PA28.3-5 | Prostate: BPH, Carcinoma & Prostatitis — Summary & Reflection

REFLECT

Before moving to the summary, take a moment to consolidate your thinking:

1. The zone matters: You evaluated a man with LUTS and a smooth enlarged prostate — the enlarged transition zone causing BPH. Then a biopsy from the peripheral zone showed carcinoma. Can you sketch, without notes, the cross-section of the prostate labelling these two zones and the disease in each?

1. DHT vs oncogene: BPH and carcinoma are both androgen-dependent but through completely different mechanisms. BPH is driven by DHT-mediated growth factor upregulation (hyperplasia). Carcinoma involves TMPRSS2-ERG fusion placing an oncogenic transcription factor under androgen control. Can you explain these two mechanisms to a colleague without conflating them?

1. Gleason 3+4 vs 4+3: Both sum to 7, yet they are different ISUP grade groups (2 vs 3) with meaningfully different prognoses. Why does the order of patterns matter? (Hint: the primary pattern is the majority — so 4+3 means most of the tumour is poorly formed fused glands.)

1. The osteoblastic puzzle: Most bone metastases from other carcinomas are osteolytic. Prostate cancer is osteoblastic. What growth factor secreted by prostate cancer cells explains this, and why does this mean serum ALP (not just PSA) is a useful monitoring tool?

1. PSA on finasteride: A patient on finasteride for BPH has a PSA of 4.0 ng/mL. Is this reassuring? What do you actually do with this result?

KEY TAKEAWAYS

Module Summary: Prostate — BPH, Carcinoma & Prostatitis

Prostatitis (PA28.5):
• Four NIH categories: I (acute bacterial) — fever, tender boggy prostate, neutrophilic suppurative inflammation; II (chronic bacterial) — recurrent UTI, same organism; III (CPPS) — commonest (90–95%), culture-negative, IIIa with WBCs/IIIb without; IV (asymptomatic, incidental).
• Granulomatous prostatitis (TB, non-specific, BCG-induced) mimics carcinoma on DRE — diagnosis by biopsy.
• Never order PSA during active prostatitis.

BPH (PA28.3) — Key Framework:
• Transition zone; requires aging + androgens; NOT premalignant.
• Pathogenesis: DHT (via 5α-reductase type 2) → AR activation → proliferation/anti-apoptosis → nodular hyperplasia.
• Morphology: large glands with intact two-layer epithelium (secretory + basal), papillary infoldings, corpora amylacea; stromal nodules also present.
• Complications: AUR, hydronephrosis, UTI, CKD.
• DRE: smooth, rubbery, symmetrically enlarged; PSA modest elevation.
• Treatment: α-blockers (immediate, dynamic) → 5α-reductase inhibitors (shrink, slow) → TURP (definitive).

Prostate Carcinoma (PA28.4) — Key Framework:
• Peripheral zone; androgen-dependent (TMPRSS2-ERG fusion); HGPIN = precursor.
• Morphology: small crowded infiltrating glands, absent basal layer, prominent nucleoli, perineural invasion — IHC: AMACR+, p63−, 34βE12−.
• Gleason grading: patterns 3→5; score = primary + secondary; ISUP Grade Groups 1–5 (GG3 = 4+3 is a key inflection).
• DRE: hard, irregular nodule, posterior; PSA often elevated; free:total PSA ratio low.
• Spread: local (neurovascular bundle, seminal vesicles) → lymphatic (obturator nodes) → osteoblastic bone metastases (lumbar spine, pelvis via Batson plexus) → ALP elevated.
• Treatment: surveillance / radical prostatectomy / radiotherapy (localised); androgen deprivation therapy (metastatic) → eventual castration resistance.

The Pathology Mindmap:
BPH = transition zone + DHT + intact basal layer + LUTS
Carcinoma = peripheral zone + TMPRSS2-ERG + absent basal layer + osteoblastic mets
PSA = not cancer-specific; double on finasteride; invalid in acute prostatitis