Prostatitis, benign prostatic hyperplasia

1. Prostatitis

Definition

• Inflammation of the prostate.

Types (5 categories)

1. Acute bacterial prostatitis (2–5 %)

• Same organisms as UTI: E. coli, gram-negative rods, enterococci, staphylococci.
• Routes:
  • Direct extension from inflamed urethra (STD) or bladder.
  • Vascular spread from distant sites.
• Histology: granulocytes + abscess formation.
• Sx: fever + dysuria + lower back pain.
• PE: enlarged + tender prostate.

2. Chronic bacterial prostatitis (2–5 %)

• May follow acute or develop insidiously.
• Caused by uropathogens.
• Major reservoir for recurrent UTI in men.
• Sx: lower back pain + dysuria + perineal discomfort.

3. Chronic granulomatous prostatitis

• Causes: TB, sarcoidosis, fungal infections, after transurethral resection.
• Non-specific (non-necrotizing) / reactive: fluid leak from ruptured prostatic ducts.
• Specific (necrotizing) granulomatous: TB — rare miliary dissemination, BCG instillation (bladder cancer Tx), fungal in immunocompromised.

4. Chronic (non-bacterial) pelvic pain syndrome (90–95 % of cases)

• No pathogen.
• Local symptoms + ↑ leukocytes in prostatic secretion.

5. Asymptomatic inflammatory prostatitis

• No pathogens, no symptoms.
• Only leukocytes in semen.

2. Benign Prostatic Hyperplasia (BPH)

Definition

• Proliferation of stromal + epithelial elements surrounding the urethra → enlargement of prostate gland.
• Extremely common; present in men from age 40; ↑ with age.
• NOT pre-malignant.

Pathogenesis

A) Excessive androgen stimulation

• Prostate stromal cells produce 5α-reductase → testosterone → dihydrotestosterone (DHT).
• DHT is 10× more potent than testosterone (slower receptor dissociation).
• T + DHT bind nuclear androgen receptors in stromal/epithelial cells → GF activation → hyperplasia.

B) ↑ Estrogen levels (with aging)

• Estradiol ↑ in aging men → ↑ androgen receptors.
• Testosterone ↓ ~1 % per year after 30, but 5α-reductase activity ↑ → net ↑ DHT.

Morphology

• Periurethral nodules in transitional zone (NOT peripheral zone, which is the cancer zone).
• Nodules compress urethra → obstructive symptoms.
• Compressed urethra → slit-like orifice.
• Histology: proliferation of stromal (fibromuscular) + epithelial (glandular) elements.

Clinical features

• Lower urinary tract obstruction:
  • Hesitancy (difficulty starting urine stream).
  • Intermittent interruption while voiding.
  • Weak stream, post-void dribbling.
  • May progress to complete urinary obstruction → painful bladder distention → hydronephrosis.
• Storage symptoms: urgency, frequency, nocturia.
• Residual urine + chronic obstruction → ↑ UTI risk.
• DRE: enlarged, firm, rubbery, smooth prostate (cancer = hard, nodular).

Treatment

• 5α-reductase inhibitors — finasteride, dutasteride (block DHT formation).
• α-adrenergic blockers — tamsulosin (Flomax) (relax SM).
• Transurethral resection (TURP) for severe obstruction.

3. Comparison — BPH vs Prostate Cancer (preview)

Feature	BPH	Prostate carcinoma
Zone	Transitional (periurethral)	Peripheral (posterior)
DRE	Enlarged, smooth, rubbery	Hard, nodular
Obstruction	Early (compresses urethra)	Late (further from urethra)
Pre-malignant	No	—
PSA	Mild ↑	Moderate-marked ↑

💡 High-yield: Prostatitis: acute bacterial (E. coli, UTI organisms, fever + dysuria + tender prostate); chronic bacterial = #1 cause of recurrent UTI in men; chronic non-bacterial pelvic pain = 90–95 % of cases. BPH = #1 prostate disorder, men > 40, NOT pre-malignant. Transitional zone (periurethral) → compresses urethra. Pathogenesis: DHT (5α-reductase converts T → DHT, 10× potency) + ↑ estradiol with aging. Sx: hesitancy + weak stream + nocturia + frequency + urgency; severe → hydronephrosis + UTI. DRE: smooth rubbery enlarged. Tx: 5α-reductase inhibitors (finasteride) + α-blockers (tamsulosin) + TURP. Cancer = peripheral zone (hard nodular on DRE).