarone have been reported. Monitor phenytoin levels in patients taking both drugs.
Dextromethorphan is a substrate for both CYP2D6 and CYP3A. Amiodarone inhibits CYP2D6 and CYP3A. Chronic (>2 weeks) amiodarone treatment impairs metabolism of dextromethorphan leading to increased serum concentration.
To avoid excessive systemic absorption, the lacrimal sac should be compressed by digital pressure for two to three minutes after installation. To avoid inducing angle closure glaucoma, an estimation of the depth of the angle of the anterior chamber should be made. Excessive topical use of this drug can potentially lead to a confusional state characterized by delirium, agitation, and rarely coma. This state is more apt to occur in the pediatric and geriatric age groups. The specific anti-dote for this systemic anticholinergic syndrome is injectable physostigmine salicylate.
Transient symptoms of stinging and burning may occur. Prolonged use may produce local irritation characterized by follicular conjunctivitis, vascular congestion, edema, exudates, and an eczematoid dermatitis. Thirst or dryness of mouth, eye irritation not present before therapy, or increased sensitivity of eyes to light may occur.
To report SUSPECTED ADVERSE REACTIONS, contact Altaire Pharmaceuticals, Inc. at (800)-258-2471.
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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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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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Interactions
Interactions
A total of 440 drugs (1549 brand and generic names) are known to interact with Imbruvica (ibrutinib). 228 major drug interactions (854 brand and generic names) 210 moderate drug interactions (691 brand and generic names) 2 minor drug interactions (4 brand and generic names) Show all medications in the database that may interact with Imbruvica (ibrutinib).