## Pathogenesis of Benign Prostatic Hyperplasia **Key Point:** BPH is fundamentally a hormone-dependent condition driven by the androgen-DHT axis, not infection or malignancy. ### Mechanism of BPH Development BPH arises from a combination of: 1. Continued androgen (testosterone) production by the testes 2. Increased expression of 5-alpha reductase in prostatic stromal and epithelial cells 3. Enhanced sensitivity of prostatic tissue to DHT, the active metabolite 4. Age-related accumulation of stromal and epithelial hyperplasia **High-Yield:** The key pathophysiologic abnormality is NOT increased testosterone levels (which remain relatively stable with age) but rather **increased local conversion to DHT and increased tissue sensitivity** to DHT in the prostate. ### Why This Matters Clinically **Clinical Pearl:** This is why 5-alpha reductase inhibitors (finasteride, dutasteride) and androgen receptor antagonists are effective treatments — they interrupt the DHT-driven proliferation pathway. ### Epidemiology - Prevalence increases with age: ~50% of men by age 60, ~90% by age 85 - Histologic BPH present in >90% of men >70 years old - Symptomatic BPH affects ~25% of men >40 years **Warning:** Do not confuse BPH with prostate cancer — they are independent conditions, though both increase with age. BPH is benign hyperplasia; cancer is malignant transformation. ### Differential Pathology | Feature | BPH | Prostatitis | Prostate Cancer | |---------|-----|-------------|------------------| | **Etiology** | Androgen-DHT sensitivity | Bacterial/inflammatory | Malignant transformation | | **Histology** | Stromal and glandular hyperplasia | Inflammatory infiltrate | Atypical glands, loss of architecture | | **PSA elevation** | Mild-moderate | Marked (acute) | Marked | | **Treatment response** | 5-AR inhibitors, alpha-blockers | Antibiotics | Surgery, radiation, hormonal therapy | [cite:Robbins 10e Ch 20]
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