Uro-MP Disease Interactions

Agents with anticholinergic activity can exacerbate many of the manifestations of autonomic neuropathy, including tachycardia, anhidrosis, bladder atony, obstipation, dry mouth and eyes, cycloplegia and blurring of vision, and sexual impotence in males. Therapy with antimuscarinic agents and higher dosages of antispasmodic agents (e.g., dicyclomine or oxybutynin) should be administered cautiously in patients with autonomic neuropathy.

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Anticholinergics are contraindicated in patients with obstructive diseases such as achalasia, esophageal stricture or stenosis, pyloroduodenal stenosis, stenosing peptic ulcer, pyloric obstruction, and paralytic ileus. Anticholinergics may further suppress intestinal motility with resultant precipitation or aggravation of toxic megacolon.

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Anticholinergic agents are contraindicated in patients with primary glaucoma, a tendency toward glaucoma (narrow anterior chamber angle), or adhesions (synechiae) between the iris and lens, as well as for the elderly and others in whom undiagnosed glaucoma or excessive pressure in the eye may be present. Because anticholinergics cause mydriasis, they may exacerbate these conditions.

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In general, the use of anticholinergic agents is contraindicated in patients with urinary retention and bladder neck obstruction caused by prostatic hypertrophy. Dysuria may occur and may require catheterization. Also, anticholinergic drugs may aggravate partial obstructive uropathy. Caution is advised even when using agents with mild to moderate anticholinergic activity, particularly in elderly patients.

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The use of systemic anticholinergics is contraindicated in the treatment of lower respiratory tract symptoms including asthma. Muscarinic receptor antagonists reduce bronchial secretions, which can result in decreased fluidity and increased thickening of secretions. However, ipratropium does not produce these effects and can be used safely in treating asthma.

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Because antimuscarinic agents have anticholinergic effects, they are contraindicated in patients with myasthenia gravis. Their use may be appropriate to reduce adverse muscarinic effects caused by an anticholinesterase agent.

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The use of drugs with antiperistaltic activity (primarily antidiarrheal and antimuscarinic agents, but also antispasmodic agents such as dicyclomine or oxybutynin at high dosages) is contraindicated in patients with diarrhea due to pseudomembranous enterocolitis or enterotoxin-producing bacteria. These drugs may prolong and/or worsen diarrhea associated with organisms that invade the intestinal mucosa, such as toxigenic E. coli, Salmonella and Shigella, and pseudomembranous colitis due to broad-spectrum antibiotics. Other symptoms and complications such as fever, shedding of organisms and extraintestinal illness may also be increased or prolonged. In general, because antiperistaltic agents decrease gastrointestinal motility, they may delay the excretion of infective gastroenteric organisms or toxins and should be used cautiously in patients with any infectious diarrhea, particularly if accompanied by high fever or pus or blood in the stool. Some cough and cold and other combination products may occasionally include antimuscarinic agents for their drying effects and may, therefore, require careful selection when necessary.

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The use of laxatives is contraindicated in patients with inflammatory bowel disease. Patients with inflammatory bowel disease may experience colonic perforation with use of stimulant laxatives.

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The use of laxatives is contraindicated in patients with intestinal obstruction disorders. Patients with intestinal obstruction disorders may need their underlying condition treated to correct the constipation. Some laxatives require reduction in the colon to their active form to be effective which may be a problem in patients with intestinal obstruction.

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The use of methenamine salts (i.e. methenamine hippurate or mandelate), but not the base, is contraindicated in patients with severe renal impairment or dehydration. Methenamine is excreted by the kidney and concentrated in the urine. In patients with low urinary output, the salts can precipitate and cause crystalluria.

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Methenamine mandelate (salts), should be avoided in patients with gout as it may precipitate urate crystals in their urine. A similar situation may arise in patients with a predisposition to the formation of uric acid stones.

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The use of methenamine and its salts (i.e. methenamine hippurate or mandelate) is contraindicated in patients with severe hepatic impairment. Methenamine is hydrolyzed to ammonia and formaldehyde in the urine under acidic conditions. Patients with liver disease may already have elevated ammonia levels, which can cause or exacerbate hepatic encephalopathy. Methenamine hippurate has also been associated with isolated cases of transient elevations in serum transaminases. The manufacturer recommends periodic liver function tests during therapy, particularly in patients with preexisting liver dysfunction.

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The use of methylene blue is contraindicated for the treatment of methemoglobinemia in patients with glucose-6-phosphate deficiency (G-6-PD). Methylene blue will not reverse the condition in patients with G-6-PD and may precipitate acute hemolysis in these patients.

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The use of phosphates is in general contraindicated in conditions where high potassium, high phosphate, or low calcium may be encountered such as hypoparathyroidism, osteomalacia, acute pancreatitis, or chronic renal disease.

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Therapy with phosphates should be administered with extreme caution in patients with hyperphosphatemia (hypoparathyroidism or severe renal impairment). Elevated serum concentrations of phosphate and calcium can exceed the solubility level and result in calcium-phosphate precipitates that deposit in vascular and renal systems as well as other soft tissues of the body. Clinical monitoring of serum calcium and phosphate concentrations is necessary.

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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.

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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.

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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.

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The use of sodium phosphates is contraindicated in patients with congenital megacolon, intestinal obstruction, imperforate anus, active inflammatory disease or congestive heart failure. Serious, potentially life-threatening electrolyte imbalance such as hypocalcemia and hyperphosphatemia can result with prolonged or excessive use of phosphate laxatives. Hypernatremia and dehydration can occur due to improper dilution of hypertonic saline laxatives. Therapy with sodium phosphates should be administered cautiously and frequency of administration limited in patients with renal dysfunction, colostomy, cardiac dysfunction, or electrolyte imbalance. Clinical monitoring of electrolyte concentrations is recommended.

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Anticholinergics block vagal inhibition of the SA nodal pacemaker. Therapy with anticholinergics should be administered cautiously to patients with tachycardia, congestive heart failure, or coronary artery disease. Premature ventricular depolarization, ventricular tachycardia, and fibrillation associated with anticholinergics are rare.

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Anticholinergics block vagal inhibition of the SA nodal pacemaker. Therapy with anticholinergics should be administered cautiously in patients with tachycardia, congestive heart failure, or coronary artery disease. Premature ventricular depolarization or ventricular tachycardia or fibrillation associated with anticholinergics is rare.

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Antimuscarinic agents block vagal inhibition of the SA nodal pacemaker. These agents should be administered cautiously in patients with tachycardia, congestive heart failure, or coronary artery disease. Premature ventricular depolarization or ventricular tachycardia or fibrillation associated with antimuscarinic drugs is rare.

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Antimuscarinic agents may cause a delay in gastric emptying and possibly antral stasis in patients with gastric ulcer. Therapy with antimuscarinic agents should be administered cautiously to patients with gastric ulcer.

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Antimuscarinic agents decrease gastric motility and relax the lower esophageal sphincter which promotes gastric retention and can aggravate reflux. These drugs should be administered cautiously in patients with gastroesophageal reflux or hiatal hernia associated with reflux esophagitis.

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Antimuscarinic agents may suppress intestinal motility and produce paralytic ileus with resultant precipitation of toxic megacolon. These drugs should be administered cautiously to patients with ulcerative colitis.

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Atropine-like agents undergo significant hepatic metabolism. Therapy with atropine-like agents should be administered cautiously to patients with liver disease.

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Atropine-like agents are primarily eliminated by the kidney. Therapy with atropine-like agents should be administered cautiously to patients with renal disease.

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Methylene blue is reduced in tissues to leukomethylene blue, and both are excreted by the kidney. The serum concentrations of methylene blue and leukomethylene blue may be increased in patients with impaired renal function. Therapy with methylene blue should be avoided in patients with severe renal impairment and administered cautiously in patients with mild to moderate renal impairment. Dosage adjustments may be necessary.

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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.

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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 if given in high dosages, should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. 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.

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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.

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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.

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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.

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Cardiovascular effects of anticholinergics may exacerbate hypertension. Therapy with anticholinergic agents should be administered cautiously in patients with hypertension.

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In general, agents with anticholinergic activity may exacerbate hyperthyroidism. Therapy with anticholinergics should be administered cautiously in patients with hyperthyroidism. Thyroid levels should be monitored if usage is prolonged.

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Diarrhea may be a symptom of incomplete intestinal obstruction, especially in patients with ileostomy or colostomy. Antimuscarinic agents may further aggravate the diarrhea. Therefore, these drugs should be administered cautiously in patients with diarrhea.

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Atropine-like agents may increase the risk of hyperthermia in patients with fever by producing anhidrosis. Therapy with atropine-like agents should be administered cautiously in febrile patients.

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