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MD Pharmacology NMC syllabus ~5 min read Recent advances last updated on 2026-06-30

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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