Urinary incontinence (UI) is the involuntary loss of urine that is objectively demonstrable and constitutes a social or hygienic problem. Understanding the pathophysiology of each type is essential for accurate diagnosis and targeted management. Stress urinary incontinence (SUI) results from inadequate urethral closure pressure during activities that increase intra-abdominal pressure (coughing, sneezing, laughing, lifting, exercise). The pathophysiology involves two mechanisms: urethral hypermobility (loss of anatomic support from weakened pelvic floor muscles and endopelvic fascia, allowing the urethra to descend during straining so the pressure transmission to the urethra is lost) and intrinsic sphincter deficiency (ISD — weakened urethral sphincter that cannot maintain closure even without hypermobility). Risk factors include vaginal delivery (especially traumatic, forceps-assisted, or with large birth weight), pelvic surgery, estrogen deficiency (postmenopausal atrophy of urethral mucosa), chronic cough, and obesity. Urge urinary incontinence (UUI) or overactive bladder (OAB) results from detrusor overactivity — involuntary detrusor muscle contractions during bladder filling that the patient cannot suppress. The pathophysiology involves disruption of the normal balance between excitatory (cholinergic/muscarinic M2 and M3 receptors) and inhibitory neural pathways controlling detrusor function. Causes...