Benign prostatic hyperplasia (BPH) (also called nodular hyperplasia; glandular and stromal hyperplasia) is extremely common. Androgens (dihydrotestosterone) play an important role in the pathogenesis, and the lesion is not premalignant. The inci-dence increases with age (age 60 is 70%; age 70 is 80%). BPH typically presents with the following:
• Decreased caliber and force of stream
• Trouble starting (hesitancy)/stopping the stream
• Postvoid dribbling
• Urinary retention
• Possible elevation in prostate specific antigen (PSA) but usually <10 ng/mL
Complications include urinary tract infection, urinary bladder trabeculation and diverticula formation, and hydronephrosis and renal failure (rare). Treatment varies, with available modalities including transurethral resection of prostate (TURP); the 5-alpha reductase inhibitor, finasteride (Proscar); and the selective alpaha-1 receptor blockers, terazosin and prazosin.
Grossly, BPH causes an enlarged prostate with well-demarcated nodules in the tran-sition and central (periurethral) zones, which often results in slit-like compression of the prostatic urethra. Microscopically, the lesion shows glandular and stromal hyperplasia resulting in the characteristic prostate enlargement.
Prostate adenocarcinoma is the most common cancer in men in the United States and the second most common cause of cancer death in men. The incidence increases with age, and the highest rate is in African Americans.
• Often clinically silent but may present with lower back pain secondary to metastasis
• Advanced localized disease may present with urinary tract obstruction or UTI (rare)
• Tumor can be detected with digital rectal exam (induration), serum PSA level, and transrectal U/S and biopsy
• Metastases most commonly involve obturator and pelvic lymph nodes
• Osteoblastic bone metastasis to lumbar spine can occur, and can be associated with elevated alkaline phosphatase
Treatment of local disease is prostatectomy and/or external beam radiation. Meta-static disease is treated with orchiectomy, estrogens, or LHRH agonists and anti-androgens. The disease course can be monitored with PSA levels.
Pathologically, an ill-defined, firm, yellow mass commonly arises in the posterior aspect of the peripheral zone. Microscopically, adenocarcinoma is graded with the Gleason system, which scores glandular differentiation. TMPRSS2-ETS fusion genes are present in nearly 50% of all prostatic carcinomas.
• Acute prostatitis is usually caused by intraprostatic reflux of urinary tract pathogens.
• Chronic prostatitis may develop following recurrent acute prostatitis, and bacterial pathogens may not be detectable. Chronic nonbacterial prostatitis (chronic pelvic pain syndrome) is more common than bacterial prostatitis.
• Clinical findings can include fever (acute prostatitis), pain (lower back, peri-neal, or suprapubic), painful prostate on rectal exam, and dysuria (with pos-sible hematuria).
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