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 81–1Medications That Influence Lower Urinary Tract Function |Favorite 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 |
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