Section 15.1: Male Genitourinary Disorders (BPH, Prostate Cancer, Testicular Torsion, ED)
Key Takeaways
- Benign prostatic hyperplasia (BPH) arises in the transition zone and presents with obstructive and irritative symptoms; digital rectal exam (DRE) shows a smooth, rubbery, symmetrically enlarged prostate.
- Alpha-1 blockers (e.g., tamsulosin) relax prostatic smooth muscle for rapid relief, while 5-alpha reductase inhibitors (e.g., finasteride) block DHT to slowly shrink the gland and halve serum PSA levels (PSA must be doubled for screening).
- Prostate cancer is predominantly adenocarcinoma arising in the peripheral zone (felt as hard, irregular nodules on DRE); advanced disease classically presents with osteoblastic bone metastases to the spine.
- Testicular torsion is a surgical emergency presenting with sudden unilateral pain, a high-riding testis with horizontal lie, and an absent cremasteric reflex; do not delay surgical detorsion for ultrasound if suspicion is high.
- Erectile dysfunction is categorized as organic (gradual onset, absent morning erections) or psychogenic (sudden onset, intact morning erections); phosphodiesterase-5 (PDE-5) inhibitors are first-line but absolutely contraindicated with nitrates.
Why This Matters for the PANCE
Male genitourinary disorders represent highly common clinical scenarios on the PANCE. You must be able to differentiate benign prostatic hyperplasia (BPH) from prostate cancer, recognize the medical and surgical management of these conditions, and quickly identify testicular torsion as a time-critical urologic emergency. Furthermore, erectile dysfunction (ED) is a highly prevalent condition that requires a thorough understanding of vascular risk factors and pharmacologic contraindications, particularly regarding phosphodiesterase-5 (PDE-5) inhibitors. Mastering these topics ensures success on both general medicine and surgical sections of the exam.
Benign Prostatic Hyperplasia (BPH)
- Definition and Pathophysiology: Benign prostatic hyperplasia (BPH) is a nonmalignant hypertrophy and hyperplasia of the transition zone of the prostate gland. This zone surrounds the proximal urethra. Hyperplasia is driven by dihydrotestosterone (DHT), which is converted from testosterone by the enzyme 5-alpha-reductase within prostatic stromal cells. As the transition zone expands, it compresses the prostatic urethra and leads to bladder outlet obstruction.
- Risk Factors: Advancing age (extremely common, affecting >50% of men over 60 and >80% of men over 80) and family history.
- Clinical Presentation: Presents with Lower Urinary Tract Symptoms (LUTS), which are clinically divided into:
- Obstructive (Voiding) Symptoms: Urinary hesitancy, weak or split stream, straining to void, post-void dribbling, and a sensation of incomplete bladder emptying.
- Irritative (Storage) Symptoms: Urinary frequency, urgency, nocturia, and urge incontinence. These symptoms occur due to detrusor muscle hypertrophy and instability in response to chronic outflow obstruction.
- Diagnostic Workup:
- Digital Rectal Examination (DRE): Demonstrates a symmetrically enlarged, smooth, firm, rubbery, and nontender prostate gland. The normal median sulcus may be obliterated.
- Urinalysis: Essential to rule out urinary tract infection (UTI) and hematuria.
- Prostate-Specific Antigen (PSA): Can be mildly elevated due to increased prostate volume, but is not diagnostic.
- Post-Void Residual (PVR) Volume: Measured via bladder ultrasound to quantify urinary retention; values >100 mL indicate significant outlet obstruction.
- Clinical Management:
- First-line Pharmacotherapy for Mild-to-Moderate Symptoms:
- Alpha-1 Adrenergic Antagonists (e.g., Tamsulosin, Alfuzosin, Terazosin, Doxazosin): Relax the smooth muscle of the bladder neck and prostatic urethra, providing rapid symptom relief (within days). Tamsulosin is uroselective (alpha-1a), minimizing systemic vascular side effects like orthostatic hypotension. Non-selective agents (doxazosin, terazosin) require titration and are often dosed at bedtime due to the risk of first-dose syncope. A classic side effect of alpha-blockers is retrograde ejaculation.
- 5-Alpha Reductase Inhibitors (e.g., Finasteride, Dutasteride): Block the conversion of testosterone to DHT. By reducing DHT levels, they progressively shrink the prostate gland (by ~20-25%) and prevent disease progression. However, they have a slow onset of action, requiring 6 to 12 months for clinical efficacy. Side effects include decreased libido, erectile dysfunction, and gynecomastia.
- High-Yield Pearl: 5-alpha-reductase inhibitors reduce serum PSA levels by approximately 50%. Therefore, for prostate cancer screening, the measured PSA level must be doubled for accurate interpretation.
- Phosphodiesterase-5 (PDE-5) Inhibitors (e.g., Tadalafil): Can be used alone or in combination with alpha-blockers, particularly in patients with co-existing erectile dysfunction.
- Surgical Management: Transurethral Resection of the Prostate (TURP) is the gold standard surgical intervention. It is indicated for patients with refractory urinary retention, recurrent UTIs, bladder calculi, persistent gross hematuria, or post-renal acute kidney injury. The most common long-term complication of TURP is retrograde ejaculation.
- First-line Pharmacotherapy for Mild-to-Moderate Symptoms:
Prostate Cancer
- Definition and Pathophysiology: Prostate cancer is the most common non-dermatologic cancer in men. Over 95% of cases are adenocarcinomas. Unlike BPH, which arises in the transition zone, prostate cancer predominantly arises in the peripheral zone of the prostate. Because the peripheral zone is anatomically distant from the urethra, early-stage prostate cancer is characteristically asymptomatic.
- Risk Factors: Advanced age (rare before 50, incidence peaks after 70), African American race, family history (especially a first-degree relative), and high-fat diet.
- Clinical Presentation:
- Early Disease: Asymptomatic; usually detected via screening (PSA or DRE).
- Locally Advanced Disease: Urinary obstruction symptoms (LUTS), hematuria, or hematospermia.
- Metastatic Disease: Bone pain is the classic presenting symptom of advanced metastatic prostate cancer, particularly in the lumbosacral spine, pelvis, or femur. These are characteristically osteoblastic metastases (which appear radiodense/white on X-ray).
- Diagnostic Workup:
- Digital Rectal Examination (DRE): Reveals a hard, irregular, asymmetric, nodular prostate gland.
- Prostate-Specific Antigen (PSA): Elevated. While PSA is prostate-specific, it is not cancer-specific. PSA can be elevated by BPH, prostatitis, urinary retention, recent ejaculation, or vigorous prostate examination. A PSA >4.0 ng/mL warrants further investigation.
- Gold Standard for Diagnosis: Transrectal Ultrasound (TRUS) guided needle biopsy is required to confirm the diagnosis. A multiparametric MRI (mpMRI) is often performed beforehand to identify target lesions.
- Grading and Staging: The Gleason Score is used to grade prostate cancer based on glandular architecture. The pathologist assigns a grade (1 to 5) to the primary and secondary growth patterns; the sum ranges from 6 (low-grade, well-differentiated) to 10 (high-grade, poorly differentiated).
- Clinical Management:
- Active Surveillance: Appropriate for patients with low-risk, localized disease or those with a life expectancy of less than 10 years.
- Localized Disease: Radical prostatectomy or radiation therapy (external beam radiation or brachytherapy). Primary side effects include erectile dysfunction and stress urinary incontinence.
- Metastatic Disease (Androgen Deprivation Therapy [ADT]): Mainstay of treatment to reduce testosterone levels.
- LHRH (GnRH) Agonists (e.g., Leuprolide, Goserelin): Cause an initial transient surge in testosterone (testosterone flare) before downregulating receptors. This flare can worsen bone pain or spinal cord compression. Thus, an antiandrogen (e.g., Bicalutamide) must be co-administered for the first 2 to 4 weeks.
- GnRH Antagonists (e.g., Degarelix): Directly block GnRH receptors, rapidly lowering testosterone without causing a flare.
Testicular Torsion
- Definition and Pathophysiology: Testicular torsion is a urologic emergency caused by the twisting of the spermatic cord, which leads to venous occlusion, subsequent arterial occlusion, ischemia, and testicular infarction if not corrected. The primary predisposing factor is the "bell-clapper deformity," a congenital anatomical variant where the tunica vaginalis attaches high on the spermatic cord, allowing the testis to rotate freely.
- Clinical Presentation: Sudden-onset, severe, unilateral scrotal pain, often accompanied by lower abdominal pain, nausea, and vomiting. On physical exam:
- The affected testis is swollen, erythematous, and tender.
- The testis is high-riding with a horizontal lie (due to shortening of the spermatic cord).
- Absent Cremasteric Reflex: Lightly stroking the ipsilateral inner thigh fails to elevate the testis. This is the most sensitive physical exam finding (its presence makes torsion highly unlikely).
- Negative Prehn Sign: Elevation of the scrotum does not relieve pain. This helps differentiate torsion from epididymitis, where elevation often provides relief (positive Prehn sign).
- Diagnostic Workup:
- Initial/Gold Standard Test: Color Doppler ultrasound of the scrotum, which demonstrates decreased or absent blood flow to the affected testis.
- Clinical Rule: Do not delay surgical intervention to obtain an ultrasound if there is high clinical suspicion. Irreversible testicular damage occurs within 6 hours of onset.
- Clinical Management:
- Surgical Emergency: Immediate surgical exploration, detorsion, and bilateral orchiopexy (anchoring the testes to the scrotum to prevent recurrence).
- Manual Detorsion: If surgery is delayed, manual detorsion can be attempted. The testis is rotated outward (from medial to lateral, like "opening a book"). Success is marked by immediate pain relief and return of Doppler flow.
Erectile Dysfunction (ED)
- Definition and Pathophysiology: Erectile dysfunction (ED) is the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance. Normal erection requires parasympathetic-mediated nitric oxide release, which activates guanylate cyclase, increasing cyclic GMP (cGMP) and causing smooth muscle relaxation and increased blood flow into the corpora cavernosa. ED is categorized as:
- Organic (Vascular, Neurogenic, Endocrine): Gradual onset, progressive loss of erections, and absence of nocturnal or morning erections. Vascular disease (atherosclerosis, hypertension) and diabetes are the most common organic causes.
- Psychogenic: Sudden onset, situational ED, with intact nocturnal or morning erections.
- Medication-Induced: Commonly caused by beta-blockers, SSRIs, and spironolactone.
- Diagnostic Workup: Detailed history, lipid panel, fasting blood glucose or HbA1c, and morning total testosterone levels.
- Clinical Management:
- First-line Pharmacotherapy: Phosphodiesterase-5 (PDE-5) Inhibitors (e.g., Sildenafil, Tadalafil, Vardenafil). They prevent the degradation of cGMP, enhancing nitric oxide-mediated vasodilation.
- Contraindications & Risks: Absolute contraindication with nitrates (leads to life-threatening hypotension). Use caution with alpha-blockers due to additive vasodilatory effects. Side effects include headache, facial flushing, dyspepsia, and transient blue-green color vision impairment (cyanopsia) due to PDE-6 inhibition in the retina. Priapism (erection >4 hours) is a rare but emergency side effect.
- Second-line: Intracavernosal or intraurethral alprostadil (prostaglandin E1).
Comparison of Scrotal Pain Etiologies
| Feature | Testicular Torsion | Epididymitis | Orchitis |
|---|---|---|---|
| Onset | Sudden, acute | Gradual | Gradual, often post-viral |
| Age Group | Neonates, adolescents (12-18) | Under 35 (STI-related); Over 35 (UTI-related) | Children/adults (associated with Mumps) |
| Cremasteric Reflex | Absent | Present | Present |
| Prehn Sign | Negative (no pain relief with elevation) | Positive (pain relief with elevation) | Negative |
| Ultrasound | Decreased/absent blood flow | Increased blood flow (hyperemia) | Increased blood flow, testicular swelling |
| Management | Emergent surgical detorsion & orchiopexy | Ceftriaxone + Doxycycline (<35); Levofloxacin (>35) | Supportive care (NSAIDs, ice, scrotal support) |
Classic PANCE Traps & Clinical Pearls
- PSA Trap: If a patient is taking a 5-alpha reductase inhibitor (like finasteride), remember to double their measured PSA level to get their true baseline. If the lab reports a PSA of 2.5 ng/mL, the clinician must interpret it as 5.0 ng/mL.
- Torsion Diagnostic Delay: Never wait for an ultrasound if the clinical presentation of testicular torsion is clear (e.g., adolescent with sudden pain, high-riding testis, and absent cremasteric reflex). Go straight to surgical consult.
- Nitrate Contraindication: Always screen patients for nitrate use (e.g., sublingual nitroglycerin, isosorbide mononitrate) before prescribing PDE-5 inhibitors. Co-administration can cause catastrophic cardiovascular collapse.
A 67-year-old male presents with urinary frequency, urgency, and nocturia. On digital rectal examination, his prostate is symmetrically enlarged, smooth, and firm, with no palpable nodules. He is started on finasteride. Six months later, his routine screening prostate-specific antigen (PSA) is reported by the lab as 2.4 ng/mL. What is the patient's estimated true PSA level?
A 16-year-old male is brought to the emergency department with sudden-onset, severe right testicular pain that began 3 hours ago. He reports nausea and one episode of emesis. On physical examination, the right testis is swollen, tender, and high-riding with a horizontal orientation. Lightly stroking the right inner thigh does not result in elevation of the right testis. Scrotal elevation does not relieve the pain. Which of the following is the most appropriate next step in management?