Interactions between Isosorbide dinitrate and Oxydose

The oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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.

Isosorbide dinitrate has a major potential interaction with Anemia.

Some manufacturers and medical references consider the use of nitrates and nitrites to be contraindicated in patients with severe anemia. Nitrates and nitrites can cause methemoglobinemia, primarily in high-dose intravenous therapy or acute poisoning and in patients with NADH reductase deficiency. However, elevations of methemoglobin may also occur with commonly used dosages. While probably not of routine clinical significance, the increases may be important in certain patient populations such as those with coronary insufficiency or anemia.

Isosorbide dinitrate has a major potential interaction with Aortic Stenosis.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.

The oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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.

Isosorbide dinitrate has a major potential interaction with Brain Tumor.

Organic nitrates and nitrites can increase cerebrospinal fluid pressure. Therapy with these agents should be administered cautiously, if at all, in patients with or at risk for intracranial hypertension, including those with cerebral hemorrhage, intracranial lesions, or recent head trauma.

The oxyCODONE in Oxydose 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.

The oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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.

Isosorbide dinitrate has a major potential interaction with Cerebrovascular Insufficiency.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.

The oxyCODONE in Oxydose 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.

Isosorbide dinitrate has a major potential interaction with Constrictive Pericarditis.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.

Isosorbide dinitrate has a major potential interaction with Dehydration.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.

The oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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.

The oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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 oxyCODONE in Oxydose has a major potential interaction with Gastrointestinal Obstruction.

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

Isosorbide dinitrate has a minor potential interaction with Glaucoma/Intraocular Hypertension.

Some medical references state that organic nitrates and nitrites may increase intraocular pressure and should be used with caution in patients with glaucoma. However, the effect on intraocular pressure is variable and brief, and there is no evidence that these drugs precipitate narrow-angle glaucoma. Amyl nitrate typically may cause a slight rise of 3+ mm for several seconds followed by a fall in intraocular pressure for 10 to 20 minutes, the latter secondary to a fall in blood pressure. Nitroglycerin rarely produces ocular side effects, and oral nitroglycerin appears to have few to no significant ocular side effects.

Isosorbide dinitrate has a major potential interaction with Head Injury.

Organic nitrates and nitrites can increase cerebrospinal fluid pressure. Therapy with these agents should be administered cautiously, if at all, in patients with or at risk for intracranial hypertension, including those with cerebral hemorrhage, intracranial lesions, or recent head trauma.

The oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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.

Isosorbide dinitrate has a major potential interaction with Heart Attack.

The benefits of organic nitrates and nitrites in patients with acute myocardial infarction (AMI) or congestive heart failure have not been established and its use is not recommended in these settings. If used, it should be accompanied by careful clinical and hemodynamic monitoring to avoid the hazards of systemic hypotension and tachycardia, which in AMI can exacerbate myocardial ischemia. In general, oral or long-acting formulations of these drugs should not be used in the early management of AMI because of the difficulty in precisely controlling and rapidly terminating their hemodynamic effects should adverse reactions occur. Sublingual and other immediate- onset nitrates or nitrites should typically be avoided in suspected AMI with marked bradycardia or tachycardia, and should be used with extreme caution, if at all, in patients with right ventricular or inferior wall infarction. Rarely, sublingual nitroglycerin has produced hypotension accompanied by paradoxical bradycardia in patients with AMI and especially right ventricular infarction. The latter group of patients are also particularly dependent on adequate right ventricular preload to maintain cardiac output and can experience profound hypotension with nitrate or nitrite administration due to reduction of right ventricular preload.

Isosorbide dinitrate has a major potential interaction with Heart Failure.

The benefits of organic nitrates and nitrites in patients with acute myocardial infarction (AMI) or congestive heart failure have not been established and its use is not recommended in these settings. If used, it should be accompanied by careful clinical and hemodynamic monitoring to avoid the hazards of systemic hypotension and tachycardia, which in AMI can exacerbate myocardial ischemia. In general, oral or long-acting formulations of these drugs should not be used in the early management of AMI because of the difficulty in precisely controlling and rapidly terminating their hemodynamic effects should adverse reactions occur. Sublingual and other immediate- onset nitrates or nitrites should typically be avoided in suspected AMI with marked bradycardia or tachycardia, and should be used with extreme caution, if at all, in patients with right ventricular or inferior wall infarction. Rarely, sublingual nitroglycerin has produced hypotension accompanied by paradoxical bradycardia in patients with AMI and especially right ventricular infarction. The latter group of patients are also particularly dependent on adequate right ventricular preload to maintain cardiac output and can experience profound hypotension with nitrate or nitrite administration due to reduction of right ventricular preload.

Isosorbide dinitrate has a major potential interaction with Hemodialysis.

The combined effect of organic nitrates or nitrites with hemodialysis, which often lowers blood pressure, can cause life-threatening hypotension. Therapy with these agents should be administered cautiously in patients requiring hemodialysis. The medication should be withheld before undergoing dialysis, and hemodynamic stability should be established prior to resumption of medication following dialysis. Nitroglycerin and isosorbide dinitrate are moderately dialyzed.

Isosorbide dinitrate has a major potential interaction with Hemorrhagic Stroke.

Organic nitrates and nitrites can increase cerebrospinal fluid pressure. Therapy with these agents should be administered cautiously, if at all, in patients with or at risk for intracranial hypertension, including those with cerebral hemorrhage, intracranial lesions, or recent head trauma.

Isosorbide dinitrate has a moderate potential interaction with Hypertrophic Cardiomyopathy.

Organic nitrates and nitrites may aggravate the angina associated with hypertrophic cardiomyopathy and should be administered cautiously in patients with this condition.

Isosorbide dinitrate has a major potential interaction with Hypotension.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.

The oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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.

The oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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.

Isosorbide dinitrate has a major potential interaction with Pseudotumor Cerebri.

Organic nitrates and nitrites can increase cerebrospinal fluid pressure. Therapy with these agents should be administered cautiously, if at all, in patients with or at risk for intracranial hypertension, including those with cerebral hemorrhage, intracranial lesions, or recent head trauma.

The oxyCODONE in Oxydose 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.

The oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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 oxyCODONE in Oxydose 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).

Isosorbide dinitrate has a major potential interaction with Shock.

Organic nitrates and nitrites may cause severe hypotension, syncope and shock, even with small doses. Hypotension induced by these agents may be accompanied by paradoxical bradycardia and increased angina pectoris. Therapy with nitrates and nitrites should be administered cautiously in patients who are volume-depleted or hypotensive (e.g., systolic blood pressure <90 mm Hg) or who, because of inadequate circulation to the brain or to other vital organs, would be unusually compromised by undue hypotension. Patients should be in a sitting or recumbent position during and immediately after drug administration, and monitored for symptoms of severe hypotension such as nausea, vomiting, weakness, pallor, perspiration, and syncope. Nitrate or nitrite therapy is considered contraindicated in patients with acute circulatory failure or shock.

The oxyCODONE in Oxydose 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.

The oxyCODONE in Oxydose 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.