Interactions between Digoxin and Endagen-HD

The HYDROcodone in Endagen-HD has a major potential interaction with Acute Alcohol Intoxication.

The use of opiate agonists is contraindicated in patients with acute alcohol intoxication exhibiting depressed vital signs. The central nervous system depressant effects of opiate agonists may be additive with those of alcohol. Severe respiratory depression and death may occur. Therapy with opiate agonists should be administered cautiously in patients who might be prone to acute alcohol intake.

The HYDROcodone in Endagen-HD has a moderate potential interaction with Adrenal Insufficiency.

Patients with Addison's disease may have increased risk of respiratory depression and prolonged CNS depression associated with the use of narcotic (opioid) analgesic agents. Conversely, these agents may cause or potentiate adrenal insufficiency. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with adrenocortical insufficiency. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

The HYDROcodone in Endagen-HD has a major potential interaction with Alcoholism.

Opiate agonists have the potential to cause dependence and abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use. Abrupt cessation, reduction in dosage, or administration of an opiate antagonist such as naloxone may precipitate withdrawal symptoms. In patients who have developed tolerance to an opiate agonist, overdosage can still produce respiratory depression and death, and cross-tolerance usually will occur with other agents in the class. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with opiate agonists. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of opiate therapy should be undertaken gradually using a dosage-tapering schedule.

The HYDROcodone in Endagen-HD has a major potential interaction with Altered Consciousness.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

The HYDROcodone in Endagen-HD has a moderate potential interaction with Arrhythmia.

Opiate agonists have cholinergic activity. Large doses and/or rapid intravenous administration may produce bradycardia and arrhythmias via stimulation of medullary vagal nuclei. Therapy with opiate agonists should be administered cautiously in patients with a history of arrhythmias. Clinical monitoring of cardiovascular status is recommended during therapy.

The HYDROcodone in Endagen-HD has a major potential interaction with Asphyxia.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

The chlorpheniramine in Endagen-HD 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 Endagen-HD 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 HYDROcodone in Endagen-HD has a moderate potential interaction with Biliary Obstruction.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

The HYDROcodone in Endagen-HD has a major potential interaction with Brain Tumor.

The hypoventilation associated with administration of opiate agonists, particularly by the intravenous route, can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Opiate agonists should not be used in patients with suspected or known head injury or increased intracranial pressure. Also, clinicians treating such patients should be aware that opiate agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

The HYDROcodone in Endagen-HD has a major potential interaction with Brain Tumor.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

Digoxin has a major potential interaction with Cardiomyopathy.

Patients with heart failure associated with preserved left ventricular systolic function, such as in restrictive cardiomyopathy, constrictive pericarditis, amyloid heart disease and acute cor pulmonale, may be particularly susceptible to experience decrease cardiac output. Therapy with digoxin should be administered cautiously in such patients. Patients with idiopathic hypertrophic subaortic stenosis may have worsening of the outflow obstruction due to the inotropic effects of digoxin.

Digoxin has a major potential interaction with Cardiomyopathy.

Digoxin can rarely precipitate vasoconstriction and may promote the development of cytokines; therefore, should be avoided in patients with myocarditis.

The phenylephrine in Endagen-HD 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 Endagen-HD 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 HYDROcodone in Endagen-HD has a major potential interaction with Cerebral Vascular Disorder.

The hypoventilation associated with administration of opiate agonists, particularly by the intravenous route, can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Opiate agonists should not be used in patients with suspected or known head injury or increased intracranial pressure. Also, clinicians treating such patients should be aware that opiate agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

The HYDROcodone in Endagen-HD has a major potential interaction with Cerebral Vascular Disorder.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

The phenylephrine in Endagen-HD 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.

The HYDROcodone in Endagen-HD has a major potential interaction with Constipation.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

Digoxin has a major potential interaction with Constrictive Pericarditis.

Patients with heart failure associated with preserved left ventricular systolic function, such as in restrictive cardiomyopathy, constrictive pericarditis, amyloid heart disease and acute cor pulmonale, may be particularly susceptible to experience decrease cardiac output. Therapy with digoxin should be administered cautiously in such patients. Patients with idiopathic hypertrophic subaortic stenosis may have worsening of the outflow obstruction due to the inotropic effects of digoxin.

The chlorpheniramine in Endagen-HD 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.

Digoxin has a major potential interaction with Cor Pulmonale.

Patients with heart failure associated with preserved left ventricular systolic function, such as in restrictive cardiomyopathy, constrictive pericarditis, amyloid heart disease and acute cor pulmonale, may be particularly susceptible to experience decrease cardiac output. Therapy with digoxin should be administered cautiously in such patients. Patients with idiopathic hypertrophic subaortic stenosis may have worsening of the outflow obstruction due to the inotropic effects of digoxin.

The HYDROcodone in Endagen-HD has a major potential interaction with Dehydration.

Opiate agonists can induce vasodilation and significant hypotension, particularly when given in high dosages and/or by rapid intravenous administration. Opiate analgesics cause vasodilatation that may exacerbate hypotension and hypoperfusion and, therefore, are contraindicated in circulatory shock. At therapeutic analgesic dosages, ambulatory patients are more likely to experience dizziness and hypotension than patients who are confined to bed. However, orthostatic hypotension may occur in supine patients upon rising. Therapy with opiate agonists should be administered cautiously and initiated at reduced dosages in patients with hypovolemia, or a predisposition to hypotension. When given by intramuscular or subcutaneous administration, clinicians should also be aware that impaired perfusion in these patients may prevent complete absorption of the drug. With repeated injections, an excessive amount may be absorbed suddenly if normal circulation is reestablished.

The phenylephrine in Endagen-HD 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.

Digoxin has a major potential interaction with Diarrhea.

Potassium and/or magnesium depletion sensitizes the myocardium to digoxin. In patients with hypokalemia or hypomagnesemia, digoxin toxicity may occur despite serum drug concentrations below 2.0 ng/mL. Therapy with digoxin should be administered cautiously in patients with or predisposed to potassium and/or magnesium deficiency, including patients on diuretic therapy; those with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; those with malnutrition; and renal dialysis patients. Electrolyte imbalances should be corrected prior to initiation of treatment. Serum potassium and magnesium concentrations should be monitored during therapy.

The HYDROcodone in Endagen-HD has a major potential interaction with Drug Dependence.

Opiate agonists have the potential to cause dependence and abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use. Abrupt cessation, reduction in dosage, or administration of an opiate antagonist such as naloxone may precipitate withdrawal symptoms. In patients who have developed tolerance to an opiate agonist, overdosage can still produce respiratory depression and death, and cross-tolerance usually will occur with other agents in the class. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with opiate agonists. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of opiate therapy should be undertaken gradually using a dosage-tapering schedule.

Digoxin has a major potential interaction with Electrolyte Abnormalities.

Potassium and/or magnesium depletion sensitizes the myocardium to digoxin. In patients with hypokalemia or hypomagnesemia, digoxin toxicity may occur despite serum drug concentrations below 2.0 ng/mL. Therapy with digoxin should be administered cautiously in patients with or predisposed to potassium and/or magnesium deficiency, including patients on diuretic therapy; those with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; those with malnutrition; and renal dialysis patients. Electrolyte imbalances should be corrected prior to initiation of treatment. Serum potassium and magnesium concentrations should be monitored during therapy.

The HYDROcodone in Endagen-HD has a moderate potential interaction with Gallbladder Disease.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

The HYDROcodone in Endagen-HD has a major potential interaction with Gastrointestinal Obstruction.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

The HYDROcodone in Endagen-HD has a major potential interaction with Gastrointestinal Obstruction.

Opioid analgesics are contraindicated in patients with known or suspected gastrointestinal obstruction, including paralytic ileus.

The chlorpheniramine in Endagen-HD 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 phenylephrine in Endagen-HD 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.

The chlorpheniramine in Endagen-HD 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 HYDROcodone in Endagen-HD has a major potential interaction with Head Injury.

The hypoventilation associated with administration of opiate agonists, particularly by the intravenous route, can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Opiate agonists should not be used in patients with suspected or known head injury or increased intracranial pressure. Also, clinicians treating such patients should be aware that opiate agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

The HYDROcodone in Endagen-HD has a major potential interaction with Head Injury.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

Digoxin has a moderate potential interaction with Heart Attack.

The use of inotropic drugs in some patients with acute myocardial infarction may lead to increases in myocardial oxygen demand and lead to ischemia. Therapy with digoxin should be administered cautiously in these patients.

Digoxin has a major potential interaction with Heart Block.

Digoxin slows sinoatrial and AV conduction, prolonging the PR interval. When treated with digoxin, patients with preexisting sinus node disease may develop severe sinus bradycardia or sinoatrial block, and patients with incomplete AV block may progress to advanced or complete heart block. In such patients, consideration should be given to the insertion of a pacemaker prior to initiating treatment with digoxin. Digoxin may be administered to patients with complete, stable AV block who have congestive heart failure, provided the block was not induced by cardiac glycosides.

Digoxin has a major potential interaction with Hemodialysis.

Potassium and/or magnesium depletion sensitizes the myocardium to digoxin. In patients with hypokalemia or hypomagnesemia, digoxin toxicity may occur despite serum drug concentrations below 2.0 ng/mL. Therapy with digoxin should be administered cautiously in patients with or predisposed to potassium and/or magnesium deficiency, including patients on diuretic therapy; those with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; those with malnutrition; and renal dialysis patients. Electrolyte imbalances should be corrected prior to initiation of treatment. Serum potassium and magnesium concentrations should be monitored during therapy.

Digoxin has a major potential interaction with Hyperaldosteronism.

Potassium and/or magnesium depletion sensitizes the myocardium to digoxin. In patients with hypokalemia or hypomagnesemia, digoxin toxicity may occur despite serum drug concentrations below 2.0 ng/mL. Therapy with digoxin should be administered cautiously in patients with or predisposed to potassium and/or magnesium deficiency, including patients on diuretic therapy; those with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; those with malnutrition; and renal dialysis patients. Electrolyte imbalances should be corrected prior to initiation of treatment. Serum potassium and magnesium concentrations should be monitored during therapy.

Digoxin has a major potential interaction with Hypercalcemia.

Calcium and digoxin have additive inotropic effects. Therefore, hypercalcemia from any cause will predispose patients to digoxin toxicity and serious arrhythmias. Hypercalcemia should be corrected prior to initiating treatment with digoxin, and serum calcium levels should be monitored during therapy.

The phenylephrine in Endagen-HD 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.

Digoxin has a moderate potential interaction with Hyperthyroidism.

Heart failure and/or atrial arrhythmias resulting from hypermetabolic or hyperdynamic states such as hyperthyroidism, hypoxia, or arteriovenous shunt are best managed by treating the underlying condition. Atrial arrhythmias associated with hypermetabolic states are particularly refractory to digoxin, possibly due to altered pharmacokinetics. Specifically, the apparent volume of distribution and renal elimination of the drug may be increased, resulting in lower serum concentrations. Therapy with digoxin should be administered cautiously in patients with hyperthyroidism. Serum digoxin levels should be monitored regularly and dosage adjustments may be required secondary to changes in their thyroid condition.

The chlorpheniramine in Endagen-HD 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.

Digoxin has a major potential interaction with Hypocalcemia.

Hypocalcemia can nullify the effects of digoxin. The drug may be ineffective in hypocalcemic patients until serum calcium levels are restored to normal. Restore serum calcium levels prior to initiating therapy with digoxin to obtain maximum results when using digoxin.

Digoxin has a major potential interaction with Hypokalemia.

Potassium and/or magnesium depletion sensitizes the myocardium to digoxin. In patients with hypokalemia or hypomagnesemia, digoxin toxicity may occur despite serum drug concentrations below 2.0 ng/mL. Therapy with digoxin should be administered cautiously in patients with or predisposed to potassium and/or magnesium deficiency, including patients on diuretic therapy; those with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; those with malnutrition; and renal dialysis patients. Electrolyte imbalances should be corrected prior to initiation of treatment. Serum potassium and magnesium concentrations should be monitored during therapy.

The HYDROcodone in Endagen-HD has a major potential interaction with Hypotension.

Opiate agonists can induce vasodilation and significant hypotension, particularly when given in high dosages and/or by rapid intravenous administration. Opiate analgesics cause vasodilatation that may exacerbate hypotension and hypoperfusion and, therefore, are contraindicated in circulatory shock. At therapeutic analgesic dosages, ambulatory patients are more likely to experience dizziness and hypotension than patients who are confined to bed. However, orthostatic hypotension may occur in supine patients upon rising. Therapy with opiate agonists should be administered cautiously and initiated at reduced dosages in patients with hypovolemia, or a predisposition to hypotension. When given by intramuscular or subcutaneous administration, clinicians should also be aware that impaired perfusion in these patients may prevent complete absorption of the drug. With repeated injections, an excessive amount may be absorbed suddenly if normal circulation is reestablished.

The chlorpheniramine in Endagen-HD 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.

The HYDROcodone in Endagen-HD has a major potential interaction with Infectious Gastroenteritis.

Narcotic (opioid) analgesic agents may prolong and/or worsen diarrhea associated with organisms that invade the intestinal mucosa, such as toxigenic Escherichia coli, Salmonella, Shigella, and pseudomembranous colitis due to broad-spectrum antibiotics. These agents decrease gastrointestinal motility, which may delay the excretion of infective gastroenteric organisms and/or their toxins. Other symptoms and complications such as fever, shedding of organisms, and extraintestinal illness may also be increased or prolonged. Therapy with opioids should be avoided or administered cautiously in patients with infectious diarrhea, particularly that due to pseudomembranous enterocolitis or enterotoxin-producing bacteria or if accompanied by high fever, pus, or blood in the stool.

The HYDROcodone in Endagen-HD has a major potential interaction with Inflammatory Bowel Disease.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

The HYDROcodone in Endagen-HD has a major potential interaction with Intestinal Anastomoses.

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

The chlorpheniramine in Endagen-HD 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.

The HYDROcodone in Endagen-HD has a moderate potential interaction with Liver Disease.

Narcotic (opioid) analgesic agents are extensively metabolized by the liver, and several of them (e.g., codeine, hydrocodone, meperidine, methadone, morphine, propoxyphene) have active metabolites that are further converted to inactive substances. The serum concentrations of these agents and their metabolites may be increased and the half-lives prolonged in patients with impaired hepatic function. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with liver disease. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

Digoxin has a major potential interaction with Magnesium Imbalance.

Potassium and/or magnesium depletion sensitizes the myocardium to digoxin. In patients with hypokalemia or hypomagnesemia, digoxin toxicity may occur despite serum drug concentrations below 2.0 ng/mL. Therapy with digoxin should be administered cautiously in patients with or predisposed to potassium and/or magnesium deficiency, including patients on diuretic therapy; those with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; those with malnutrition; and renal dialysis patients. Electrolyte imbalances should be corrected prior to initiation of treatment. Serum potassium and magnesium concentrations should be monitored during therapy.

Digoxin has a major potential interaction with Malnourishment.

Potassium and/or magnesium depletion sensitizes the myocardium to digoxin. In patients with hypokalemia or hypomagnesemia, digoxin toxicity may occur despite serum drug concentrations below 2.0 ng/mL. Therapy with digoxin should be administered cautiously in patients with or predisposed to potassium and/or magnesium deficiency, including patients on diuretic therapy; those with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; those with malnutrition; and renal dialysis patients. Electrolyte imbalances should be corrected prior to initiation of treatment. Serum potassium and magnesium concentrations should be monitored during therapy.

The HYDROcodone in Endagen-HD has a moderate potential interaction with Pancreatitis.

Opioid agonists may cause spasm of the sphincter of Oddi, which may increase biliary tract pressure. Other opioid-induced effects may include a reduction in biliary and pancreatic secretions and transient elevations in serum amylase. Patients with biliary tract disease (including acute pancreatitis) should be regularly evaluated for worsening symptoms. Therapy with opioids should be administered cautiously in patients with biliary tract disease, gallbladder disease, or acute pancreatitis.

The phenylephrine in Endagen-HD 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.

Digoxin has a major potential interaction with Preexcitation Syndrome.

Digoxin may enhance accessory pathway conduction in conditions such as the Wolff-Parkinson-White syndrome. Patients with Wolf-Parkinson-White syndrome that presents atrial fibrillation are at higher risk for ventricular fibrillation. Treatment with digoxin should be used with caution in these patients.

The HYDROcodone in Endagen-HD has a major potential interaction with Prematurity/Underweight in Infancy.

The use of narcotic (opioid) analgesic agents is contraindicated in premature infants. These agents may cross the immature blood-brain barrier to a greater extent than in adults, resulting in disproportionate respiratory depression.

The phenylephrine in Endagen-HD 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 HYDROcodone in Endagen-HD has a major potential interaction with Pulmonary Impairment.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

Digoxin has a major potential interaction with Renal Dysfunction.

Digoxin is primarily eliminated by the kidney. Patients with renal impairment may be at increased risk for digoxin toxicity, including ventricular arrhythmias and AV conduction disturbances, due to decreased drug clearance. Therapy with digoxin should be administered cautiously in patients with impaired renal function. Dosage adjustments should be made according to product package labeling and patient attributes such as age, ideal body weight, and other concomitant disease states and medication usage. Dosage increments should be made very gradually, since the elimination half-life may be prolonged in these patients and a longer period of time is required to establish steady-state serum concentrations than normal. These patients should be monitored closely for manifestations of toxicity, and dosages further adjusted as necessary. If toxicity occurs, clinicians should be aware that the adverse effects may also be prolonged.

The chlorpheniramine in Endagen-HD 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.

The HYDROcodone in Endagen-HD has a moderate potential interaction with Renal Dysfunction.

Although narcotic (opioid) analgesic agents are generally metabolized by the liver, renal impairment can alter the elimination of these agents and their metabolites (some of which are pharmacologically active), resulting in drug accumulation and increased risk of toxicity. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with significantly impaired renal function. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

The HYDROcodone in Endagen-HD has a major potential interaction with Respiratory Arrest.

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

The HYDROcodone in Endagen-HD has a moderate potential interaction with Seizures.

Narcotic (opioid) analgesic agents may increase the frequency of seizures in patients with seizure disorders, may increase the risk of seizures occurring in other clinical settings associated with seizures, and, at higher dosages, have been reported to induce seizures in patients without history of seizures. Patients with history of seizure disorders should be regularly evaluated for worsened seizure control during therapy. Prolonged meperidine use may increase the risk of toxicity (e.g., seizures) from the accumulation of the active metabolite (normeperidine).

The HYDROcodone in Endagen-HD has a major potential interaction with Shock.

Opiate agonists can induce vasodilation and significant hypotension, particularly when given in high dosages and/or by rapid intravenous administration. Opiate analgesics cause vasodilatation that may exacerbate hypotension and hypoperfusion and, therefore, are contraindicated in circulatory shock. At therapeutic analgesic dosages, ambulatory patients are more likely to experience dizziness and hypotension than patients who are confined to bed. However, orthostatic hypotension may occur in supine patients upon rising. Therapy with opiate agonists should be administered cautiously and initiated at reduced dosages in patients with hypovolemia, or a predisposition to hypotension. When given by intramuscular or subcutaneous administration, clinicians should also be aware that impaired perfusion in these patients may prevent complete absorption of the drug. With repeated injections, an excessive amount may be absorbed suddenly if normal circulation is reestablished.

Digoxin has a major potential interaction with Sinus Node Dysfunction.

Digoxin slows sinoatrial and AV conduction, prolonging the PR interval. When treated with digoxin, patients with preexisting sinus node disease may develop severe sinus bradycardia or sinoatrial block, and patients with incomplete AV block may progress to advanced or complete heart block. In such patients, consideration should be given to the insertion of a pacemaker prior to initiating treatment with digoxin. Digoxin may be administered to patients with complete, stable AV block who have congestive heart failure, provided the block was not induced by cardiac glycosides.

Digoxin has a moderate potential interaction with Underactive Thyroid.

Hypothyroidism may reduce the requirements for digoxin due to decreased volume of distribution and plasma clearance of the drug. Therapy with digoxin should be initiated at lower dosages in patients with hypothyroidism to avoid toxicity. Serum digoxin levels should be monitored regularly and dosage adjustments may be required secondary to changes in thyroid condition.

The HYDROcodone in Endagen-HD has a moderate potential interaction with Urinary Retention.

Narcotic (opioid) analgesic agents may inhibit the urinary voiding reflex and increase the tone of the vesical sphincter in the bladder. Acute urinary retention requiring catheterization may occur, particularly in patients with prostatic hypertrophy or urethral stricture and in older adult patients. These agents may also decrease urine production via direct effects on the kidney and central stimulation of the release of vasopressin. Therapy with opioids should be administered cautiously in patients with or predisposed to urinary retention and/or oliguria. The effects on smooth muscle tone appear to be the most pronounced with morphine.

The chlorpheniramine in Endagen-HD 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.

Digoxin has a major potential interaction with Ventricular Arrhythmia.

The use of digoxin is contraindicated in patients with ventricular fibrillation. Digoxin toxicity is associated with adverse cardiac effects, including ventricular arrhythmias, which are most commonly seen in chronic toxicity. Digoxin-induced ventricular tachycardia is associated with a high mortality rate, since ventricular fibrillation or asystole may result. Therapy with digoxin should be administered cautiously in patients with frequent ventricular premature contractions or ventricular tachycardia, especially if these arrhythmias are not caused by heart failure.

Digoxin has a moderate potential interaction with Vitamin B1 Deficiency.

Patients with beri beri heart disease may fail to respond adequately to digoxin if the underlying thiamine deficiency is not treated concomitantly.

Digoxin has a major potential interaction with Vomiting.

Potassium and/or magnesium depletion sensitizes the myocardium to digoxin. In patients with hypokalemia or hypomagnesemia, digoxin toxicity may occur despite serum drug concentrations below 2.0 ng/mL. Therapy with digoxin should be administered cautiously in patients with or predisposed to potassium and/or magnesium deficiency, including patients on diuretic therapy; those with primary or secondary aldosteronism (may have low potassium levels); those with severe or prolonged diarrhea or vomiting; those with malnutrition; and renal dialysis patients. Electrolyte imbalances should be corrected prior to initiation of treatment. Serum potassium and magnesium concentrations should be monitored during therapy.