Can you take Aspirin with Nitro-Bid IV?

Aspirin has a major potential interaction with Alcoholism.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

The nitroglycerin in Nitro-Bid IV 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.

Aspirin has a moderate potential interaction with Anemia.

Occult, often asymptomatic GI blood loss occurs quite frequently with the use of normal dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. Other salicylates reportedly cause little or no GI blood loss at usual dosages, but may do so at high dosages. Prolonged therapy with salicylates, particularly aspirin, should be administered cautiously in patients with or predisposed to anemia. Periodic monitoring of hematocrit is recommended. The same precautions should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

The nitroglycerin in Nitro-Bid IV 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.

Aspirin has a major potential interaction with Asthma.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are contraindicated in patients with history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other NSAIDs; severe, sometimes fatal, anaphylactic reactions to NSAIDs have been reported in such patients. A subpopulation of patients with asthma may have aspirin-sensitive asthma which may include chronic rhinosinusitis complicated by nasal polyps, severe potentially fatal bronchospasm, and/or intolerance to aspirin and other NSAIDs. Since cross-reactivity between aspirin and other NSAIDs has been reported in such aspirin-sensitive patients, therapy with any NSAID should be avoided in patients with this form of aspirin sensitivity. NSAIDs should be used with caution in patients with preexisting asthma (without known aspirin sensitivity), and these patients should be monitored for changes in the signs and symptoms of asthma.

Aspirin has a major potential interaction with Bleeding Disorder.

The use of aspirin is contraindicated in patients with significant active bleeding or hemorrhagic disorders such as hemophilia, von Willebrand's disease, or telangiectasia. Aspirin interferes with coagulation by irreversibly inhibiting platelet aggregation and prolonging bleeding time. The non-aceylated salicylates (i.e. salicylate salts such as sodium or magnesium salicylate) do not demonstrate these effects and may be appropriate substitutions in these patients. However, all salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially aspirin, should be administered with extreme caution in patients with hypoprothrombinemia, vitamin K deficiency, thrombocytopenia, thrombotic thrombocytopenic purpura, severe hepatic impairment, or anticoagulant use.

The nitroglycerin in Nitro-Bid IV 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 nitroglycerin in Nitro-Bid IV 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.

Aspirin has a major potential interaction with Coagulation Defects and Disorders.

The use of aspirin is contraindicated in patients with significant active bleeding or hemorrhagic disorders such as hemophilia, von Willebrand's disease, or telangiectasia. Aspirin interferes with coagulation by irreversibly inhibiting platelet aggregation and prolonging bleeding time. The non-aceylated salicylates (i.e. salicylate salts such as sodium or magnesium salicylate) do not demonstrate these effects and may be appropriate substitutions in these patients. However, all salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially aspirin, should be administered with extreme caution in patients with hypoprothrombinemia, vitamin K deficiency, thrombocytopenia, thrombotic thrombocytopenic purpura, severe hepatic impairment, or anticoagulant use.

Aspirin has a major potential interaction with Colonic Ulceration.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

The nitroglycerin in Nitro-Bid IV 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.

The nitroglycerin in Nitro-Bid IV has a major potential interaction with Constrictive Pericarditis.

The use of intravenous nitroglycerin is contraindicated in patients with constrictive pericarditis, pericardial tamponade, or restrictive cardiomyopathy. In these patients, cardiac output is dependent upon venous return, which can be reduced by nitroglycerin due to venous pooling. Also, nitroglycerin-induced hypotension may lead to paradoxical bradycardia and increased angina pectoris.

The nitroglycerin in Nitro-Bid IV 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.

Aspirin has a moderate potential interaction with G-6-PD Deficiency.

Salicylates, particularly aspirin, may cause or aggravate hemolysis in patients with pyruvate kinase or glucose-6-phosphate dehydrogenase (G-6-PD) deficiency. However, this effect has not been clearly established. Until more data are available, therapy with salicylates should be administered cautiously in patients with G-6-PD deficiency. The same precaution should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate.

Aspirin has a major potential interaction with Gastritis/Duodenitis.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

Aspirin has a major potential interaction with Gastrointestinal Hemorrhage.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

Aspirin has a major potential interaction with Gastrointestinal Perforation.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

The nitroglycerin in Nitro-Bid IV 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.

The nitroglycerin in Nitro-Bid IV 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 nitroglycerin in Nitro-Bid IV 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.

The nitroglycerin in Nitro-Bid IV 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.

The nitroglycerin in Nitro-Bid IV 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.

Aspirin has a moderate potential interaction with Hemodialysis.

Salicylate and its metabolites are readily removed by hemodialysis and, to a lesser extent, by peritoneal dialysis. Doses should either be scheduled for administration after dialysis or supplemental doses be given after dialysis.

The nitroglycerin in Nitro-Bid IV 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.

Aspirin has a major potential interaction with History, Peptic Ulcer.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

The nitroglycerin in Nitro-Bid IV 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.

The nitroglycerin in Nitro-Bid IV 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.

Aspirin has a major potential interaction with Influenza.

The use of salicylates, primarily aspirin, in children with varicella infections or influenza-like illnesses has been associated with an increased risk of Reye's syndrome. Although a causal relationship has not been established, the majority of evidence to date seems to support the association. Most authorities, including the American Academy of Pediatrics Committee on Infectious Diseases, recommend avoiding the use of salicylates in children and teenagers with known or suspected varicella or influenza and during presumed outbreaks of influenza. If antipyretic or analgesic therapy is indicated under these circumstances, acetaminophen may be an appropriate alternative. The same precautions should also be observed with related agents such as salicylamide or diflunisal because of their structural and pharmacological similarities to salicylate.

Aspirin has a moderate potential interaction with Liver Disease.

The use of salicylates has occasionally been associated with acute, reversible hepatotoxicity, primarily manifested as elevations of serum transaminases, alkaline phosphatase and/or, rarely, bilirubin. Hepatic injury consistent with chronic active hepatitis has also been reported in a few patients, which resulted rarely in encephalopathy or death. Salicylate-induced hepatotoxicity appears to be dependent on serum salicylate concentration (> 25 mg/dL) and has occurred most frequently in patients with juvenile arthritis, active systemic lupus erythematosus, rheumatic fever, or preexisting hepatic impairment. Therapy with salicylates, particularly when given in high dosages, should be administered cautiously in these patients, and periodic monitoring of liver function is recommended. The same precautions should also be observed with the use of related agents such as salicylamide because of their structural and pharmacological similarities to salicylate. A dosage reduction may be necessary if liver function abnormalities develop and serum salicylate concentration exceeds 25 mg/dL, although serum transaminase elevations may sometimes be transient and return to pretreatment values despite continued therapy without dosage adjustment.

Aspirin has a major potential interaction with Noninfectious Colitis.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

Aspirin has a major potential interaction with Peptic Ulcer.

Salicylates, particularly aspirin, can cause dose-related gastrointestinal bleeding and mucosal damage, which may occur independently of each other. Occult, often asymptomatic GI blood loss is quite common with usual dosages of aspirin and stems from the drug's local effect on the GI mucosa. During chronic therapy, this type of bleeding may occasionally produce iron deficiency anemia. In contrast, major upper GI bleeding rarely occurs except in patients with active peptic ulcers or recent GI bleeding. However, these patients generally do not experience greater occult blood loss than healthy patients following small doses of aspirin. Mucosal damage associated with the use of salicylates may lead to development of peptic ulcers with or without bleeding, reactivation of latent ulcers, and ulcer perforation. Therapy with salicylates and related agents such as salicylamide should be considered and administered cautiously in patients with a history of GI disease or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than other individuals. Extreme caution and thorough assessment of risks and benefits are warranted in patients with active or recent GI bleeding or lesions. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If salicylates are used, close monitoring for toxicity is recommended. Some adverse GI effects may be minimized by administration with high dosages of antacids, use of enteric-coated or extended-release formulations, and/or concurrent use of a histamine H2-receptor antagonist or a cytoprotective agent such as misoprostol. Patients with active peptic ulceration or GI bleeding treated with salicylates should generally be administered a concomitant anti-ulcer regimen.

The nitroglycerin in Nitro-Bid IV has a major potential interaction with Pericardial Tamponade.

The use of intravenous nitroglycerin is contraindicated in patients with constrictive pericarditis, pericardial tamponade, or restrictive cardiomyopathy. In these patients, cardiac output is dependent upon venous return, which can be reduced by nitroglycerin due to venous pooling. Also, nitroglycerin-induced hypotension may lead to paradoxical bradycardia and increased angina pectoris.

The nitroglycerin in Nitro-Bid IV 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.

Aspirin has a major potential interaction with Renal Dysfunction.

Salicylate and its metabolites are eliminated almost entirely by the kidney. Therapy with salicylate drugs should be administered cautiously in patients with renal impairment, especially if it is severe. Reduced dosages may be necessary to avoid drug accumulation. Clinical monitoring of renal function is recommended during prolonged therapy, since the use of salicylate drugs has rarely been associated with renal toxicities, including elevations in serum creatinine, renal papillary necrosis, and acute tubular necrosis with renal failure. Most of the data have been derived from experience with aspirin but may apply to other salicylates as well. In patients with impaired renal function, aspirin has caused reversible and sometimes marked decreases in renal blood flow and glomerular filtration rate. Adverse renal effects have usually reversed rapidly following withdrawal of aspirin therapy.

The nitroglycerin in Nitro-Bid IV has a major potential interaction with Restrictive Cardiomyopathy.

The use of intravenous nitroglycerin is contraindicated in patients with constrictive pericarditis, pericardial tamponade, or restrictive cardiomyopathy. In these patients, cardiac output is dependent upon venous return, which can be reduced by nitroglycerin due to venous pooling. Also, nitroglycerin-induced hypotension may lead to paradoxical bradycardia and increased angina pectoris.

The nitroglycerin in Nitro-Bid IV 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.

Aspirin has a major potential interaction with Thrombocytopathy.

The use of aspirin is contraindicated in patients with significant active bleeding or hemorrhagic disorders such as hemophilia, von Willebrand's disease, or telangiectasia. Aspirin interferes with coagulation by irreversibly inhibiting platelet aggregation and prolonging bleeding time. The non-aceylated salicylates (i.e. salicylate salts such as sodium or magnesium salicylate) do not demonstrate these effects and may be appropriate substitutions in these patients. However, all salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially aspirin, should be administered with extreme caution in patients with hypoprothrombinemia, vitamin K deficiency, thrombocytopenia, thrombotic thrombocytopenic purpura, severe hepatic impairment, or anticoagulant use.

Aspirin has a major potential interaction with Thrombocytopenia.

The use of aspirin is contraindicated in patients with significant active bleeding or hemorrhagic disorders such as hemophilia, von Willebrand's disease, or telangiectasia. Aspirin interferes with coagulation by irreversibly inhibiting platelet aggregation and prolonging bleeding time. The non-aceylated salicylates (i.e. salicylate salts such as sodium or magnesium salicylate) do not demonstrate these effects and may be appropriate substitutions in these patients. However, all salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially aspirin, should be administered with extreme caution in patients with hypoprothrombinemia, vitamin K deficiency, thrombocytopenia, thrombotic thrombocytopenic purpura, severe hepatic impairment, or anticoagulant use.

Aspirin has a major potential interaction with Varicella-Zoster.

The use of salicylates, primarily aspirin, in children with varicella infections or influenza-like illnesses has been associated with an increased risk of Reye's syndrome. Although a causal relationship has not been established, the majority of evidence to date seems to support the association. Most authorities, including the American Academy of Pediatrics Committee on Infectious Diseases, recommend avoiding the use of salicylates in children and teenagers with known or suspected varicella or influenza and during presumed outbreaks of influenza. If antipyretic or analgesic therapy is indicated under these circumstances, acetaminophen may be an appropriate alternative. The same precautions should also be observed with related agents such as salicylamide or diflunisal because of their structural and pharmacological similarities to salicylate.

Aspirin has a major potential interaction with Vitamin K Deficiency.

The use of aspirin is contraindicated in patients with significant active bleeding or hemorrhagic disorders such as hemophilia, von Willebrand's disease, or telangiectasia. Aspirin interferes with coagulation by irreversibly inhibiting platelet aggregation and prolonging bleeding time. The non-aceylated salicylates (i.e. salicylate salts such as sodium or magnesium salicylate) do not demonstrate these effects and may be appropriate substitutions in these patients. However, all salicylates can interfere with the action of vitamin K and induce a dose-dependent alteration in hepatic synthesis of coagulation factors VII, IX and X. At usual recommended dosages, a slight increase in prothrombin time (PT) may occur. Therapy with salicylates, especially aspirin, should be administered with extreme caution in patients with hypoprothrombinemia, vitamin K deficiency, thrombocytopenia, thrombotic thrombocytopenic purpura, severe hepatic impairment, or anticoagulant use.