Drug Interaction Report

Spironolactone has a major potential interaction with Acidosis.

Acidosis alters the ratio of extracellular to intracellular potassium and may commonly lead to rapid increases in serum potassium levels. Conversely, high serum potassium concentrations may potentiate acidosis. Because of their hyperkalemic effects, therapy with potassium-sparing diuretics should be avoided in patients with metabolic or respiratory acidosis. These agents should be used cautiously in patients in whom acidosis may occur, such as patients with cardiopulmonary disease, severe respiratory disease, or poorly controlled diabetes. Acid-base balance and serum potassium levels should be monitored at regular intervals.

The pilocarpine ophthalmic in Pilocar has a major potential interaction with Aphakia.

The use of miotic agents may occasionally cause retinal detachment due to drug-induced ciliary or accommodative spasm, which causes the lens and vitreous to move forward and create a retinal tear. Therapy with miotic agents should be administered with extreme caution, if at all, in patients with risk factors for retinal detachment, such as old age, retinal degenerative changes or other retinal disorders, aphakia, prior cataract extraction, or a history of severe myopia or retinal detachment.

The pilocarpine ophthalmic in Pilocar 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.

The pilocarpine ophthalmic in Pilocar 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 pilocarpine ophthalmic in Pilocar has a moderate potential interaction with Cataract.

The use of miotic agents has been associated with the development of lens opacities characterized by the appearance of anterior subcapsular vacuoles. The incidence of cataracts appears to be highest in patients treated with long-acting cholinesterase inhibitors (e.g., demecarium and echothiophate) and may also be related to age (higher in patients > 60 years of age), drug concentration, frequency of use, and duration of therapy (>= 6 months). Lens opacities usually regress if miotic therapy is withdrawn early in their development but often become progressive once they are established. Therapy with miotic agents should be administered cautiously in patients with or predisposed to cataracts. Slit-lamp examinations should be performed regularly, and miotic therapy discontinued if necessary.

The pilocarpine ophthalmic in Pilocar 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 pilocarpine ophthalmic in Pilocar 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.

Spironolactone has a major potential interaction with Diabetes Mellitus.

Potassium-sparing diuretics can cause hyperkalemia, which may result in life-threatening cardiac arrhythmias. Patients with diabetes mellitus, with or without nephropathy, may be particularly susceptible to the hyperkalemic effect of these drugs due to a defect in the renin-angiotensin-aldosterone axis. Therapy with potassium-sparing diuretics should be avoided, if possible, in patients with diabetes, especially uncontrolled or insulin-dependent diabetes mellitus. If these drugs are used, serum potassium levels and renal function should be monitored at regular intervals. Determination of serum electrolytes is especially important during initiation of therapy, after a dosage adjustment, and during illness that could alter renal function.

Spironolactone has a major potential interaction with Diabetes Mellitus.

Acidosis alters the ratio of extracellular to intracellular potassium and may commonly lead to rapid increases in serum potassium levels. Conversely, high serum potassium concentrations may potentiate acidosis. Because of their hyperkalemic effects, therapy with potassium-sparing diuretics should be avoided in patients with metabolic or respiratory acidosis. These agents should be used cautiously in patients in whom acidosis may occur, such as patients with cardiopulmonary disease, severe respiratory disease, or poorly controlled diabetes. Acid-base balance and serum potassium levels should be monitored at regular intervals.

Spironolactone has a major potential interaction with Electrolyte Abnormalities.

All diuretics may cause or aggravate fluid and electrolyte disturbances. Potassium-sparing diuretics may cause hyperkalemia and, infrequently, hyponatremia. The latter generally occurs when these agents are combined with other diuretics such as thiazides or used in markedly edematous patients with restricted sodium intake. Therapy with potassium-sparing diuretics should be administered cautiously in patients with or predisposed to electrolyte abnormalities. Electrolyte imbalances should be corrected prior to initiating therapy, and serum electrolyte concentrations should be monitored periodically and maintained at normal ranges during therapy. Determination of serum electrolytes is especially important during initiation of therapy, after a dosage adjustment, and during illness that could alter renal function.

Spironolactone has a moderate potential interaction with Gout.

Potassium-sparing diuretics have been reported to elevate serum uric acid levels. Therapy with these agents should be administered cautiously in patients with a history of gout.

The pilocarpine ophthalmic in Pilocar 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.

The pilocarpine ophthalmic in Pilocar 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.

The pilocarpine ophthalmic in Pilocar 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.

Spironolactone has a major potential interaction with Hyperkalemia.

The use of potassium-sparing diuretics is contraindicated in the presence of elevated serum potassium concentrations (> 5.5 mEq/L). Potassium-sparing diuretics can cause hyperkalemia, which may result in life-threatening cardiac arrhythmias. Careful monitoring of serum potassium levels is necessary in all patients treated with potassium-sparing diuretics, especially during initiation of therapy, after dosage adjustment, and during illness that could alter renal function. The diuretic should be withdrawn immediately if hyperkalemia develops, and measures should be initiated to lower serum potassium if it exceeds 6.5 mEq/L. The combined use of a potassium-sparing diuretic with a kaliuretic diuretic (e.g., thiazides) may decrease the risk of hyperkalemia.

Spironolactone has a major potential interaction with Hyponatremia.

All diuretics may cause or aggravate fluid and electrolyte disturbances. Potassium-sparing diuretics may cause hyperkalemia and, infrequently, hyponatremia. The latter generally occurs when these agents are combined with other diuretics such as thiazides or used in markedly edematous patients with restricted sodium intake. Therapy with potassium-sparing diuretics should be administered cautiously in patients with or predisposed to electrolyte abnormalities. Electrolyte imbalances should be corrected prior to initiating therapy, and serum electrolyte concentrations should be monitored periodically and maintained at normal ranges during therapy. Determination of serum electrolytes is especially important during initiation of therapy, after a dosage adjustment, and during illness that could alter renal function.

The pilocarpine ophthalmic in Pilocar 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 pilocarpine ophthalmic in Pilocar 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.

The pilocarpine ophthalmic in Pilocar 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.

Spironolactone has a moderate potential interaction with Liver Disease.

Rapid alterations in fluid and electrolyte balance may precipitate hepatic coma in patients with liver disease. Hepatic encephalopathy has been associated with the use of diuretics, most frequently thiazides but also some potassium-sparing diuretics. Therapy with all diuretics should be administered cautiously in patients with impaired hepatic function. These patients should be monitored carefully for signs and symptoms of hepatic encephalopathy such as tremors, confusion, increased jaundice, and coma.

The pilocarpine ophthalmic in Pilocar has a major potential interaction with Myopia.

The use of miotic agents may occasionally cause retinal detachment due to drug-induced ciliary or accommodative spasm, which causes the lens and vitreous to move forward and create a retinal tear. Therapy with miotic agents should be administered with extreme caution, if at all, in patients with risk factors for retinal detachment, such as old age, retinal degenerative changes or other retinal disorders, aphakia, prior cataract extraction, or a history of severe myopia or retinal detachment.

The pilocarpine ophthalmic in Pilocar 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.

The pilocarpine ophthalmic in Pilocar 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 pilocarpine ophthalmic in Pilocar 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.

Spironolactone has a major potential interaction with Pulmonary Impairment.

Acidosis alters the ratio of extracellular to intracellular potassium and may commonly lead to rapid increases in serum potassium levels. Conversely, high serum potassium concentrations may potentiate acidosis. Because of their hyperkalemic effects, therapy with potassium-sparing diuretics should be avoided in patients with metabolic or respiratory acidosis. These agents should be used cautiously in patients in whom acidosis may occur, such as patients with cardiopulmonary disease, severe respiratory disease, or poorly controlled diabetes. Acid-base balance and serum potassium levels should be monitored at regular intervals.

Spironolactone has a major potential interaction with Renal Dysfunction.

The use of potassium-sparing diuretics is contraindicated in patients with anuria, acute or progressive renal insufficiency, or diabetic nephropathy. Potassium-sparing diuretics can cause hyperkalemia, which may result in life-threatening cardiac arrhythmias. Patients with impaired renal function may be particularly susceptible to the hyperkalemic effect of these drugs. Therapy with potassium-sparing diuretics should be administered cautiously in patients with evidence of renal function impairment (BUN > 30 mg/dL or serum creatinine > 1.5 mg/dL). If these drugs are used, serum potassium levels and renal function should be monitored at regular intervals. Determination of serum electrolytes is especially important during initiation of therapy, after a dosage adjustment, and during illness that could alter renal function.

The pilocarpine ophthalmic in Pilocar has a major potential interaction with Retinal Disorders.

The use of miotic agents may occasionally cause retinal detachment due to drug-induced ciliary or accommodative spasm, which causes the lens and vitreous to move forward and create a retinal tear. Therapy with miotic agents should be administered with extreme caution, if at all, in patients with risk factors for retinal detachment, such as old age, retinal degenerative changes or other retinal disorders, aphakia, prior cataract extraction, or a history of severe myopia or retinal detachment.

The pilocarpine ophthalmic in Pilocar 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.

The pilocarpine ophthalmic in Pilocar 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 pilocarpine ophthalmic in Pilocar 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.

The pilocarpine ophthalmic in Pilocar has a major potential interaction with Uveitis, Anterior.

The use of miotic agents is contraindicated in patients with active anterior uveitis and/or glaucoma associated with iridocyclitis. Pupillary constriction produced by these agents may aggravate the inflammation and predispose these patients to the development of posterior synechiae.