Can you take Alphagan P with Famotidine?

The brimonidine ophthalmic in Alphagan P has a moderate potential interaction with Cardiovascular Conditions and Disorders.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. In the central nervous system, alpha adrenergic stimulation causes an inhibition of sympathetic vasomotor centers, resulting in decreased peripheral resistance and bradycardia. While the commercially available agents in the U.S. (apraclonidine and brimonidine) are hydrophilic and do not readily distribute across the ocular-blood barrier into the CNS, prolonged use may increase the risk of systemic effects. There have been occasional reports of bradycardia, chest heaviness or burning, palpitation, reduced blood pressure, and orthostatic hypotension when apraclonidine 1% was administered once or twice a day for 4 weeks to individuals not undergoing laser surgery. Therapy with ophthalmic alpha-2 adrenergic agents should be administered cautiously in patients with severe, uncontrolled cardiovascular disease, including hypertension, coronary or cerebrovascular insufficiency, recent myocardial infarction, chronic renal failure, Raynaud's disease, thromboangiitis obliterans, and a predisposition for orthostatic hypotension.

The brimonidine ophthalmic in Alphagan P has a moderate potential interaction with Cerebrovascular Insufficiency.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. In the central nervous system, alpha adrenergic stimulation causes an inhibition of sympathetic vasomotor centers, resulting in decreased peripheral resistance and bradycardia. While the commercially available agents in the U.S. (apraclonidine and brimonidine) are hydrophilic and do not readily distribute across the ocular-blood barrier into the CNS, prolonged use may increase the risk of systemic effects. There have been occasional reports of bradycardia, chest heaviness or burning, palpitation, reduced blood pressure, and orthostatic hypotension when apraclonidine 1% was administered once or twice a day for 4 weeks to individuals not undergoing laser surgery. Therapy with ophthalmic alpha-2 adrenergic agents should be administered cautiously in patients with severe, uncontrolled cardiovascular disease, including hypertension, coronary or cerebrovascular insufficiency, recent myocardial infarction, chronic renal failure, Raynaud's disease, thromboangiitis obliterans, and a predisposition for orthostatic hypotension.

The brimonidine ophthalmic in Alphagan P has a moderate potential interaction with Depression.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. Depression has infrequently been associated with the ocular use of these drugs due to their inhibiting effect on the sympathetic nervous system. Depressed patients should be monitored for exacerbation of their condition during therapy with ophthalmic alpha-2 adrenergic agents.

Famotidine has a major potential interaction with Gastrointestinal Hemorrhage.

Histamine H2 receptor antagonists should not be used in the presence of vomit with blood, or bloody or black stools. These might be serious conditions and the diagnosis needs to be ruled out.

The brimonidine ophthalmic in Alphagan P has a moderate potential interaction with Hypotension.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. In the central nervous system, alpha adrenergic stimulation causes an inhibition of sympathetic vasomotor centers, resulting in decreased peripheral resistance and bradycardia. While the commercially available agents in the U.S. (apraclonidine and brimonidine) are hydrophilic and do not readily distribute across the ocular-blood barrier into the CNS, prolonged use may increase the risk of systemic effects. There have been occasional reports of bradycardia, chest heaviness or burning, palpitation, reduced blood pressure, and orthostatic hypotension when apraclonidine 1% was administered once or twice a day for 4 weeks to individuals not undergoing laser surgery. Therapy with ophthalmic alpha-2 adrenergic agents should be administered cautiously in patients with severe, uncontrolled cardiovascular disease, including hypertension, coronary or cerebrovascular insufficiency, recent myocardial infarction, chronic renal failure, Raynaud's disease, thromboangiitis obliterans, and a predisposition for orthostatic hypotension.

The brimonidine ophthalmic in Alphagan P has a moderate potential interaction with Liver Disease.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. There are limited data concerning the pharmacokinetic disposition or the clinical use of these drugs in patients with renal and/or liver disease. Therapy with ophthalmic alpha-2 adrenergic agents should be administered cautiously in patients with significantly impaired renal or hepatic function.

The brimonidine ophthalmic in Alphagan P has a moderate potential interaction with Renal Dysfunction.

Topically applied alpha-2 adrenergic receptor agonists are systemically absorbed, with the potential for producing rare but clinically significant systemic effects. There are limited data concerning the pharmacokinetic disposition or the clinical use of these drugs in patients with renal and/or liver disease. Therapy with ophthalmic alpha-2 adrenergic agents should be administered cautiously in patients with significantly impaired renal or hepatic function.

Famotidine has a moderate potential interaction with Renal Dysfunction.

Famotidine is partially eliminated by the kidney as unchanged drug, the extent of which is dependent upon the route of administration (25% to 30% oral; 65% to 70% intravenous). The elimination half-life of famotidine may be prolonged considerably in patients with severe renal impairment (CrCl < 10 mL/min), possibly exceeding 20 hours and approaching approximately 24 hours in anuric patients. Since central nervous system adverse effects such as grand mal seizures and psychic disturbances have been reported in patients with moderate (CrCl < 50 mL/min) and severe renal impairment, dosage adjustments are recommended for these patients. Reducing the normally recommended dosage by one-half or prolonging the dosing interval to 36 to 48 hours may be appropriate, depending on the patient's clinical response.