BPH pathogenesis centers on DHT-mediated androgen receptor signaling within the prostate transition zone. Testosterone enters prostatic cells and is converted to DHT by 5-alpha reductase (type II predominates in prostate). DHT binds androgen receptors, forming homodimers that translocate to the nucleus and activate transcription of genes promoting growth (PSA, cell survival, proliferation pathways). Stromal-epithelial paracrine signaling involving FGF, KGF, and IGF-1 further drives hyperplasia, while TGF-beta provides counterbalancing antiproliferative signals. The dynamic component involves alpha-1A adrenergic receptor-mediated smooth muscle contraction: epinephrine activates PLC, generating IP3 and DAG, triggering intracellular calcium release from the sarcoplasmic reticulum and extracellular calcium entry, culminating in actin-myosin cross-bridge formation and urethral smooth muscle contraction. Alpha-blockers competitively inhibit this sequence. PDE5 inhibitors increase cGMP in prostatic smooth muscle, promoting relaxation through a distinct pathway. Surgical interventions (TURP, laser enucleation, prostatic urethral lift, water vapor thermal therapy) address refractory cases. The clinician must select pharmacotherapy based on prostate size, symptom severity, and comorbidities, manage surgical referral timing, and handle post-operative complications.