Drug Interactions between Bromfed DM and guanfacine

Avoid consuming grapefruit or grapefruit juice during treatment with guanFACINE, as it may increase blood levels and effects of the medication. This may cause blood pressure to fall excessively, especially when you rise from a sitting or lying position. The risk of other side effects such as drowsiness, dizziness, lightheadedness, fainting, headache, palpitations, and heart rate changes may also increase. Additionally, you should avoid or limit the use of alcohol while being treated with guanFACINE. Combining the medication with alcohol can intensify sedative and blood pressure lowering effects, which may increase the risk of falls and injury. Avoid driving or operating hazardous machinery until you know how the medication affects you, and use caution when getting up from a sitting or lying position. If you are using a long-acting or extended-release formulation of the medication, make sure you do not take it with a high-fat meal. Doing so results in increased absorption and elevated blood levels of the medication. Talk to your doctor or pharmacist if you have any questions or concerns.

Alcohol can increase the nervous system side effects of dextromethorphan such as dizziness, drowsiness, and difficulty concentrating. Some people may also experience impairment in thinking and judgment. You should avoid or limit the use of alcohol while being treated with dextromethorphan. Do not use more than the recommended dose of dextromethorphan, and avoid activities requiring mental alertness such as driving or operating hazardous machinery until you know how the medication affects you. Talk to your doctor or pharmacist if you have any questions or concerns.

Alcohol can increase the nervous system side effects of brompheniramine such as dizziness, drowsiness, and difficulty concentrating. Some people may also experience impairment in thinking and judgment. You should avoid or limit the use of alcohol while being treated with brompheniramine. Do not use more than the recommended dose of brompheniramine, and avoid activities requiring mental alertness such as driving or operating hazardous machinery until you know how the medication affects you. Talk to your doctor or pharmacist if you have any questions or concerns.

Both pseudoephedrine and caffeine can increase blood pressure and heart rate, and combining them may enhance these effects. Talk to your doctor before using these medications, especially if you have a history of high blood pressure or heart disease. You may need a dose adjustment or more frequent monitoring by your doctor to safely use both medications. Contact your doctor if your condition changes or you experience increased side effects. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

Sympathomimetic agents may cause adverse cardiovascular effects, particularly when used in high dosages and/or in susceptible patients. In cardiac tissues, these agents may produce positive chronotropic and inotropic effects via stimulation of beta- 1 adrenergic receptors. Cardiac output, oxygen consumption, and the work of the heart may be increased. In the peripheral vasculature, vasoconstriction may occur via stimulation of alpha-1 adrenergic receptors. Palpitations, tachycardia, arrhythmia, hypertension, reflex bradycardia, coronary occlusion, cerebral vasculitis, myocardial infarction, cardiac arrest, and death have been reported. Some of these agents, particularly ephedra alkaloids (ephedrine, ma huang, phenylpropanolamine), may also predispose patients to hemorrhagic and ischemic stroke. Therapy with sympathomimetic agents should generally be avoided or administered cautiously in patients with sensitivity to sympathomimetic amines, hyperthyroidism, or underlying cardiovascular or cerebrovascular disorders. These agents should not be used in patients with severe coronary artery disease or severe/uncontrolled hypertension.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

Central alpha-2 adrenoreceptor agonists reduce sympathetic outflow from the central nervous system, resulting in decreases in heart rate, peripheral and renovascular resistance, and blood pressure. Therapy with these agents should be administered cautiously in patients with hypotension or conditions that may be exacerbated by decreased blood pressure and perfusion, such as coronary insufficiency, peripheral vascular disease (e.g., Raynaud's syndrome), cerebrovascular disease, or recent myocardial infarction.

It has been suggested that the anticholinergic effect of antihistamines may reduce the volume and cause thickening of bronchial secretions, resulting in obstruction of respiratory tract. Some manufacturers and clinicians recommend that therapy with antihistamines be administered cautiously in patients with asthma or chronic obstructive pulmonary disease.

Central alpha-2 adrenoreceptor agonists may occasionally cause mental depression and should be used cautiously in patients with a history of depression.

Sympathomimetic agents may cause increases in blood glucose concentrations. These effects are usually transient and slight but may be significant with dosages higher than those normally recommended. Therapy with sympathomimetic agents should be administered cautiously in patients with diabetes mellitus. Closer monitoring of blood glucose concentrations may be appropriate.

The extended-release formulation of pseudoephedrine (Sudafed 24 Hour) contains a non-deformable material. There have been rare reports of obstructive symptoms in patients with known strictures following the ingestion of similar sustained-release products. Therapy with the extended-release formulation of pseudoephedrine should be administered cautiously in patients with preexisting severe gastrointestinal narrowing or obstruction, whether pathologic or iatrogenic.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

Sympathomimetic agents can induce transient mydriasis via stimulation of alpha-1 adrenergic receptors. In patients with anatomically narrow angles or narrow-angle glaucoma, pupillary dilation can provoke an acute attack. In patients with other forms of glaucoma, mydriasis may occasionally increase intraocular pressure. Therapy with sympathomimetic agents should be administered cautiously in patients with or predisposed to glaucoma, particularly narrow-angle glaucoma.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.

Central alpha-2 adrenoreceptor agonists reduce sympathetic outflow from the central nervous system. Heart rate is decreased, which may lead to or exacerbate sinus bradycardia and atrioventricular block. Therapy with central alpha-2 adrenoreceptor agonists should be administered cautiously in patients with conduction disturbances such as sinus node dysfunction or AV nodal disease.

The safety and effectiveness of guanfacine in children under 12 years of age has not been demonstrated and its use in this age group is not recommended. However, there have been some spontaneous postmarketing reports of mania and aggressive behavioral changes in pediatric patients with attention- deficit hyperactivity disorder (ADHD) that received this drug. All patients had medical or family risks of bipolar disorder, and all of them recovered after treatment discontinuation. Hallucinations have also been reported in pediatric patients receiving guanfacine for the treatment of ADHD.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

Antihistamines may infrequently cause cardiovascular adverse effects related to their anticholinergic and local anesthetic (quinidine-like) activities. Tachycardia, palpitation, ECG changes, arrhythmias, hypotension, and hypertension have been reported. Although these effects are uncommon and usually limited to overdosage situations, the manufacturers and some clinicians recommend that therapy with antihistamines be administered cautiously in patients with cardiovascular disease, hypertension, and/or hyperthyroidism.

Central alpha-2 adrenoreceptor agonists reduce sympathetic outflow from the central nervous system, resulting in decreases in heart rate, peripheral and renovascular resistance, and blood pressure. Therapy with these agents should be administered cautiously in patients with hypotension or conditions that may be exacerbated by decreased blood pressure and perfusion, such as coronary insufficiency, peripheral vascular disease (e.g., Raynaud's syndrome), cerebrovascular disease, or recent myocardial infarction.

Central alpha-2 adrenoreceptor agonists reduce sympathetic outflow from the central nervous system, resulting in decreases in heart rate, peripheral and renovascular resistance, and blood pressure. Therapy with these agents should be administered cautiously in patients with hypotension or conditions that may be exacerbated by decreased blood pressure and perfusion, such as coronary insufficiency, peripheral vascular disease (e.g., Raynaud's syndrome), cerebrovascular disease, or recent myocardial infarction.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

Normally, approximately 50% of a guanfacine dose is eliminated unchanged by the kidney and the rest metabolized by the liver. However, neither the parent drug nor its metabolites accumulate significantly during chronic dosing in patients with severe renal impairment due to increased hepatic metabolism of the drug in these patients. Thus, initial dosage adjustments are generally not necessary in renal impairment. Dosage titration, however, should be made cautiously if hepatic function is also compromised. The pharmacokinetics of guanfacine has not been studied in patients with liver disease. The manufacturer recommends caution when the drug is used in such patients.

Central alpha-2 adrenoreceptor agonists reduce sympathetic outflow from the central nervous system, resulting in decreases in heart rate, peripheral and renovascular resistance, and blood pressure. Therapy with these agents should be administered cautiously in patients with hypotension or conditions that may be exacerbated by decreased blood pressure and perfusion, such as coronary insufficiency, peripheral vascular disease (e.g., Raynaud's syndrome), cerebrovascular disease, or recent myocardial infarction.

Chewable products frequently may contain aspartame, which is metabolized in the gastrointestinal tract to phenylalanine. Sudafed (brand of pseudoephedrine) chewable 15 mg tablets provide the equivalent of 0.78 mg of phenylalanine per each tablet. The aspartame/phenylalanine content should be considered when this and similar products are used in patients who must restrict their intake of phenylalanine (i.e. phenylketonurics).

Sympathomimetic agents may cause or worsen urinary difficulty in patients with prostate enlargement due to smooth muscle contraction in the bladder neck via stimulation of alpha-1 adrenergic receptors. Therapy with sympathomimetic agents should be administered cautiously in patients with hypertrophy or neoplasm of the prostate.

Normally, approximately 50% of a guanfacine dose is eliminated unchanged by the kidney and the rest metabolized by the liver. However, neither the parent drug nor its metabolites accumulate significantly during chronic dosing in patients with severe renal impairment due to increased hepatic metabolism of the drug in these patients. Thus, initial dosage adjustments are generally not necessary in renal impairment. Dosage titration, however, should be made cautiously if hepatic function is also compromised. The pharmacokinetics of guanfacine has not been studied in patients with liver disease. The manufacturer recommends caution when the drug is used in such patients.

Limited pharmacokinetic data are available for the older, first-generation antihistamines. Many appear to be primarily metabolized by the liver, and both parent drugs and metabolites are excreted in the urine. Patients with renal and/or liver disease may be at greater risk for adverse effects from antihistamines due to drug and metabolite accumulation. Therapy with antihistamines should be administered cautiously in such patients. Lower initial dosages may be appropriate.

Central alpha-2 adrenoreceptor agonists reduce sympathetic outflow from the central nervous system. Heart rate is decreased, which may lead to or exacerbate sinus bradycardia and atrioventricular block. Therapy with central alpha-2 adrenoreceptor agonists should be administered cautiously in patients with conduction disturbances such as sinus node dysfunction or AV nodal disease.

Antihistamines often have anticholinergic activity, to which elderly patients are particularly sensitive. Therapy with antihistamines should be administered cautiously, if at all, in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as urinary retention or obstruction; angle-closure glaucoma, untreated intraocular hypertension, or uncontrolled primary open-angle glaucoma; and gastrointestinal obstructive disorders. Conventional, first-generation antihistamines such as the ethanolamines (bromodiphenhydramine, carbinoxamine, clemastine, dimenhydrinate, diphenhydramine, doxylamine, phenyltoloxamine) tend to exhibit substantial anticholinergic effects. In contrast, the newer, relatively nonsedating antihistamines (e.g., cetirizine, fexofenadine, loratadine) reportedly have low to minimal anticholinergic activity at normally recommended dosages and may be appropriate alternatives.