Overactive Bladder Pharmacotherapy
Detrusor Overactivity & Storage LUTS — Antimuscarinics (M₃-selectivity & anticholinergic burden), β₃-Agonists (Mirabegron, Vibegron), Intravesical OnabotulinumtoxinA, Combination Therapy; Bethanechol for the Underactive Bladder & Desmopressin for Nocturia
Introduction & terminology
- Overactive bladder (OAB) — a symptom syndrome of urinary urgency, usually with frequency and nocturia, with or without urgency urinary incontinence (UUI), in the absence of UTI or obvious pathology — mapping mechanistically onto detrusor overactivity during the storage phase.
- Urgency — the sudden compelling desire to void that is difficult to defer — the cornerstone symptom distinguishing OAB from simple frequency.
- UUI vs stress incontinence — UUI is leakage preceded by urgency; it contrasts with stress incontinence (leakage on effort — a sphincteric/anatomical problem). Antimuscarinics & β3-agonists treat the urgency/UUI component, not stress leakage.
- Therapeutic aim — drugs act during storage to lower intravesical pressure, increase functional bladder capacity, reduce uninhibited detrusor contractions and alter filling sensation.
- Aetiological subtypes — idiopathic (majority, no neurological cause) vs neurogenic detrusor overactivity (suprapontine/suprasacral lesions — stroke, MS, spinal-cord injury, spina bifida). Both respond to antimuscarinics; the neurogenic group is the classical target for intravesical and higher-dose strategies. (KDT uses the older labels detrusor instability / hyperreflexia.)
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Overactive Bladder Pharmacotherapy
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