Anticholinergic drugs urinary tract

Drug therapy may also cause renal insufficiency due to lower urinary tract obstruction. Ureteral obstruction can be caused by calculi or retroperitoneal fibrosis. Bladder dysfunction with urinary outflow obstruction can result, particularly in males with prostatic hypertrophy, from anticholinergic drugs including tricyclic antidepressants and disopyramide. Bladder outlet and ureteral obstruction may result from bladder fibrosis following hemorrhagic cystitis with cyclophosphamide or ifosfamide therapy. Concurrent treatment with mesna can prevent cystitis and this complication. 

Urinary tract Drug-induced urinary retention has been reviewed, emphasizing the anticholinergic activity of some antipsychotic drugs [56" ]. 

Disopyramide phosphate is used orally for the treatment of certain ventricular and atrial arrhythmias. Despite its structural dissimilarity to procainamide (Fig. 26.10), its cardiac effects are very similar. Disopyramide is rapidly and completely absorbed from the gastrointestinal tract. Peak plasma level is usually reached within 1 to 3 hours, and a plasma half-life of 5 to 7 hours is common. Approximately half of an oral dose is excreted unchanged in the urine. The remaining drug undergoes hepatic metabolism, principally to the corresponding N-dealkylated form. This metabolite retains approximately half the antiarrhythmic activity of disopyramide and also is subject to renal excretion. Adverse effects of disopyramide frequently are observed. These effects are primarily anticholinergic in nature and include dry mouth, blurred vision, constipation, and urinary retention. 

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