Benign prostatic hyperplasia (BPH) arises from proliferation of which zone of the prostate gland?

Explanation

## Zonal Anatomy and BPH Pathogenesis ### Prostatic Zones | Zone | % of Normal Gland | Origin of BPH | Malignancy Risk | | --- | --- | --- | --- | | **Transition zone** | 5–10% | Yes (95% of BPH) | Low | | **Central zone** | 20–25% | No | Low | | **Peripheral zone** | 70% | No | High (70% of cancers) | | **Anterior fibromuscular stroma** | Variable | No | No | **Key Point:** Benign prostatic hyperplasia arises almost exclusively from the **transition zone**, which normally comprises only 5–10% of the prostate but undergoes progressive nodular hyperplasia with age. ### Pathophysiology of BPH 1. **Androgen-dependent process**: Requires DHT (dihydrotestosterone) produced by 5α-reductase 2. **Age-related**: Incidence increases dramatically after age 50 3. **Stromal-epithelial interaction**: Both smooth muscle and glandular epithelium proliferate 4. **Nodular growth**: Forms discrete nodules that compress the urethra, causing lower urinary tract symptoms (LUTS) **Mnemonic:** **TZ-BPH** — Transition Zone = Benign Prostatic Hyperplasia **Clinical Pearl:** Although the transition zone is small in the normal prostate, it can enlarge dramatically in BPH, sometimes reaching 100+ grams. This is why BPH-related obstruction can be severe despite originating from a small anatomical region. ### Why This Matters Clinically - **TURP (transurethral resection of prostate)** targets the transition zone - **5α-reductase inhibitors** (finasteride, dutasteride) are effective because they reduce DHT-driven hyperplasia in this zone - **Peripheral zone cancers** are NOT related to BPH pathology