Can you take Acetylcholine ophthalmic with Tussplex DM?

Acetylcholine ophthalmic has a moderate potential interaction with Arrhythmia.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

Acetylcholine ophthalmic has a moderate potential interaction with Asthma.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

The chlorpheniramine in Tussplex DM has a moderate potential interaction with Asthma.

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.

The phenylephrine in Tussplex DM has a moderate potential interaction with Benign Prostatic Hyperplasia.

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.

The phenylephrine in Tussplex DM has a major potential interaction with Cardiovascular Conditions and Disorders.

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.

The chlorpheniramine in Tussplex DM has a moderate potential interaction with Cardiovascular Conditions and Disorders.

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.

The phenylephrine in Tussplex DM has a major potential interaction with Cerebrovascular Insufficiency.

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.

Acetylcholine ophthalmic has a moderate potential interaction with COPD.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

The chlorpheniramine in Tussplex DM has a moderate potential interaction with COPD.

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.

Acetylcholine ophthalmic has a moderate potential interaction with Corneal Abrasion.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

The phenylephrine in Tussplex DM has a moderate potential interaction with Diabetes Mellitus.

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 chlorpheniramine in Tussplex DM has a moderate potential interaction with Gastrointestinal Obstruction.

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.

The chlorpheniramine in Tussplex DM has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

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.

The phenylephrine in Tussplex DM has a moderate potential interaction with Glaucoma/Intraocular Hypertension.

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.

Acetylcholine ophthalmic has a moderate potential interaction with Heart Attack.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

Acetylcholine ophthalmic has a moderate potential interaction with Heart Failure.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

Acetylcholine ophthalmic has a moderate potential interaction with High Blood Pressure.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

The phenylephrine in Tussplex DM has a major potential interaction with Hyperthyroidism.

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.

The chlorpheniramine in Tussplex DM has a moderate potential interaction with 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.

Acetylcholine ophthalmic has a moderate potential interaction with Hypotension.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

The chlorpheniramine in Tussplex DM has a moderate potential interaction with Hypotension.

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.

Acetylcholine ophthalmic has a moderate potential interaction with Indigestion.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

Acetylcholine ophthalmic has a moderate potential interaction with Irritable Bowel Syndrome.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

The chlorpheniramine in Tussplex DM has a moderate potential interaction with Liver Disease.

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.

Acetylcholine ophthalmic has a moderate potential interaction with Parkinsonism.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

Acetylcholine ophthalmic has a moderate potential interaction with Peptic Ulcer.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

The phenylephrine in Tussplex DM has a major potential interaction with Pheochromocytoma.

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.

Acetylcholine ophthalmic has a moderate potential interaction with Post MI Syndrome.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

The phenylephrine in Tussplex DM has a moderate potential interaction with Prostate Tumor, Benign.

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.

The chlorpheniramine in Tussplex DM has a moderate potential interaction with Renal Dysfunction.

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.

Acetylcholine ophthalmic has a moderate potential interaction with Seizures.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

Acetylcholine ophthalmic has a moderate potential interaction with Sinus Node Dysfunction.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.

The chlorpheniramine in Tussplex DM has a moderate potential interaction with Urinary Retention.

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.

Acetylcholine ophthalmic has a moderate potential interaction with Urinary Tract Obstruction.

Topically applied cholinergic agents are systemically absorbed, with the potential for producing rare but clinically significant systemic effects, including urinary incontinence, tightness of the bladder, increased gastric contractility and acid secretion, bradycardia, severe hypotension, bronchospasm, seizures, and coma. Increases in blood pressure may occur rarely due to a nicotinic effect on sympathetic ganglia. Therapy with ophthalmic cholinergic agents, particularly the long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate), should be administered cautiously in patients with corneal abrasion (which may increase drug penetration), bronchospastic diseases, spastic gastrointestinal disturbances, urinary tract obstruction, peptic ulcer, pronounced bradycardia and hypotension, vascular hypertension, acute cardiac failure, recent myocardial infarction, epilepsy, parkinsonism, and other conditions that may respond adversely to vagotonic effects. The usual precautions should be followed to minimize the risk of systemic toxicity, including digital compression of the nasolacrimal ducts (1 to 2 minutes) following instillation to limit drainage into the nasal chamber, where extensive absorption may occur, and washing hands after use to prevent skin absorption. Excessive cholinergic effects may be reversed with parenterally administered atropine.