Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content +++ INTRODUCTION ++ Urinary incontinence (UI) is the complaint of involuntary leakage of urine. +++ PATHOPHYSIOLOGY ++ The urethral sphincter, a combination of smooth and striated muscles within and external to the urethra, maintains adequate resistance to the flow of urine from the bladder until voluntary voiding is initiated. Volitional and involuntary bladder contractions are mediated by activation of postsynaptic muscarinic receptors by acetylcholine. Bladder smooth muscle cholinergic receptors are mainly of the M2 variety; however, M3 receptors are responsible for both emptying contraction of normal micturition and involuntary bladder contractions, which can result in UI. Therefore, most pharmacologic antimuscarinic therapy is anti-M3 based. UI occurs as a result of overactivity or underactivity of the urethra, bladder, or both. Urethral underactivity is known as stress UI (SUI) and occurs during activities such as exercise, running, lifting, coughing, and sneezing. The urethral sphincter no longer resists the flow of urine from the bladder during periods of physical activity. Bladder overactivity is known as urge UI (UUI) and is associated with increased urinary frequency and urgency, with or without urge incontinence. The detrusor muscle is overactive and contracts inappropriately during the filling phase. Urethral overactivity and/or bladder underactivity is known as overflow incontinence. The bladder is filled to capacity but is unable to empty, causing urine to leak from a distended bladder past a normal outlet and sphincter. Common causes of urethral overactivity include benign prostatic hyperplasia (see Chap. 79); prostate cancer (see Chap. 64); and, in women, cystocele formation or surgical overcorrection after SUI surgery. Mixed incontinence includes the combination of bladder overactivity and urethral underactivity. Functional incontinence is not caused by bladder- or urethra-specific factors but rather occurs in patients with conditions such as cognitive or mobility deficits. Many medications may precipitate or aggravate voiding dysfunction and UI (Table 81–1). ++Table Graphic Jump LocationTABLE 81–1Medications That Influence Lower Urinary Tract FunctionView Table||Download (.pdf) TABLE 81–1 Medications That Influence Lower Urinary Tract Function Medication Effect Diuretics, acetylcholinesterase inhibitors Polyuria resulting in urinary frequency, urgency α-Receptor antagonists Urethral muscle relaxation and stress urinary incontinence α-Receptor agonists Urethral muscle contraction (increased urethral closure forces) resulting in urinary retention (more common in men) Calcium channel blockers Urinary retention due to reduced bladder contractility Narcotic analgesics Urinary retention due to reduced bladder contractility Sedative hypnotics Functional incontinence caused by delirium, immobility Antipsychotic agents Anticholinergic effects resulting in reduced bladder contractility and urinary retention Anticholinergics Urinary retention due to reduced bladder contractility Antidepressants, tricyclic Anticholinergic effects resulting in reduced bladder contractility, and α-antagonist effects resulting in urethral smooth muscle contraction (increased urethral closure forces) both contributing to urinary retention Alcohol Polyuria resulting in urinary frequency, urgency ACEIs Cough as a result of ACEIs may aggravate stress urinary incontinence (ACEIs, angiotensin-converting enzyme inhibitors.) +++ CINICAL PRESENTATION ++ Signs and symptoms of UI depend on ... Your MyAccess profile is currently affiliated with '[InstitutionA]' and is in the process of switching affiliations to '[InstitutionB]'. Please click ‘Continue’ to continue the affiliation switch, otherwise click ‘Cancel’ to cancel signing in. Get Free Access Through Your Institution Learn how to see if your library subscribes to McGraw Hill Medical products. Subscribe: Institutional or Individual Sign In Username Error: Please enter User Name Password Error: Please enter Password Forgot Username? Forgot Password? Sign in via OpenAthens Sign in via Shibboleth