Urology

Every diagnosis, procedure, surgical technique, classification, complication, medication, and management algorithm across the full scope of urology in one place.

01 Upper Urinary Tract Anatomy

Kidneys

The kidneys are paired retroperitoneal organs lying at the T12-L3 vertebral level. The right kidney sits slightly lower than the left due to the liver. Each kidney measures approximately 10-12 cm in length, 5-7 cm in width, and 3 cm in anteroposterior diameter, weighing 120-170 g. The kidney is surrounded by Gerota fascia (renal fascia), within which lies perinephric fat. Deep to this is the true renal capsule.

The renal parenchyma consists of an outer cortex and an inner medulla. The medulla is organized into 8-18 renal pyramids, each with its apex (papilla) projecting into a minor calyx. Minor calyces merge into 2-3 major calyces, which join to form the renal pelvis. The functional unit is the nephron — each kidney contains approximately 1 million nephrons. The renal hilum transmits the renal artery, renal vein, renal pelvis, lymphatics, and autonomic nerves. The relationship from anterior to posterior at the hilum is: vein, artery, pelvis (mnemonic: VAP).

Renal Vascular Anatomy

The renal arteries arise from the aorta at the L1-L2 level. The right renal artery passes posterior to the IVC. Each renal artery divides into 5 segmental arteries (apical, upper, middle, lower, posterior) — these are end arteries with no collateral circulation, meaning occlusion causes segmental infarction. The segmental arteries further divide: segmental → interlobar → arcuate → interlobular → afferent arteriolar → glomerular capillaries → efferent arteriolar → peritubular capillaries/vasa recta.

The left renal vein is longer than the right, passing anterior to the aorta and posterior to the SMA (the "nutcracker" position). It receives the left gonadal vein, left adrenal vein, and lumbar veins — making left-sided donor nephrectomy preferred (longer vein for anastomosis). The right renal vein drains directly into the IVC with no major tributaries. The right gonadal vein drains directly into the IVC, while the left gonadal vein drains into the left renal vein — this explains why left varicoceles are far more common than right.

A new right-sided varicocele, especially one that does not decompress with recumbency, should raise concern for retroperitoneal pathology (e.g., renal cell carcinoma with IVC thrombus) because the right gonadal vein drains directly into the IVC.

Ureters

The ureters are 25-30 cm muscular tubes that transport urine from the renal pelvis to the bladder via peristalsis. They cross the pelvic brim at the bifurcation of the common iliac artery. Three anatomic points of narrowing (sites where stones commonly impact): (1) the ureteropelvic junction (UPJ), (2) the crossing of the iliac vessels at the pelvic brim, and (3) the ureterovesical junction (UVJ) — the narrowest point.

The ureter has a three-layered wall: inner transitional epithelium (urothelium), middle smooth muscle (inner longitudinal, middle circular, outer longitudinal), and outer adventitia. Blood supply comes from multiple sources: renal artery superiorly, gonadal artery and aorta in the mid-portion, and iliac and superior vesical arteries inferiorly. The blood supply approaches medially in the upper ureter and laterally in the lower ureter — critical during surgical mobilization to avoid devascularization.

During pelvic surgery, the ureter is at greatest risk of injury at three points: (1) where it crosses the iliac vessels at the pelvic brim, (2) where it passes under the uterine artery ("water under the bridge"), and (3) at the ureterovesical junction. Always identify the ureter before ligating any pelvic structure.
Cross-section of the kidney showing cortex, medulla, pyramids, calyces, and renal pelvis
Figure 1 — Kidney Cross-Section. The cortex, medulla with renal pyramids, minor and major calyces, renal pelvis, and renal hilum structures. Source: Wikimedia Commons. Public domain.

Adrenal Glands

The adrenal glands sit atop the kidneys within Gerota fascia. The right adrenal is pyramidal and sits behind the IVC; its venous drainage is a short vein directly into the IVC (injury here during right adrenalectomy or nephrectomy can cause significant hemorrhage). The left adrenal is crescent-shaped and drains via a longer vein into the left renal vein.

Lymphatic Drainage of the GU Tract

Knowledge of lymphatic drainage is critical for surgical oncology. The kidneys drain to para-aortic and paracaval lymph nodes (left kidney → left para-aortic; right kidney → right paracaval and interaortocaval). The testes drain to the retroperitoneal (para-aortic) lymph nodes at the level of the renal hilum — NOT the inguinal nodes (unless the scrotal skin has been violated). The bladder drains to the obturator and internal iliac nodes, then external iliac and common iliac nodes. The prostate drains primarily to the obturator lymph nodes (most common site of prostate cancer lymph node metastasis), followed by internal iliac and presacral nodes. The penis and scrotal skin drain to the superficial and deep inguinal lymph nodes.

Innervation of the Lower Urinary Tract

Three neural pathways control micturition: (1) Parasympathetic (S2-S4, pelvic nerve) — acetylcholine acts on M3 receptors on the detrusor, causing contraction (voiding). (2) Sympathetic (T10-L2, hypogastric nerve) — norepinephrine acts on beta-3 receptors in the detrusor body (relaxation/storage) and alpha-1 receptors at the bladder neck and prostatic urethra (contraction/continence). (3) Somatic (S2-S4, pudendal nerve) — voluntary control of the external urethral sphincter (striated muscle) via acetylcholine at nicotinic receptors. The pontine micturition center (Barrington nucleus) coordinates the voiding reflex — simultaneous detrusor contraction and sphincter relaxation. Understanding these pathways is essential for pharmacologic management of LUTS and neurogenic bladder.

02 Lower Urinary Tract & Male Genital Anatomy

Urinary Bladder

The bladder is a hollow muscular organ with a capacity of 400-600 mL. It lies in the retropubic space (space of Retzius) when empty. The bladder wall consists of: mucosa (transitional epithelium/urothelium), lamina propria, detrusor muscle (three layers of smooth muscle — inner longitudinal, middle circular, outer longitudinal), and serosa/adventitia. The trigone is the triangular area bounded by the two ureteral orifices and the internal urethral meatus — it is the most fixed and least distensible part of the bladder. The detrusor muscle is innervated by parasympathetic fibers (S2-S4) via the pelvic nerve; contraction causes voiding.

The bladder blood supply comes from the superior and inferior vesical arteries (branches of the internal iliac artery). Venous drainage is via the vesical venous plexus into the internal iliac veins. In males, the vesical plexus communicates with the prostatic venous plexus (Santorini plexus) — this valveless venous system (Batson plexus) communicates with the vertebral venous plexus, providing a route for hematogenous metastasis of prostate and bladder cancer to the spine without passing through the lungs.

Prostate

The prostate is a walnut-sized gland (~20 g in young men) that surrounds the prostatic urethra below the bladder neck. It is divided into zones (McNeal): the peripheral zone (70% of glandular tissue — site of ~70-80% of prostate cancers and where DRE palpates), the transition zone (5-10% of tissue — site of BPH), the central zone (25% — surrounds ejaculatory ducts), and the anterior fibromuscular stroma (nonglandular). The prostate is bounded posteriorly by Denonvilliers fascia (separating it from the rectum) and laterally by the neurovascular bundles (NVB) — containing the cavernous nerves responsible for erectile function. Preservation of the NVBs during radical prostatectomy is critical for postoperative potency.

Diagram of prostate zonal anatomy showing peripheral, transition, and central zones
Figure 2 — Prostate Zonal Anatomy (McNeal). The peripheral zone (site of most cancers), transition zone (site of BPH), and central zone. The neurovascular bundles course posterolaterally. Source: Wikimedia Commons. Public domain.

Male Urethra

The male urethra is approximately 18-22 cm and has four segments: (1) prostatic urethra (~3-4 cm, widest and most distensible — verumontanum marks the opening of ejaculatory ducts and prostatic utricle), (2) membranous urethra (~1-2 cm, passes through the external urethral sphincter and urogenital diaphragm — the most common site of traumatic urethral injury in pelvic fractures), (3) bulbar urethra (~3-4 cm, surrounded by bulbospongiosus muscle, most common site of stricture from instrumentation/infection), and (4) penile (pendulous) urethra (~15 cm, within the corpus spongiosum, terminating at the fossa navicularis and external meatus).

Female Urethra

The female urethra is approximately 3-5 cm in length, running from the bladder neck to the external meatus anterior to the vaginal opening. It is supported by the pubourethral ligaments and the anterior vaginal wall. The external urethral sphincter (rhabdosphincter) provides voluntary continence and is innervated by the pudendal nerve (S2-S4). The internal sphincter (smooth muscle at the bladder neck) provides involuntary continence and is innervated by sympathetic fibers (alpha-1 adrenergic). The shorter urethral length and proximity to the vaginal introitus and anus contribute to the higher incidence of urinary tract infections in women compared to men.

Support of the female urethra is provided by the pubourethral ligaments, endopelvic fascia, and the levator ani muscles (specifically the pubococcygeus component). Weakening of these support structures — from childbirth, aging, chronic straining, or connective tissue disorders — leads to urethral hypermobility, which is the most common mechanism of stress urinary incontinence in women.

Penis

The penis contains three erectile bodies: two dorsal corpora cavernosa (responsible for rigidity during erection) and one ventral corpus spongiosum (surrounds the urethra, expands distally into the glans penis). The corpora cavernosa are surrounded by the tunica albuginea — a tough, fibrous sheath. Arterial supply is from the internal pudendal artery, which gives rise to the cavernosal (deep) arteries, dorsal artery, and bulbourethral artery. Venous drainage occurs via the deep dorsal vein (beneath Buck fascia) draining into the prostatic venous plexus. Erection is a parasympathetic event (S2-S4, via NO-mediated smooth muscle relaxation); ejaculation is sympathetic (T10-L2).

Testes, Epididymis & Spermatic Cord

The testes are ovoid organs (~4 × 3 × 2.5 cm, ~20 mL volume) within the scrotum. Each testis is covered by the tunica vaginalis (a peritoneal remnant) and the tunica albuginea. The testicular parenchyma contains seminiferous tubules (site of spermatogenesis) and Leydig cells (produce testosterone in the interstitium). Spermatozoa pass from the seminiferous tubules through the rete testis into the epididymis (head/caput → body/corpus → tail/cauda). The cauda epididymis is continuous with the vas deferens.

The spermatic cord contains: vas deferens, testicular artery (from aorta), artery of the vas deferens (from inferior vesical artery), cremasteric artery (from inferior epigastric artery), pampiniform venous plexus, genital branch of the genitofemoral nerve, lymphatics, and the processus vaginalis remnant. Three fascial layers cover the cord (corresponding to abdominal wall layers encountered during inguinal descent): external spermatic fascia (from external oblique aponeurosis), cremasteric fascia and muscle (from internal oblique), and internal spermatic fascia (from transversalis fascia). The ilioinguinal nerve (L1) runs on the surface of the spermatic cord within the inguinal canal and provides sensation to the medial thigh, root of the penis, and anterior scrotum — it can be injured during inguinal surgery causing chronic groin pain.

The seminal vesicles are paired accessory glands posterior to the bladder base that contribute ~70% of ejaculate volume (fructose-rich alkaline fluid). They lie just superior to the prostate and lateral to the ampullae of the vas deferens. Each seminal vesicle duct joins with the ipsilateral vas deferens to form the ejaculatory duct, which traverses the prostate to empty at the verumontanum. Ejaculatory duct obstruction (EDO) is a treatable cause of male infertility — diagnosed by low ejaculate volume, azoospermia/oligospermia, and dilated seminal vesicles on TRUS; treated by transurethral resection of the ejaculatory ducts (TURED).

The testicular artery arises directly from the aorta. During inguinal orchiopexy, if the testicular artery must be divided (Fowler-Stephens technique for high undescended testes), the testis can survive on collateral supply from the artery of the vas deferens and cremasteric artery — but only if these vessels are carefully preserved.
Male urogenital anatomy showing kidneys, ureters, bladder, prostate, urethra, and external genitalia
Figure 3 — Male Urogenital Anatomy. Overview of kidneys, ureters, bladder, prostate, seminal vesicles, and external genitalia. Source: Wikimedia Commons. Public domain.

03 Renal Physiology & Fluid/Electrolyte Basics

Glomerular Filtration

The glomerular filtration rate (GFR) is approximately 120 mL/min (180 L/day) in a healthy adult. Filtration is driven by net filtration pressure — the balance of hydrostatic and oncotic pressures across the glomerular capillary. The GFR is regulated by: myogenic reflex (afferent arteriolar constriction in response to increased pressure), tubuloglomerular feedback (macula densa senses NaCl delivery and modulates afferent tone), and RAAS (angiotensin II preferentially constricts the efferent arteriole, maintaining GFR in low-flow states). ACE inhibitors and ARBs reduce efferent arteriolar tone, which lowers intraglomerular pressure — protective in diabetic nephropathy but can precipitate acute kidney injury in bilateral renal artery stenosis.

Tubular Function

The proximal convoluted tubule (PCT) reabsorbs ~65% of filtered Na+, water, glucose, amino acids, bicarbonate, phosphate, and uric acid. The loop of Henle establishes the medullary concentration gradient via countercurrent multiplication — the thick ascending limb actively reabsorbs NaCl via the Na-K-2Cl cotransporter (target of loop diuretics). The distal convoluted tubule (DCT) reabsorbs NaCl via the Na-Cl cotransporter (target of thiazides). The collecting duct is regulated by aldosterone (ENaC, Na reabsorption/K secretion) and ADH/vasopressin (aquaporin-2 insertion for water reabsorption).

Acid-Base Balance

The kidneys maintain acid-base homeostasis by: (1) reabsorbing filtered HCO3- (primarily in the PCT via carbonic anhydrase), (2) generating new HCO3- through ammonium (NH4+) excretion, and (3) excreting titratable acid. Renal tubular acidosis (RTA) is relevant to urology because Type I (distal) RTA causes alkaline urine → calcium phosphate stones, while Type II (proximal) RTA causes bicarbonate wasting. Uric acid stones form in persistently acidic urine (pH < 5.5).

Urologic Electrolyte Considerations

Post-TURP syndrome (TUR syndrome) occurs from absorption of hypotonic irrigation fluid (glycine or sorbitol) during monopolar TURP — causing dilutional hyponatremia, hypo-osmolality, volume overload, and glycine toxicity (visual disturbances, encephalopathy). Symptoms include confusion, nausea, bradycardia, and seizures when Na+ falls below 120 mEq/L. Treatment: stop the procedure, administer IV hypertonic saline (3% NaCl) carefully, and give loop diuretics. Bipolar TURP uses normal saline irrigation and has essentially eliminated this complication.

Hyperchloremic metabolic acidosis is the most common metabolic complication of urinary diversion using bowel segments. Ileal and colonic segments reabsorb urinary chloride (via Cl-/HCO3- exchange) and ammonium, leading to non-anion-gap metabolic acidosis. Treatment: oral sodium bicarbonate supplementation. Jejunal segments cause hyponatremic, hyperkalemic, metabolic acidosis (least commonly used for this reason).

Metabolic Complications by Bowel Segment in Urinary Diversion

Bowel SegmentMetabolic ComplicationMechanism
Ileum / ColonHyperchloremic metabolic acidosis (non-anion gap)Cl-/HCO3- exchange across bowel mucosa + NH4+ reabsorption
JejunumHyponatremic, hyperkalemic metabolic acidosisNa+/Cl- secretion with K+/H+ absorption; rarely used
StomachHypochloremic metabolic alkalosis + hematuria-dysuria syndromeHCl secretion into urine; rarely used except in patients with renal insufficiency

Additional long-term complications of bowel-based urinary diversion: vitamin B12 deficiency (if > 60 cm of terminal ileum resected — monitor levels annually after 3-5 years), fat-soluble vitamin malabsorption (ileal resection impairs bile salt reabsorption), diarrhea (bile salt malabsorption), urinary tract stones (hyperoxaluria from fat malabsorption + mucus nidus), recurrent UTIs (mucus-producing bowel epithelium), and secondary malignancy at the bowel-urine interface (adenocarcinoma — rare but reported, typically > 10 years after diversion; recommend annual endoscopic surveillance after 10 years for continent diversions).

After ileal conduit or neobladder creation, monitor for hyperchloremic metabolic acidosis — the most common metabolic complication of urinary diversion. Patients may require lifelong oral bicarbonate supplementation. Also monitor B12 levels in patients with ileal resections exceeding 60 cm.

04 The Urologic Exam & Assessment

History & Physical Examination

The urologic history should address: voiding symptoms (LUTS — frequency, urgency, nocturia, hesitancy, weak stream, straining, incomplete emptying, terminal dribbling), storage symptoms (urgency, incontinence, frequency), hematuria (gross vs microscopic, timing — initial/terminal/total, painful vs painless), pain (flank, suprapubic, perineal, scrotal, penile), sexual function (erectile dysfunction, ejaculatory disorders), and fertility. The digital rectal exam (DRE) assesses prostate size, consistency (normal = firm, rubbery), nodularity, and tenderness. A hard, irregular, asymmetric prostate suggests malignancy. Rectal tone is assessed to evaluate sphincter function.

Urinalysis & Urine Studies

Urinalysis is the most fundamental urologic test. Key findings: hematuria (> 3 RBCs/HPF — requires evaluation for malignancy in adults ≥ 35 years per AUA guidelines), pyuria (> 5 WBCs/HPF — suggests infection), bacteriuria, proteinuria, crystals (calcium oxalate = envelope-shaped, uric acid = rhomboid/rosette, struvite = coffin-lid, cystine = hexagonal). Urine culture is indicated for suspected UTI, with ≥ 105 CFU/mL considered significant.

Urine cytology has high specificity but low sensitivity for urothelial carcinoma, particularly high-grade tumors. It is useful for surveillance of bladder cancer and CIS. 24-hour urine collection is the cornerstone of metabolic stone evaluation — measures volume, calcium, oxalate, citrate, uric acid, sodium, pH, and supersaturation indices.

PSA — Prostate-Specific Antigen

PSA is a serine protease produced by prostatic epithelium. Normal value is age-dependent but generally < 4.0 ng/mL. PSA is organ-specific but NOT cancer-specific — elevated in BPH, prostatitis, instrumentation, ejaculation, and cancer. PSA density = PSA / prostate volume (suspicious if > 0.15). PSA velocity = rate of change over time (suspicious if > 0.75 ng/mL/year). Free-to-total PSA ratio: lower percentage free PSA (< 10%) is more suspicious for cancer. PSA values 4-10 ng/mL represent a "diagnostic gray zone" with ~25% cancer detection rate on biopsy.

Uroflowmetry & Post-Void Residual

Uroflowmetry measures the rate of urine flow. The key parameter is Qmax (maximum flow rate): normal > 15 mL/s; values < 10 mL/s suggest obstruction. A voided volume of ≥ 150 mL is required for a reliable study. The flow pattern helps distinguish obstruction (prolonged, plateau-shaped) from detrusor weakness (low, extended curve). Post-void residual (PVR) is measured by catheterization or ultrasound immediately after voiding. PVR > 200 mL is generally significant; PVR > 300 mL suggests significant bladder dysfunction.

AUA Symptom Score (IPSS)

The International Prostate Symptom Score (IPSS) is a validated 7-question self-assessment tool scoring voiding symptoms from 0-35: mild (0-7), moderate (8-19), severe (20-35). An additional quality-of-life (QoL) question is scored 0-6. The IPSS is used for baseline assessment and monitoring treatment response in BPH. It is not diagnostic of any specific condition.

Hematuria Evaluation Algorithm

The AUA/SUFU guideline for microhematuria (updated 2020) stratifies patients by risk: Low risk: age < 40 (women) or < 25 (men), 3-10 RBC/HPF, no risk factors, never smoker → repeat UA in 6 months. Intermediate risk: age 40-59 (women) or 25-59 (men), 11-25 RBC/HPF, or 3-25 RBC/HPF with risk factors (smoking history, chemical exposure) → cystoscopy + renal US. High risk: age ≥ 60, > 25 RBC/HPF, or any history of gross hematuria, or prior urologic cancer → cystoscopy + CT urogram. All patients with gross hematuria require full urologic evaluation (cystoscopy + CT urogram) regardless of age.

Gross painless hematuria in an adult is bladder cancer until proven otherwise. All patients with gross hematuria require cystoscopy and upper tract imaging (CT urogram). Anticoagulation does NOT cause hematuria — it unmasks an underlying pathologic source. Never attribute hematuria solely to anticoagulation without performing a complete evaluation.
Illustration of digital rectal examination technique for prostate assessment
Figure 4 — Digital Rectal Examination. DRE allows assessment of prostate size, consistency, symmetry, and nodularity. The peripheral zone (where most cancers arise) is the palpable portion. Source: Wikimedia Commons. Public domain.

05 Prostate Cancer

Epidemiology & Risk Factors

Prostate cancer is the most commonly diagnosed non-cutaneous malignancy in men and the second leading cause of cancer death in American men. Risk factors: age (rare before 50; median age at diagnosis ~66), race (African American men have ~60% higher incidence and 2-3× higher mortality), family history (first-degree relative → 2× risk; BRCA2 carriers have 3-5× risk), and diet (high animal fat).

PSA Screening

Current AUA/NCCN guidelines recommend shared decision-making for PSA screening starting at age 55-69 (or age 40-45 for high-risk men: African American, BRCA2, strong family history). Screening is not recommended for men with < 10-year life expectancy. A baseline PSA at age 40-45 can help stratify future risk: PSA > 0.7 ng/mL at age 40 or > 0.9 at age 50 confers significantly higher lifetime risk.

Gleason Grading & ISUP Grade Groups

The Gleason score is the sum of the two most prevalent architectural patterns (each graded 1-5). The primary pattern (most prevalent) is listed first. The ISUP Grade Group system (2014) simplifies reporting:

ISUP Grade GroupGleason ScorePrognosis
13+3 = 6Favorable — candidate for active surveillance
23+4 = 7Favorable intermediate
34+3 = 7Unfavorable intermediate
44+4 = 8, 3+5, 5+3High risk
54+5, 5+4, 5+5 = 9-10Very high risk

TNM Staging (Prostate Cancer, AJCC 8th Edition)

StageDescription
T1aIncidental, ≤ 5% of resected tissue
T1bIncidental, > 5% of resected tissue
T1cIdentified by needle biopsy (PSA elevation)
T2aInvolves ≤ one half of one lobe
T2bInvolves > one half of one lobe
T2cInvolves both lobes
T3aExtracapsular extension (unilateral or bilateral)
T3bSeminal vesicle invasion
T4Invasion of adjacent structures (bladder neck, external sphincter, rectum, levator muscles, pelvic wall)
N1Regional lymph node metastasis
M1aNon-regional lymph node metastasis
M1bBone metastasis
M1cOther distant metastasis

Risk Stratification (NCCN/D'Amico)

Very low risk: T1c, Gleason 6, PSA < 10, fewer than 3 positive cores, ≤ 50% cancer in any core, PSA density < 0.15. Low risk: T1-T2a, Gleason 6, PSA < 10. Intermediate risk: T2b-T2c, or Gleason 7, or PSA 10-20. High risk: T3a, or Gleason 8-10, or PSA > 20. Very high risk: T3b-T4, primary Gleason pattern 5, or > 4 cores with Gleason 8-10.

Active Surveillance

Active surveillance (AS) is the preferred strategy for very-low-risk and low-risk prostate cancer in men with ≥ 10-year life expectancy. Protocol includes: PSA every 3-6 months, DRE every 12 months, confirmatory MRI-targeted biopsy within 6-12 months, then repeat biopsy every 1-2 years. Reclassification triggers intervention (Gleason upgrade to 4+3 or higher, increased tumor volume). The landmark ProtecT trial showed no difference in prostate-cancer-specific mortality at 15 years between AS, radical prostatectomy, and radiotherapy for localized disease.

Radical Prostatectomy

Radical prostatectomy (RP) involves removal of the entire prostate, seminal vesicles, and often pelvic lymph nodes. Approaches: robot-assisted laparoscopic (RARP) — now the most common approach in the US, offering improved visualization and nerve-sparing precision; open retropubic (RRP); and perineal (rarely used). Key steps include apical dissection, dorsal venous complex ligation, nerve-sparing (when oncologically appropriate), vesicourethral anastomosis, and lymph node dissection. Major complications: erectile dysfunction (30-70% depending on nerve-sparing status and age) and urinary incontinence (5-20% at 1 year). Positive surgical margins occur in 10-30% of cases.

Radiation Therapy

External beam radiation therapy (EBRT) — intensity-modulated radiation therapy (IMRT) or stereotactic body radiation therapy (SBRT) — is an alternative to surgery for localized disease. Brachytherapy (permanent seed implantation, typically I-125) is used for low-risk disease. For intermediate and high-risk disease, radiation is combined with androgen deprivation therapy (ADT) — 6 months for intermediate risk, 18-36 months for high risk (per DART/STAMPEDE data). Radiation side effects: proctitis, cystitis, erectile dysfunction (delayed onset), and secondary malignancies.

Androgen Deprivation Therapy (ADT)

ADT is the backbone of treatment for advanced and metastatic prostate cancer. Methods: (1) GnRH agonists (leuprolide, goserelin) — cause initial testosterone flare then suppression (co-administer anti-androgen for first 2-4 weeks to prevent flare); (2) GnRH antagonists (degarelix, relugolix) — immediate suppression without flare; (3) bilateral orchiectomy — surgical castration; (4) anti-androgens (bicalutamide, enzalutamide, apalutamide, darolutamide) — block androgen receptor. Target testosterone level: < 50 ng/dL (castrate). ADT side effects: hot flashes, sexual dysfunction, osteoporosis, metabolic syndrome, cardiovascular risk, cognitive changes, and anemia.

Castration-Resistant Prostate Cancer (CRPC)

CRPC is defined as disease progression despite castrate testosterone levels (< 50 ng/dL). Treatment options include: novel hormonal agents (enzalutamide, abiraterone + prednisone, apalutamide, darolutamide), chemotherapy (docetaxel, cabazitaxel), radiopharmaceuticals (radium-223 for bone metastases, Lu-177-PSMA-617 for PSMA-positive disease), PARP inhibitors (olaparib, rucaparib for BRCA/HRR-mutated tumors), immunotherapy (sipuleucel-T), and bone-protective agents (denosumab, zoledronic acid).

In newly diagnosed metastatic hormone-sensitive prostate cancer (mHSPC), the standard of care is now ADT PLUS at least one additional agent — either a novel hormonal agent (abiraterone, enzalutamide, apalutamide, darolutamide) and/or docetaxel chemotherapy (CHAARTED, LATITUDE, ENZAMET, TITAN, ARASENS trials). The era of ADT monotherapy for mHSPC is over.

Salvage Therapy & Biochemical Recurrence

Biochemical recurrence (BCR) after radical prostatectomy is defined as a detectable and rising PSA ≥ 0.2 ng/mL (confirmed on two measurements). After radiation therapy, BCR is defined as a PSA nadir + 2.0 ng/mL (Phoenix definition). For BCR after RP: salvage radiation therapy (SRT) is most effective when PSA is < 0.5 ng/mL (ideally < 0.2 ng/mL) and when Gleason score, margin status, and PSA kinetics suggest local recurrence. GETUG-AFU 16 and RTOG 9601 trials demonstrated benefit of concurrent ADT with salvage radiation. For BCR after radiation: salvage prostatectomy, cryotherapy, HIFU, or ADT depending on risk profile. PSMA PET-CT has revolutionized BCR evaluation — it detects recurrence at PSA levels as low as 0.2-0.5 ng/mL with high sensitivity, enabling more precise targeting of salvage therapy.

Prostate Biopsy Techniques

The standard approach has evolved from TRUS-guided systematic biopsy (12-core template) to MRI-TRUS fusion targeted biopsy. In fusion biopsy, suspicious lesions identified on mpMRI (PI-RADS ≥ 3) are co-registered with real-time TRUS, and targeted cores are obtained from each lesion in addition to systematic cores. The transperineal approach is increasingly preferred over transrectal due to lower infection risk (near-zero sepsis rate without antibiotics vs ~1-4% with transrectal approach despite prophylaxis). MRI-targeted biopsy improves detection of clinically significant cancer (Gleason ≥ 7) and reduces detection of clinically insignificant cancer (Gleason 6).

Histopathology of prostate cancer showing Gleason pattern 4
Figure 5 — Prostate Cancer Histopathology. Gleason pattern 4 showing poorly formed glands and fused cribriform architecture. Source: Wikimedia Commons. Public domain.

Hamdy FC et al. "10-Year outcomes after monitoring, surgery, or radiotherapy for localized prostate cancer." N Engl J Med. 2016;375(15):1415-1424. PMID: 27048165 (ProtecT Trial)

Epstein JI et al. "The 2014 International Society of Urological Pathology (ISUP) Consensus Conference on Gleason Grading." Am J Surg Pathol. 2016;40(2):244-252. PMID: 25099515

06 Bladder Cancer

Epidemiology & Risk Factors

Bladder cancer is the 6th most common cancer overall and the most common malignancy of the urinary tract. Approximately 90% of bladder cancers in the Western world are urothelial carcinoma (transitional cell carcinoma, TCC). Other histologies: squamous cell carcinoma (associated with chronic inflammation, Schistosoma haematobium), adenocarcinoma (urachal remnant), and small cell carcinoma. Risk factors: cigarette smoking (strongest risk factor, 3-4× risk, accounts for ~50% of cases), occupational exposure to aromatic amines (2-naphthylamine, benzidine — rubber, dye, chemical industries), cyclophosphamide, pelvic radiation, and chronic irritation (catheters, stones, Schistosoma).

Presentation & Diagnosis

The hallmark presentation is painless gross hematuria — present in ~80-90% of patients. Irritative voiding symptoms (frequency, urgency, dysuria) may suggest carcinoma in situ (CIS). Diagnosis requires cystoscopy with biopsy/resection. Urine cytology has high specificity for high-grade tumors and CIS but low sensitivity for low-grade tumors. CT urogram evaluates the upper tracts for synchronous disease.

TNM Staging (Bladder Cancer)

StageDescriptionCategory
TaNoninvasive papillary carcinoma (confined to urothelium)Non-muscle-invasive (NMIBC)
Tis (CIS)Carcinoma in situ — flat, high-grade, confined to urothelium
T1Invades lamina propria (subepithelial connective tissue)
T2aInvades superficial muscle (inner half of detrusor)Muscle-invasive (MIBC)
T2bInvades deep muscle (outer half of detrusor)
T3Invades perivesical tissue (T3a microscopically, T3b macroscopically)
T4Invades adjacent organs (T4a: prostate stroma/uterus/vagina; T4b: pelvic wall/abdominal wall)

TURBT — Transurethral Resection of Bladder Tumor

TURBT is both diagnostic (staging) and therapeutic (for NMIBC). Critical technique: resection must include detrusor muscle in the specimen to accurately stage — absence of muscle requires re-TURBT. A re-TURBT is performed 2-6 weeks after initial resection for high-grade T1 tumors and when no muscle was in the specimen. Approximately 40-50% of re-TURBTs show residual disease, and up to 25% are upstaged.

Intravesical Therapy for NMIBC

BCG (Bacillus Calmette-Guérin) is the gold standard intravesical immunotherapy for intermediate-risk and high-risk NMIBC. Induction: 6 weekly instillations. Maintenance (SWOG protocol): 3 weekly instillations at 3, 6, 12, 18, 24, 30, and 36 months — proven to reduce recurrence and progression. BCG is the only intravesical agent shown to reduce progression to muscle-invasive disease. Contraindications: active UTI, traumatic catheterization, immunosuppression. Complications: BCG cystitis (common), BCG sepsis (rare but life-threatening — treat with isoniazid + rifampin + fluoroquinolone). Intravesical chemotherapy (mitomycin C, gemcitabine) is used for low-risk NMIBC or BCG failures.

Radical Cystectomy & Urinary Diversion

Radical cystectomy is the gold standard for muscle-invasive bladder cancer (T2-T4a, N0-Nx, M0) and BCG-unresponsive high-risk NMIBC. In men: removal of bladder, prostate, seminal vesicles, and pelvic lymph nodes. In women: removal of bladder, uterus, ovaries, anterior vaginal wall, and pelvic lymph nodes. Pelvic lymph node dissection (extended template to the aortic bifurcation) is critical — ~25% of patients are upstaged by LND.

Urinary diversion options: (1) Ileal conduit (Bricker) — the most common diversion; a segment of ileum serves as a urine conduit to an abdominal stoma (requires external appliance). (2) Orthotopic neobladder (Studer, Hautmann) — detubularized ileal segment fashioned into a spherical reservoir anastomosed to the urethra; allows volitional voiding (no stoma). Requires intact external sphincter and negative urethral margin. Patients void by Valsalva/abdominal straining. (3) Continent cutaneous diversion (Indiana pouch) — catheterizable stoma, no external appliance.

Neoadjuvant cisplatin-based chemotherapy (MVAC or dose-dense MVAC or gemcitabine/cisplatin) provides a 5-8% absolute overall survival benefit and should be offered to eligible patients before cystectomy. Adjuvant immunotherapy (nivolumab) is now standard for patients at high risk of recurrence post-cystectomy. Trimodal therapy (maximal TURBT + concurrent chemoradiation) is a bladder-preserving alternative for select patients.

Immunotherapy for Metastatic Urothelial Carcinoma

Immune checkpoint inhibitors have transformed treatment of advanced urothelial carcinoma. First-line: For cisplatin-eligible patients, pembrolizumab + enfortumab vedotin (EV-302/KEYNOTE-A39 trial) is the new standard; cisplatin-based chemotherapy followed by avelumab maintenance (JAVELIN Bladder 100) is an established option. For cisplatin-ineligible patients: pembrolizumab or atezolizumab (if PD-L1 positive) or carboplatin-based chemotherapy. Second-line: Enfortumab vedotin (antibody-drug conjugate targeting Nectin-4), erdafitinib (FGFR inhibitor for FGFR2/3-altered tumors), sacituzumab govitecan (Trop-2 ADC). The urothelial carcinoma treatment landscape is rapidly evolving with novel ADCs and targeted therapies.

CIS (carcinoma in situ) of the bladder is a flat, high-grade lesion that appears as erythematous, velvety mucosa on cystoscopy. Despite being "non-invasive," it has a 50-80% risk of progression to muscle-invasive disease if untreated. CIS is the most aggressive form of NMIBC and requires BCG therapy. Failure to respond to BCG mandates radical cystectomy.
Histopathology of urothelial carcinoma of the bladder
Figure 6 — Urothelial Carcinoma Histopathology. High-grade papillary urothelial carcinoma showing architectural disorder and nuclear atypia. Source: Wikimedia Commons. Public domain.

Grossman HB et al. "Neoadjuvant chemotherapy plus cystectomy compared with cystectomy alone for locally advanced bladder cancer." N Engl J Med. 2003;349(9):859-866. PMID: 14645423

07 Renal Cell Carcinoma

Epidemiology & Subtypes

Renal cell carcinoma (RCC) accounts for ~90% of renal malignancies and ~3% of all adult cancers. Peak incidence age 60-70; M:F ratio 2:1. Risk factors: smoking, obesity, hypertension, acquired cystic kidney disease (dialysis patients), von Hippel-Lindau (VHL) syndrome, and hereditary papillary RCC. Histologic subtypes:

SubtypeFrequencyKey Features
Clear cell70-80%VHL gene mutation (chromosome 3p); highly vascular; most responsive to targeted therapy and immunotherapy
Papillary (Type 1 & 2)10-15%Type 1: MET mutation, better prognosis; Type 2: worse prognosis, associated with hereditary leiomyomatosis and RCC (HLRCC)
Chromophobe5%Best prognosis of RCC subtypes; associated with Birt-Hogg-Dubé syndrome
Collecting duct (Bellini)< 1%Aggressive, poor prognosis
MedullaryRareAlmost exclusively in patients with sickle cell trait; highly aggressive

Presentation

The classic triad of flank pain, hematuria, and palpable abdominal mass is present in only ~10% of cases and usually indicates advanced disease. Most RCCs today are discovered incidentally on imaging. Paraneoplastic syndromes occur in ~20%: hypercalcemia (PTHrP), erythrocytosis (EPO), hypertension (renin), hepatic dysfunction without liver metastases (Stauffer syndrome — resolves after nephrectomy), and non-metastatic hepatic dysfunction.

Bosniak Classification for Renal Cysts

CategoryFeaturesMalignancy RiskManagement
ISimple cyst: thin wall, no septa/calcification/enhancement< 1%No follow-up
IIFew thin septa, fine calcification, < 3 cm hyperdense cyst, no enhancement< 5%No follow-up
IIFMultiple thin septa, minimal smooth thickening, thick calcification, ≥ 3 cm hyperdense, no enhancement5-15%Follow-up imaging
IIIThick/irregular septa or wall, measurable enhancement40-60%Surgery or active surveillance
IVEnhancing soft tissue component> 80%Surgery

Surgical Management

For localized RCC (T1-T2), surgery is the primary treatment. Partial nephrectomy (nephron-sparing surgery) is the gold standard for T1a tumors (≤ 4 cm) and preferred for T1b (≤ 7 cm) when technically feasible — equivalent oncologic outcomes with better renal function preservation. Approaches: robotic-assisted (most common), laparoscopic, or open. Radical nephrectomy is indicated for larger tumors (T2, > 7 cm), centrally located tumors not amenable to partial nephrectomy, and locally advanced disease. Includes removal of Gerota fascia and kidney en bloc. Ipsilateral adrenalectomy is only indicated if imaging suggests adrenal involvement.

For tumors with IVC tumor thrombus (occurs in ~4-10% of RCC), surgical thrombectomy is performed with radical nephrectomy. Level of thrombus dictates approach: Level I (renal vein) — simple vein control; Level II (infrahepatic IVC) — IVC clamping; Level III (intrahepatic/retrohepatic IVC) — may require liver mobilization; Level IV (supradiaphragmatic/intra-atrial) — requires cardiopulmonary bypass with cardiothoracic surgery. Despite the IVC thrombus, if there is no distant metastatic disease, 5-year survival is 40-65% after complete resection.

IMDC Risk Stratification (Metastatic RCC)

The International Metastatic RCC Database Consortium (IMDC/Heng criteria) stratifies mRCC prognosis using 6 risk factors: (1) KPS < 80%, (2) time from diagnosis to treatment < 1 year, (3) hemoglobin < lower limit of normal, (4) corrected calcium > upper limit of normal, (5) neutrophils > upper limit of normal, (6) platelets > upper limit of normal. Favorable risk: 0 factors (median OS ~43 months). Intermediate risk: 1-2 factors (median OS ~23 months). Poor risk: 3-6 factors (median OS ~8 months). IMDC risk group guides treatment selection in mRCC.

Systemic Therapy for Advanced/Metastatic RCC

First-line treatment for clear cell mRCC has shifted to immune checkpoint inhibitor (ICI) combinations: ipilimumab + nivolumab (IMDC intermediate/poor risk — CheckMate 214), pembrolizumab + axitinib (KEYNOTE-426), nivolumab + cabozantinib (CheckMate 9ER), or pembrolizumab + lenvatinib (KEYNOTE-581/CLEAR). For favorable-risk patients, ICI combinations or single-agent TKI (cabozantinib, sunitinib, pazopanib) are options. Cytoreductive nephrectomy is selectively offered in the immunotherapy era (no longer standard for all patients — CARMENA and SURTIME trials).

Small Renal Masses & Active Surveillance

Small renal masses (SRM) are defined as enhancing renal tumors ≤ 4 cm. Approximately 20-30% of SRMs are benign (oncocytoma, angiomyolipoma). Active surveillance is appropriate for patients with significant comorbidities, limited life expectancy, or high surgical risk. Growth rate is typically slow (~0.3 cm/year). Renal mass biopsy can help guide management — high diagnostic accuracy for distinguishing benign from malignant lesions and determining histologic subtype. Thermal ablation (cryoablation, radiofrequency ablation, microwave ablation) is an option for T1a tumors in patients who are poor surgical candidates — lower cancer-specific survival than partial nephrectomy but acceptable for appropriately selected patients.

RCC is classically resistant to conventional chemotherapy and radiotherapy. The VHL-HIF-VEGF pathway drives clear cell RCC angiogenesis, making it responsive to VEGF-targeted TKIs. The addition of immune checkpoint inhibitors has transformed mRCC outcomes — 5-year OS for intermediate/poor-risk mRCC now exceeds 40% with ipilimumab + nivolumab.
Histopathology of clear cell renal cell carcinoma showing clear cytoplasm and vascular stroma
Figure 7 — Clear Cell RCC Histopathology. Tumor cells with abundant clear cytoplasm (lipid and glycogen-rich) arranged around a delicate vascular network. Source: Wikimedia Commons. Public domain.

Motzer RJ et al. "Nivolumab plus ipilimumab versus sunitinib in advanced renal-cell carcinoma." N Engl J Med. 2018;378(14):1277-1290. PMID: 29562145 (CheckMate 214)

08 Testicular Cancer

Epidemiology & Risk Factors

Testicular cancer is the most common solid malignancy in men aged 15-35. Incidence has been increasing over recent decades. Risk factors: cryptorchidism (3-8× increased risk; orchiopexy before puberty may reduce risk but does not eliminate it), prior testicular cancer (contralateral risk ~2-5%), family history (brother with testicular cancer → 8-10× risk), disorders of sex development (gonadal dysgenesis), and infertility/testicular atrophy.

Classification — Germ Cell Tumors (95%)

CategorySubtypesKey Features
Seminoma (~55%)Classical, spermatocyticPeak age 30-40; homogeneous on US; exquisitely radiosensitive; AFP is NEVER elevated (if AFP elevated, treat as NSGCT regardless of histology)
Nonseminomatous GCT (NSGCT, ~45%)Embryonal carcinoma, yolk sac tumor, choriocarcinoma, teratoma, mixedPeak age 20-30; more aggressive; choriocarcinoma produces hCG; yolk sac tumor produces AFP; teratoma is chemoresistant — must be resected

Tumor Markers

AFP (α-fetoprotein): Elevated in yolk sac tumors and some embryonal carcinomas. Half-life: 5-7 days. NEVER elevated in pure seminoma (if elevated, treat as NSGCT). hCG (β-human chorionic gonadotropin): Elevated in choriocarcinoma (very high levels) and ~10-20% of seminomas (modest elevation). Half-life: 24-36 hours. LDH: Nonspecific marker of tumor burden/cell turnover. Marker decline after orchiectomy follows predictable half-lives — failure to normalize or rising markers indicates residual/metastatic disease.

Staging & IGCCCG Risk Classification

Stage I: confined to testis (no lymph node or distant metastasis). Stage II: retroperitoneal lymph node involvement (IIA: ≤ 2 cm; IIB: 2-5 cm; IIC: > 5 cm). Stage III: distant metastatic disease (IIIA: lung/non-regional LN; IIIB-C: based on marker levels or non-pulmonary visceral metastasis). The International Germ Cell Cancer Collaborative Group (IGCCCG) classifies metastatic GCT into good, intermediate, and poor prognosis groups based on site of primary, presence of non-pulmonary visceral metastases, and marker levels — 5-year survival: good 90-92%, intermediate 72-80%, poor 48-54%.

Management

Radical inguinal orchiectomy is the initial treatment for all suspected testicular tumors. An inguinal approach is mandatory (NOT transscrotal) — a transscrotal biopsy or orchiectomy violates the scrotal skin, alters lymphatic drainage (scrotal skin drains to inguinal nodes, testis drains to retroperitoneal nodes), and may necessitate hemiscrotectomy. A testicular prosthesis can be placed at the time of orchiectomy.

Stage I seminoma: Options include surveillance (preferred for most — recurrence rate ~15-20%, nearly all curable at relapse), single-agent carboplatin (1-2 cycles), or adjuvant radiation (less used now due to long-term toxicity). Stage I NSGCT: Options include surveillance (if markers normalize and risk factors absent), retroperitoneal lymph node dissection (RPLND), or adjuvant BEP × 1 cycle.

BEP chemotherapy (bleomycin, etoposide, cisplatin) is the standard regimen for metastatic GCT: 3 cycles for good-prognosis, 4 cycles for intermediate/poor-prognosis. Cure rates for metastatic testicular cancer are among the highest of any solid tumor (>90% for good-prognosis disease). Post-chemotherapy RPLND is indicated for residual retroperitoneal masses > 1 cm in NSGCT (may contain residual viable tumor, teratoma, or necrosis). For seminoma, residual masses are observed with PET/CT — post-chemotherapy surgery only if PET-positive and ≥ 3 cm.

Testicular cancer is one of the most curable solid tumors. Even widely metastatic disease has a > 50% cure rate. Sperm banking should be offered to ALL patients before orchiectomy and chemotherapy, as fertility may be compromised. The contralateral testis should be examined, and if cryptorchid, should undergo biopsy to assess for GCNIS (germ cell neoplasia in situ).
Gross pathology specimen of testicular seminoma
Figure 8 — Testicular Seminoma (Gross Specimen). Homogeneous, cream-colored, lobulated tumor replacing normal testicular parenchyma. Source: Wikimedia Commons. Public domain.

Late Effects of Testicular Cancer Treatment

Given the young age of most patients and high cure rates, long-term survivorship is critical. Cardiovascular disease: Cisplatin-based chemotherapy increases long-term cardiovascular risk (metabolic syndrome, coronary artery disease) — 2-3× risk of cardiovascular events; ongoing surveillance recommended. Secondary malignancies: Radiation and chemotherapy increase risk of solid tumors (GI, lung, thyroid, melanoma) and leukemia; risk rises with time. Fertility: Chemotherapy impairs spermatogenesis — recovery occurs in ~80% by 5 years for BEP; sperm banking before treatment is essential. Hypogonadism: ~10-20% of long-term survivors develop testosterone deficiency. Nephrotoxicity, ototoxicity, neurotoxicity: Cisplatin-related effects may persist or worsen over time (tinnitus, hearing loss, peripheral neuropathy). Retrograde ejaculation: After RPLND (even nerve-sparing); rates ~5-10% with nerve-sparing technique vs ~70-100% without. Long-term follow-up protocols should be individualized based on tumor stage, histology, and treatment received.

International Germ Cell Consensus Classification. "International Germ Cell Consensus Classification: a prognostic factor-based staging system for metastatic germ cell cancers." J Clin Oncol. 1997;15(2):594-603. PMID: 9058731

09 Upper Tract Urothelial Carcinoma

Overview

Upper tract urothelial carcinoma (UTUC) accounts for 5-10% of urothelial cancers. It involves the renal pelvis (~60%) or ureter (~40%). Risk factors mirror those of bladder cancer (smoking, aromatic amines) with additional associations: aristolochic acid (Balkan endemic nephropathy, Chinese herbal nephropathy) and Lynch syndrome (MSH2 mutations — lifetime UTUC risk ~8%). UTUC has a higher rate of invasive disease at presentation (~60% are invasive at diagnosis vs ~25% for bladder cancer).

Diagnosis

Presentation: hematuria (gross or microscopic) is the most common symptom (~70-80%); flank pain from obstruction (~20-30%). Diagnosis: CT urogram (sensitivity ~96% for detecting UTUC — filling defect or urothelial thickening in the excretory phase), urine cytology (higher sensitivity for high-grade UTUC), and diagnostic ureteroscopy with biopsy and barbotage. Selective upper tract washing cytology improves diagnostic accuracy. All patients with UTUC should undergo cystoscopy to evaluate for concurrent bladder cancer (~17% have synchronous bladder lesions).

Management

Radical nephroureterectomy (RNU) with excision of a bladder cuff is the gold standard for high-risk UTUC (high grade, invasive, large, multifocal). The bladder cuff must be removed because of high rates (~30-50%) of subsequent bladder recurrence if the distal ureter/intramural segment is left behind. Kidney-sparing endoscopic management (ureteroscopic laser ablation) is appropriate for low-risk UTUC (low grade, small, unifocal) in patients with a solitary kidney, bilateral disease, or significant CKD. Adjuvant instillation of mitomycin C within the bladder after RNU reduces intravesical recurrence (ODMIT-C trial). Neoadjuvant cisplatin-based chemotherapy is increasingly considered given the loss of one kidney after RNU.

10 Penile Cancer

Overview

Penile cancer is rare in developed countries (< 1% of male cancers) but more common in developing nations. The vast majority (~95%) are squamous cell carcinoma. Risk factors: lack of circumcision (phimosis and chronic balanitis), poor hygiene, HPV infection (types 16 and 18 — present in ~50% of cases), smoking, and immunosuppression. Precursor lesions include erythroplasia of Queyrat (CIS of the glans), Bowen disease (CIS of the shaft), and bowenoid papulosis (HPV-associated, multifocal).

Staging & Management

Treatment of the primary tumor depends on stage: Tis/Ta — topical therapy (5-FU, imiquimod) or laser ablation; T1 (low grade, no LVI) — wide local excision or glansectomy; T1 (high grade or LVI) through T2 — partial penectomy (2 cm margin historically, though recent evidence supports narrower margins for lower-stage tumors); T3-T4 — total penectomy with perineal urethrostomy. A minimum penile stump length of ~2 cm is desired for standing voiding after partial penectomy.

Inguinal lymph node management is critical — the most important prognostic factor is inguinal lymph node status. For clinically node-negative patients with intermediate/high-risk primary tumors (T1 high grade or higher): dynamic sentinel node biopsy (DSNB) or modified inguinal lymphadenectomy. For clinically positive nodes: fine-needle aspiration followed by inguinal lymphadenectomy if positive. Pelvic lymph node dissection is indicated if ≥ 2 positive inguinal nodes or extranodal extension.

Penile Cancer TNM Staging

StageDescription
TisCarcinoma in situ (penile intraepithelial neoplasia)
TaNoninvasive verrucous carcinoma
T1aInvades subepithelial tissue, no LVI, grade 1-2
T1bInvades subepithelial tissue, with LVI or grade 3
T2Invades corpus spongiosum or corpora cavernosa
T3Invades urethra
T4Invades adjacent structures (prostate, pubic bone)
Penile cancer has an orderly, predictable pattern of lymph node spread: first to superficial inguinal nodes, then deep inguinal nodes, then pelvic (iliac) nodes. Skip metastases are rare. The 5-year survival drops from ~85% for node-negative disease to ~30-40% for node-positive disease, making accurate lymph node assessment critical for prognosis and treatment planning.

11 Nephrolithiasis — Evaluation & Medical Management

Epidemiology & Stone Types

Nephrolithiasis affects ~10% of the population, with a recurrence rate of ~50% within 5-10 years. Peak incidence age 30-60; M:F ratio ~2:1 (narrowing with rising female obesity rates). Stone composition:

Stone TypeFrequencyCrystal AppearanceKey Features
Calcium oxalate70-80%Envelope-shaped (monohydrate: dumbbell)Most common; associated with hypercalciuria, hyperoxaluria, hypocitraturia; radiopaque on X-ray
Calcium phosphate10-15%AmorphousAssociated with RTA Type I (alkaline urine pH > 7.0), hyperparathyroidism; radiopaque
Uric acid5-10%Rhomboid/rosetteRADIOLUCENT on X-ray (visible on CT); formed in acidic urine (pH < 5.5); associated with gout, metabolic syndrome, myeloproliferative disorders; can be dissolved with urinary alkalinization
Struvite (MAP)5-10%Coffin-lidMagnesium ammonium phosphate; caused by urease-producing bacteria (Proteus, Klebsiella, Pseudomonas); form staghorn calculi; alkaline urine pH > 7.2
Cystine1-3%HexagonalAutosomal recessive cystinuria; recurrent stones starting in childhood/adolescence; semi-opaque on X-ray

Acute Renal Colic — Presentation & Workup

Presentation: sudden-onset, severe colicky flank pain radiating to the groin/ipsilateral testicle or labium, often with nausea/vomiting, hematuria (present in ~85%), and restlessness (cannot find a comfortable position). Pain location correlates with stone position: upper ureteral stones → flank/costovertebral angle pain; mid-ureteral stones (crossing iliac vessels) → anterior abdominal pain mimicking appendicitis or diverticulitis; distal ureteral stones (near UVJ) → suprapubic pain, urinary urgency/frequency, pain radiating to the ipsilateral testicle/labium. The gold standard imaging is non-contrast CT abdomen/pelvis — sensitivity ~97%, specificity ~96% for ureteral stones. Also identifies stone size, location, number, and alternative diagnoses. Ultrasound is the initial study in pregnant patients and children. KUB X-ray is useful for follow-up of known radiopaque stones.

Indications for Urgent Intervention in Stone Disease

While most ureteral stones can be managed expectantly, certain situations require urgent decompression (ureteral stent or nephrostomy tube): (1) Emergency infected obstructed kidney (fever + obstructing stone = pyonephrosis until proven otherwise — can progress to urosepsis rapidly), (2) impending renal failure (bilateral obstruction, solitary kidney, pre-existing CKD), (3) intractable pain/vomiting despite adequate analgesia, and (4) high-grade obstruction with declining renal function on serial labs.

Medical Expulsive Therapy (MET)

For distal ureteral stones ≤ 10 mm, spontaneous passage is possible (likelihood decreases with size: < 5 mm ~68%, 5-10 mm ~47%). Tamsulosin 0.4 mg daily (alpha-blocker) is the most commonly used MET agent — relaxes ureteral smooth muscle, facilitating stone passage, particularly for distal ureteral stones 5-10 mm. Nifedipine (calcium channel blocker) is a second-line option. Pain management: NSAIDs (ketorolac) are first-line (also reduce ureteral edema and spasm), with opioids for breakthrough pain. MET trial duration: 4-6 weeks with close follow-up.

Metabolic Evaluation

Indicated for recurrent stone formers, first-time formers with risk factors, and all children. Includes: 24-hour urine collection (× 2 for reliability) measuring volume, calcium, oxalate, citrate, uric acid, sodium, pH, magnesium, phosphorus, creatinine, and cystine (if suspected). Serum studies: calcium, PTH, uric acid, bicarbonate, BUN/creatinine. Stone analysis (infrared spectroscopy or X-ray diffraction) should be performed on every recovered stone.

Prevention Strategies

Universal: fluid intake to achieve > 2.5 L/day urine output (most impactful intervention); dietary sodium restriction (< 2,300 mg/day — reduces calcium excretion); moderate protein intake; avoid excessive oxalate-rich foods; maintain normal calcium intake (1,000-1,200 mg/day — dietary calcium restriction INCREASES stone risk by reducing intestinal oxalate binding). Specific: thiazide diuretics (hydrochlorothiazide, chlorthalidone, indapamide) for hypercalciuria; potassium citrate for hypocitraturia and uric acid stones (alkalinizes urine to pH 6.5-7.0); allopurinol for hyperuricosuric calcium stones and uric acid stones; tiopronin or D-penicillamine for cystine stones (chelate cystine).

Uric acid stones are the only common stone type that can be completely dissolved medically — alkalinize urine to pH 6.5-7.0 with potassium citrate. Uric acid stones are radiolucent on plain X-ray but visible on CT. A large radiolucent stone on KUB that is visible on CT should prompt consideration of uric acid composition and a dissolution trial before surgical intervention.
Various types of kidney stones showing different compositions and appearances
Figure 9 — Kidney Stones by Composition. Gross appearance varies by stone type — calcium oxalate (dark, spiculated), calcium phosphate (smooth, pale), uric acid (orange-brown), and struvite (large, branched). Source: Wikimedia Commons. Public domain.

12 Surgical Stone Management

Indications for Surgical Intervention

Surgery is indicated when: stone fails to pass with MET after 4-6 weeks, stone > 10 mm (unlikely to pass spontaneously), intractable pain, persistent obstruction with infection (Emergency — sepsis risk), bilateral obstruction, solitary kidney with obstruction, and patient preference. Choice of surgical modality depends on stone size, location, composition, anatomy, and patient factors.

Shock Wave Lithotripsy (SWL)

SWL uses focused extracorporeal shock waves to fragment stones. Best for: renal and proximal ureteral stones ≤ 20 mm (ideally ≤ 10-15 mm), lower pole stones ≤ 10 mm. Success rate: ~80-85% for stones < 10 mm, decreasing with size. Contraindications: pregnancy, uncorrected coagulopathy, aortic or renal artery aneurysm, distal obstruction. Limitations: less effective for hard stones (calcium oxalate monohydrate, cystine, brushite), large stones, lower pole stones > 10 mm (poor clearance due to gravity-dependent calyx), and obese patients (skin-to-stone distance > 10 cm). Complications: steinstrasse (stone street — column of fragments obstructing the ureter), subcapsular hematoma, and perinephric hematoma.

Ureteroscopy (URS)

Ureteroscopy uses a semirigid or flexible endoscope introduced retrograde through the urethra, bladder, and ureteral orifice. Stones are fragmented with a holmium:YAG laser (gold standard for intracorporeal lithotripsy) and fragments retrieved with baskets. URS is first-line for: mid and distal ureteral stones (any size), proximal ureteral stones ≤ 15-20 mm, renal stones ≤ 20 mm, and when SWL has failed. Stone-free rates: ~95% for distal ureteral stones, ~85-90% for proximal ureteral and renal stones ≤ 15 mm. A ureteral access sheath (UAS) facilitates multiple passes and reduces intrarenal pressure. A post-procedural double-J stent is often placed for 1-2 weeks. Complications: ureteral injury/perforation, stricture (long-term), UTI/sepsis, and stone migration.

Percutaneous Nephrolithotomy (PCNL)

PCNL is the procedure of choice for large renal stones (> 20 mm), staghorn calculi, lower pole stones > 10-15 mm, and stones resistant to SWL/URS. Technique: percutaneous renal access is obtained under fluoroscopic or ultrasound guidance (typically through a posterior calyx), the tract is dilated to 24-30 Fr, and a nephroscope is introduced. Stones are fragmented with ultrasonic, pneumatic, or laser lithotripsy and extracted. Stone-free rates: ~85-95% for large stones. Miniaturized PCNL (mini-PCNL, micro-PCNL, ultra-mini-PCNL) uses smaller tracts (11-20 Fr) with reduced morbidity. Complications: bleeding (most common significant complication — 2-5% require transfusion), pneumothorax (supracostal access above 12th rib), colonic injury, urosepsis, and AV fistula.

Obstructing ureteral stone with concurrent UTI/sepsis is a UROLOGIC EMERGENCY requiring urgent decompression — either ureteral stent placement or percutaneous nephrostomy tube. Definitive stone treatment should be deferred until infection is controlled. Do NOT attempt ureteroscopy/lithotripsy on an infected, obstructed system — this risks life-threatening sepsis.
ModalityBest IndicationStone-Free RateKey Advantage
SWLRenal/proximal ureteral ≤ 15 mm70-85%Noninvasive, outpatient
URSAny ureteral; renal ≤ 20 mm85-95%High success, direct visualization
PCNLRenal > 20 mm, staghorn85-95%Best for large stone burden

Staghorn Calculi

Staghorn calculi are branched stones that fill the renal pelvis and extend into at least two calyces. Most are composed of struvite (infection stones) or, less commonly, cystine or uric acid. Struvite staghorn calculi form in the setting of chronic infection with urease-producing organisms (Proteus mirabilis is the most common; also Klebsiella, Pseudomonas, Staphylococcus saprophyticus). Urease splits urea into ammonia and CO2, raising urine pH > 7.2 and promoting crystallization of magnesium ammonium phosphate (struvite) and calcium phosphate (apatite). Untreated staghorn calculi cause progressive renal damage, recurrent sepsis, and eventual loss of renal function. Treatment: PCNL (first-line) — may require staged procedures or multiple access tracts for complete clearance. SWL monotherapy has a low stone-free rate for large staghorn calculi (< 50%). Concurrent and prolonged antibiotic therapy is essential. Acetohydroxamic acid (urease inhibitor) may be used adjunctively to prevent recurrence.

X-ray showing a large staghorn calculus filling the renal collecting system
Figure 17 — Staghorn Calculus. KUB radiograph demonstrating a large, branching radiopaque stone filling the renal pelvis and extending into multiple calyces. Source: Wikimedia Commons. Public domain.

Assimos D et al. "AUA/Endourology Society Guideline: Surgical Management of Stones." J Urol. 2016;196(4):1153-1160. PMID: 27021000

13 Ureteral Obstruction & Stenting

Acute Ureteral Obstruction

Causes: nephrolithiasis (most common), malignant extrinsic compression (cervical, colorectal, ovarian cancer, retroperitoneal lymphadenopathy), retroperitoneal fibrosis (idiopathic/Ormond disease or drug-induced — methysergide, ergotamine), iatrogenic ureteral injury (pelvic surgery), UPJ obstruction, ureteral stricture, and blood clots. Bilateral obstruction or obstruction of a solitary kidney causes obstructive renal failure (post-renal AKI). Unilateral obstruction may be asymptomatic if the contralateral kidney is normal.

Pathophysiology of Obstruction

Acute unilateral obstruction produces a triphasic renal hemodynamic response: Phase 1 (0-1.5 hrs) — increased renal blood flow and ureteral pressure (prostaglandin-mediated vasodilation); Phase 2 (1.5-5 hrs) — decreased renal blood flow with continued elevated ureteral pressure; Phase 3 (> 5 hrs) — decreased renal blood flow AND decreased ureteral pressure. Prolonged obstruction causes progressive tubular damage, cortical thinning, and eventual loss of renal function. Recovery potential decreases with duration of obstruction: complete recovery is expected if obstruction is relieved within 1-2 weeks; after 6-8 weeks of complete obstruction, recovery is unlikely. Post-obstructive diuresis may occur after relief of bilateral obstruction or obstruction of a solitary kidney — characterized by massive polyuria (may exceed 500 mL/hr) requiring careful fluid and electrolyte monitoring. Replace urine output with 0.45% saline, monitoring electrolytes every 4-6 hours.

Ureteral Stents

The double-J (DJ) ureteral stent is the most commonly placed ureteral stent. It has coiled ends (J-shaped) to anchor in the renal pelvis proximally and bladder distally. Indications: relief of ureteral obstruction, post-URS (to prevent edema-related obstruction), after ureteral injury/repair, and pre-SWL for large stones (to prevent steinstrasse). Stents are typically 6 Fr in diameter and 22-28 cm in length (patient height-dependent). Stent-related symptoms (frequency, urgency, flank pain with voiding, hematuria) are common and can be managed with alpha-blockers (tamsulosin) and anticholinergics.

A "forgotten stent" can result in encrustation, stone formation along the stent, recurrent UTI, and loss of renal function. Stents should be removed within 3-6 months (manufacturer-specific dwell time). Patients must receive clear instructions regarding stent removal timing, and a tracking system should be in place to prevent retained stents.

Percutaneous Nephrostomy

Percutaneous nephrostomy (PCN) provides external urinary drainage via a tube placed through the flank into the renal collecting system under ultrasound/fluoroscopic guidance. Preferred over retrograde stent placement in: infected obstructed system (pyonephrosis/sepsis — often technically easier and faster), patients too unstable for general anesthesia, failed retrograde stent placement, and severely ill patients. PCN can be converted to an antegrade ureteral stent once the patient stabilizes.

UPJ Obstruction

Ureteropelvic junction (UPJ) obstruction is the most common cause of hydronephrosis in children but also presents in adults. May be intrinsic (adynamic segment, high insertion of ureter) or extrinsic (crossing vessel — lower pole renal artery compressing the UPJ, present in ~30-50% of adult cases). Diagnosis: diuretic renography (MAG3 scan with furosemide) showing delayed drainage (T½ > 20 min). Definitive treatment: dismembered pyeloplasty (Anderson-Hynes) — excision of the obstructed segment and reanastomosis of the ureter to a spatulated renal pelvis. Success rate > 95%. Robotic-assisted pyeloplasty is now the most common approach. Endopyelotomy (endoscopic incision) is an alternative but has lower long-term success (~70-80%).

CT scan showing hydronephrosis with dilated renal pelvis and calyces
Figure 10 — Hydronephrosis. CT image demonstrating dilated renal pelvis and calyces due to ureteral obstruction. Source: Wikimedia Commons. Public domain.

14 Benign Prostatic Hyperplasia (BPH)

Pathophysiology

BPH is a histologic diagnosis characterized by proliferation of stromal and epithelial cells in the prostatic transition zone, leading to glandular enlargement and potential bladder outlet obstruction (BOO). BPH affects ~50% of men aged 50-60 and ~90% of men > 80. The relationship between prostate size and symptom severity is not linear — a small prostate with median lobe enlargement can cause more obstruction than a very large prostate. Two components contribute to obstruction: static (tissue bulk) and dynamic (smooth muscle tone mediated by alpha-1 adrenergic receptors in the prostate and bladder neck).

Clinical Assessment

Lower urinary tract symptoms (LUTS) include storage symptoms (frequency, urgency, nocturia) and voiding symptoms (hesitancy, weak stream, intermittency, straining, incomplete emptying). Assessment: IPSS/AUA symptom score, DRE, urinalysis, PSA, uroflowmetry (Qmax), and post-void residual (PVR). Optional: transrectal or transabdominal ultrasound for prostate volume, pressure-flow urodynamics for equivocal cases.

Medical Therapy

Drug ClassExamplesMechanismKey Effects/Side Effects
Alpha-1 blockersTamsulosin, alfuzosin, silodosin, doxazosin, terazosinRelax prostatic smooth muscle (dynamic component)Rapid symptom relief (days-weeks); side effects: orthostatic hypotension (less with tamsulosin/alfuzosin), retrograde ejaculation, intraoperative floppy iris syndrome (IFIS)
5-alpha reductase inhibitors (5-ARIs)Finasteride (type 2), dutasteride (type 1 & 2)Block conversion of testosterone to DHT → reduce prostate volume by 20-30%Full effect takes 6-12 months; reduce PSA by ~50% (must double PSA value for cancer screening); side effects: decreased libido, ED, gynecomastia
Combination therapyTamsulosin + dutasteride (Jalyn)Both mechanismsSuperior to monotherapy for large prostates (> 30-40 mL) — MTOPS and CombAT trials
PDE5 inhibitorsTadalafil 5 mg dailyRelax smooth muscle via NO/cGMP pathwayImproves both LUTS and erectile dysfunction; FDA-approved for BPH
Anticholinergics / Beta-3 agonistsOxybutynin, mirabegronReduce detrusor overactivity (storage symptoms)Used cautiously with BPH; check PVR (risk of retention)

Surgical Management

Surgical indications: refractory to medical therapy, recurrent urinary retention, recurrent UTI, bladder stones secondary to BPH, renal insufficiency due to BOO, recurrent gross hematuria from BPH, and patient preference.

ProcedureProstate SizeTechniqueKey Features
TURP30-80 mLTransurethral resection with monopolar or bipolar electrocauteryGold standard; bipolar eliminates TUR syndrome; retrograde ejaculation ~65-75%
HoLEPAny sizeHolmium laser enucleation — laser dissects adenoma from capsule, tissue morcellated in bladderSize-independent; lowest retreatment rate; steep learning curve; equivalent to open prostatectomy for large glands
Greenlight PVP30-80 mL532 nm laser photoselective vaporizationGood for anticoagulated patients (minimal bleeding); may require retreatment
Rezum30-80 mLTransurethral water vapor (steam) injection → thermal ablation of prostatic tissueOffice-based; preserves ejaculatory function; effect develops over weeks
UroLift (PUL)30-80 mL (no median lobe)Implants retract obstructing lateral lobesPreserves ejaculatory and erectile function; may need retreatment
Aquablation30-150 mLRobotic waterjet ablation using real-time TRUS guidanceAutomated resection; preserves ejaculation in some; emerging technology
Simple prostatectomy> 80-100 mLEnucleation of adenoma — robotic, laparoscopic, or open (suprapubic/retropubic)For very large glands; robotic approach increasingly common

Prostate Artery Embolization (PAE)

Prostate artery embolization is an interventional radiology procedure that selectively embolizes prostatic arteries to cause ischemic necrosis and shrinkage of the prostate. It is performed through a transfemoral or transradial approach. PAE is offered to men who are poor surgical candidates, those who decline surgery, or those who prioritize preservation of sexual function. Evidence shows modest improvement in IPSS and Qmax, but outcomes are generally inferior to TURP and HoLEP. PAE is not endorsed as first-line by AUA guidelines but is recognized as an option by some guidelines (NICE).

Medical therapy with alpha-blockers and/or 5-ARIs is first-line for bothersome BPH/LUTS. The MTOPS trial showed that combination therapy (doxazosin + finasteride) was superior to either agent alone in reducing clinical progression. 5-ARIs reduce PSA by approximately 50% — always double the measured PSA value in patients on finasteride or dutasteride when screening for prostate cancer.

Acute Urinary Retention (AUR)

Acute urinary retention is the sudden inability to void, presenting with severe suprapubic pain and a distended, palpable bladder. Most common cause in men: BPH (precipitated by medications — anticholinergics, sympathomimetics, opioids — or constipation, UTI, anesthesia). Immediate management: urethral catheterization (Foley or intermittent). If urethral catheterization fails: coude-tip catheter (angled tip navigates the prostatic urethra), or if still unsuccessful, suprapubic catheter placement. After decompression, initiate alpha-blocker (tamsulosin) and attempt trial without catheter (TWOC) in 3-7 days. Success rate of TWOC: ~40-60% with alpha-blocker. Failed TWOC or recurrent AUR is an indication for surgical management of BPH.

McConnell JD et al. "The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of BPH." N Engl J Med. 2003;349(25):2387-2398. PMID: 14695427 (MTOPS Trial)

15 Overactive Bladder & Urinary Incontinence

Types of Urinary Incontinence

TypeMechanismKey Features
Stress urinary incontinence (SUI)Urethral hypermobility or intrinsic sphincter deficiency (ISD)Leakage with cough, sneeze, lifting, exertion; more common in women (after childbirth, menopause) and post-prostatectomy in men
Urgency urinary incontinence (UUI)Detrusor overactivity (involuntary detrusor contractions)Sudden, compelling urge to void with inability to defer; associated with OAB syndrome
Mixed incontinenceCombination of SUI + UUIVery common in women; treat the predominant component first
Overflow incontinenceChronic urinary retention (BOO or detrusor underactivity)Continuous dribbling; high PVR; may be painless; causes: BPH, neurogenic bladder, medications
Functional incontinenceCognitive/mobility impairment preventing timely toiletingCommon in elderly/dementia; bladder function may be normal

Overactive Bladder (OAB)

OAB is a symptom complex of urgency, with or without urgency incontinence, usually with frequency and nocturia, in the absence of infection or other pathology. Prevalence increases with age, affecting ~15-30% of adults. Diagnosis is clinical; urodynamics are not required for initial management but indicated for refractory or complex cases.

Treatment of OAB/UUI

First-line: Behavioral therapy — bladder training (scheduled voiding, progressively increasing intervals), pelvic floor muscle exercises (Kegels), fluid management, caffeine restriction, and weight loss. Second-line: Pharmacotherapy — antimuscarinics (oxybutynin, tolterodine, solifenacin, darifenacin, fesoterodine, trospium) block M3 receptors on the detrusor; side effects include dry mouth, constipation, blurred vision, and cognitive impairment (avoid in elderly — use trospium or darifenacin, which have less CNS penetration). Mirabegron (beta-3 agonist) relaxes the detrusor via a different mechanism — no anticholinergic side effects; can be combined with antimuscarinics. Vibegron is another beta-3 agonist with fewer drug interactions.

Third-line: OnabotulinumtoxinA (Botox) injection — 100-200 units injected cystoscopically into the detrusor; effective for 6-9 months; risk of urinary retention (must be willing to perform CIC). Sacral neuromodulation (SNM, InterStim) — implanted lead at S3 modulates sacral nerve function; indicated for refractory OAB and non-obstructive urinary retention. Percutaneous tibial nerve stimulation (PTNS) — office-based, weekly for 12 weeks then monthly maintenance.

Stress Urinary Incontinence — Female

Evaluation: cough stress test, voiding diary, PVR, and urodynamics for complex cases. Conservative management: pelvic floor muscle training (PFMT, Kegels) — first-line for all SUI; vaginal pessary. Surgical management: midurethral sling (MUS) — retropubic (TVT) or transobturator (TOT) polypropylene mesh tape placed tension-free at the midurethra; success rate ~80-90%. Burch colposuspension (open or laparoscopic) — sutures the periurethral tissue to Cooper ligament; durable results but more invasive. Urethral bulking agents (Bulkamid) — office-based injection of hydrogel at the bladder neck; less invasive, lower long-term success; good for ISD or patients unfit for surgery.

Stress Urinary Incontinence — Male (Post-Prostatectomy)

Post-radical-prostatectomy incontinence affects ~5-20% of men at 1 year. Conservative: PFMT (ideally started preoperatively). Surgical: Artificial urinary sphincter (AUS, AMS 800) — the gold standard for moderate-to-severe male SUI; an inflatable cuff placed around the bulbar urethra with a control pump in the scrotum; success rate ~75-90%. Male sling (AdVance, ATOMS) — for mild-to-moderate SUI; repositions/compresses the bulbar urethra.

Diagram illustrating types of urinary incontinence including stress and urge
Figure 11 — Types of Urinary Incontinence. Stress incontinence occurs with increased abdominal pressure; urge incontinence results from involuntary detrusor contractions. Source: Wikimedia Commons. Public domain.

16 Neurogenic Bladder

Overview

Neurogenic bladder refers to bladder dysfunction caused by neurologic disease or injury. The clinical presentation depends on the level of the neurologic lesion:

Lesion LevelTypeBladder BehaviorExamples
Suprapontine (above pons)Upper motor neuronDetrusor overactivity with coordinated sphincter; incontinenceStroke, Parkinson disease, brain tumors, MS (can be any pattern)
Suprasacral spinal cord (above S2-S4)Upper motor neuronDetrusor overactivity with detrusor-sphincter dyssynergia (DSD) — the most dangerous pattern (high pressures → upper tract damage)Spinal cord injury (above conus), MS, transverse myelitis
Sacral (S2-S4) / infrasacralLower motor neuronAcontractile/areflexic detrusor; overflow incontinence; open/denervated sphincterCauda equina syndrome, conus medullaris injury, pelvic surgery, diabetic neuropathy

Evaluation

Urodynamic study (UDS) is essential — measures detrusor pressure during filling and voiding, assesses compliance, detects involuntary contractions, and identifies DSD. Key parameters: detrusor leak point pressure (DLPP) > 40 cm H2O is associated with upper tract deterioration and requires intervention. Renal ultrasound is performed to assess for hydronephrosis. VCUG evaluates for vesicoureteral reflux. Serum creatinine and GFR monitor renal function.

Management

Clean intermittent catheterization (CIC) is the gold standard for bladder emptying in neurogenic bladder — preferred over indwelling catheters (which increase UTI risk, stone formation, urethral erosion, and squamous cell carcinoma of the bladder with long-term use). CIC typically performed 4-6 times daily. Antimuscarinics or beta-3 agonists reduce detrusor overactivity and improve compliance. OnabotulinumtoxinA (200 units) injected into the detrusor is effective for neurogenic detrusor overactivity refractory to oral medications. Augmentation cystoplasty (enterocystoplasty) — using ileum or sigmoid colon to enlarge the bladder — is a last resort for refractory low-compliance bladders threatening upper tract function. Complications: mucus production, metabolic acidosis, stones, perforation, and theoretical malignancy risk.

Detrusor-sphincter dyssynergia (DSD) in spinal cord injury patients creates dangerously high intravesical pressures that can cause bilateral vesicoureteral reflux, hydronephrosis, recurrent pyelonephritis, and progressive renal failure. A DLPP > 40 cm H2O on urodynamics mandates treatment to protect the upper tracts. CIC with antimuscarinics is the cornerstone of management.

Spinal Cord Injury — Acute Phase

During spinal shock (immediately after SCI, lasting days to weeks), the bladder is areflexic and acontractile. Management during this phase: indwelling urethral catheter initially, then transition to CIC as soon as feasible. After spinal shock resolves, patients with suprasacral injuries typically develop detrusor overactivity with DSD, while those with conus/cauda equina injuries develop areflexic bladder. Annual urologic surveillance (renal US, serum creatinine, urodynamics) is recommended for all SCI patients to monitor for upper tract deterioration.

Autonomic Dysreflexia

Emergency Autonomic dysreflexia (AD) is a potentially life-threatening emergency in patients with SCI at T6 or above. Triggered by noxious stimuli below the level of injury — the most common trigger is bladder distension (blocked catheter, urinary retention). Presentation: severe paroxysmal hypertension (SBP > 200 mmHg possible), pounding headache, flushing and sweating above the injury level, bradycardia, and piloerection. Management: sit the patient upright, remove tight clothing, identify and relieve the trigger (catheterize the bladder or relieve catheter obstruction), and if BP remains elevated, give fast-acting antihypertensive (nifedipine SL, nitrate paste, or IV hydralazine). Prevention: regular bladder emptying, bowel program, and avoidance of triggers.

17 Urethral Stricture Disease

Etiology

Urethral stricture is fibrotic narrowing of the urethra caused by spongiofibrosis (scar tissue in the corpus spongiosum). Etiologies: iatrogenic (most common in developed countries — urethral catheterization, instrumentation, hypospadias repair, TURP), idiopathic (~30-40%, likely related to unrecognized lichen sclerosus or trauma), traumatic (straddle injury → bulbar urethra; pelvic fracture → membranous/prostatic urethra — posterior urethral disruption injury), infectious (gonococcal urethritis — historically common; Chlamydia), and lichen sclerosus (balanitis xerotica obliterans/BXO — affects glans and fossa navicularis, may extend to penile urethra).

Diagnosis

Retrograde urethrogram (RUG) is the gold standard imaging study — demonstrates the location, length, and degree of stricture. Combined with voiding cystourethrogram (VCUG) for posterior urethral evaluation. Uroflowmetry shows an obstructive pattern (low Qmax, prolonged curve). Cystourethroscopy provides direct visualization and is both diagnostic and used for planning repair.

Management

Urethral dilation — progressive passage of dilators (filiform and followers, balloon, or sounds); temporary relief but high recurrence rate (~50-60% at 1 year). Appropriate as initial treatment for short, non-recurrent strictures. Direct vision internal urethrotomy (DVIU) — endoscopic cold-knife incision of the stricture (typically at the 12 o'clock position); similar recurrence rate to dilation (~50-60%); best results for short (< 2 cm), single, bulbar strictures. Repeated DVIU has diminishing returns — after 2 failed DVIU/dilations, urethroplasty should be strongly considered.

Urethroplasty is the definitive treatment with the highest long-term success rates (85-95%). Types: (1) Excision and primary anastomosis (EPA) — for short (≤ 2 cm) bulbar strictures; strictured segment is excised, and the healthy urethral ends are spatulated and anastomosed; success rate > 95%. (2) Buccal mucosal graft (BMG) urethroplasty — for longer strictures (> 2 cm); a graft harvested from the inner cheek is placed dorsally (Barbagli dorsal onlay), ventrally, or as a dorsal inlay (Asopa) on the urethral plate; success rate ~85-90%. (3) Staged urethroplasty — for complex, long, or panurethral strictures (especially in lichen sclerosus); first stage opens the stricture and places BMG; second stage tubularizes the neourethra after 3-6 months.

For posterior urethral disruption injuries (pelvic fracture urethral injury — PFUI): initial management is suprapubic catheter placement; delayed posterior urethroplasty at 3-6 months after the pelvic fracture has healed. Immediate attempts at realignment are an option but carry risk of stricture, incontinence, and ED. The classic presentation of PFUI is blood at the urethral meatus, inability to void, and high-riding prostate on DRE in the setting of pelvic fracture. A retrograde urethrogram must be performed before any attempt at urethral catheterization.

Urethral Trauma Classification

TypeDescriptionManagement
Anterior (bulbar)Straddle injury; direct blow to perineum; most common cause of anterior urethral injuryUrethral catheter if partial; suprapubic catheter if complete; delayed urethroplasty
Posterior (membranous/prostatic)Pelvic fracture urethral injury; occurs in ~5-10% of pelvic fractures; disruption at prostatomembranous junctionSuprapubic catheter; delayed posterior urethroplasty at 3-6 months; primary realignment is an option but controversial

Lichen Sclerosus (Balanitis Xerotica Obliterans)

Lichen sclerosus (LS), formerly BXO, is a chronic inflammatory dermatosis that affects the glans, prepuce, and urethral meatus. It causes progressive fibrosis with a characteristic white, sclerotic appearance. LS is the most common cause of acquired phimosis in adults and a major cause of meatal stenosis and fossa navicularis strictures. The etiology is autoimmune. LS is associated with long, panurethral strictures that are challenging to manage. Buccal mucosal grafts are preferred for LS-related strictures because BMG is resistant to LS recurrence (unlike genital skin grafts). LS carries a small risk (~5%) of squamous cell carcinoma — long-term surveillance is recommended.

Retrograde urethrogram showing urethral stricture
Figure 12 — Retrograde Urethrogram. Contrast study demonstrating a urethral stricture with proximal dilation. The RUG is the gold standard for delineating stricture location and length. Source: Wikimedia Commons. Public domain.

18 Testicular Torsion & Scrotal Emergencies

Testicular Torsion

Emergency Testicular torsion is a surgical emergency caused by twisting of the spermatic cord with resultant ischemia of the testis. Peak incidence: bimodal — neonates and adolescents (12-18 years). The underlying anomaly is the "bell clapper" deformity — high attachment of the tunica vaginalis allowing the testis to rotate freely on the spermatic cord (present bilaterally in most cases).

Presentation: sudden-onset severe testicular pain (often during sleep or physical activity), nausea/vomiting, high-riding testis with a horizontal lie, absent cremasteric reflex (most sensitive physical exam finding — ~99% sensitivity in torsion), and a thickened/twisted spermatic cord. The cremasteric reflex is absent in testicular torsion.

Time to Salvage

Duration of TorsionSalvage Rate
< 6 hours~90-100%
6-12 hours~50%
12-24 hours~20%
> 24 hours~0-10%

Diagnosis & Management

If clinical suspicion is high, do NOT delay surgery for imaging — proceed directly to scrotal exploration. Color Doppler ultrasound (decreased or absent blood flow to the affected testis) is obtained when the diagnosis is uncertain. Sensitivity ~88-100%, specificity ~90-100%.

Treatment: emergent scrotal exploration, detorsion, and bilateral orchiopexy. The affected testis is untwisted, assessed for viability (return of color/bleeding after warm-saline wraps), and fixed to the dartos fascia in 3-point fixation. The contralateral testis must also be fixed (bilateral orchiopexy) because the bell clapper deformity is usually bilateral. If the testis is nonviable, orchiectomy is performed. Manual detorsion (outward rotation — "open the book") can be attempted while preparing for surgery but should not delay definitive operative exploration.

Torsion of Appendages

Torsion of the appendix testis (Müllerian duct remnant) or appendix epididymis is the most common cause of acute scrotum in prepubertal boys. Presents with gradual-onset scrotal pain, often with a visible "blue dot sign" (infarcted appendage visible through the scrotal skin). Cremasteric reflex is typically present. Management is conservative: NSAIDs, rest, scrotal support. Surgery only if torsion of the testis itself cannot be excluded.

Epididymitis & Epididymo-Orchitis

Epididymitis presents with gradual-onset scrotal pain, swelling of the epididymis (starting posterolaterally), fever, and urinary symptoms. In young men (< 35): commonly caused by Chlamydia trachomatis or Neisseria gonorrhoeae — treat with ceftriaxone 500 mg IM + doxycycline 100 mg BID × 10 days. In older men or boys: commonly caused by coliforms (E. coli) — treat with fluoroquinolone or TMP-SMX. Prehn sign (relief of pain with testicular elevation) is classically positive in epididymitis but is unreliable for excluding torsion.

Testicular torsion is a clinical diagnosis — if suspicion is high based on history and physical exam (sudden pain, absent cremasteric reflex, high-riding testis), take the patient directly to the operating room. A normal-appearing ultrasound does NOT exclude early or intermittent torsion. The salvage window is 6 hours — every minute counts.
Diagram illustrating testicular torsion with twisting of the spermatic cord
Figure 13 — Testicular Torsion. Twisting of the spermatic cord compromises blood supply to the testis. The bell clapper deformity allows free rotation of the testis within the tunica vaginalis. Source: Wikimedia Commons. Public domain.

19 Cryptorchidism & Inguinal Disorders

Cryptorchidism

Cryptorchidism (undescended testis) is the most common congenital anomaly of the male genitalia, affecting ~3% of full-term and ~30% of premature male neonates. By 6 months of age, most undescended testes will spontaneously descend — prevalence stabilizes at ~1% after 1 year. The testis may be palpable (80% — in the inguinal canal, prescrotal, or ectopic) or nonpalpable (20% — intra-abdominal, absent/vanishing testis, or ectopic).

Complications of Cryptorchidism

Infertility: Bilateral cryptorchidism causes infertility in ~75% if untreated; even unilateral cryptorchidism reduces fertility. Elevated temperature impairs spermatogenesis. Malignancy: 3-8× increased risk of testicular cancer (most commonly seminoma) — the risk is highest for intra-abdominal testes. Orchiopexy before puberty may reduce cancer risk but does not eliminate it; orchiopexy facilitates examination and tumor detection. Torsion: Higher risk due to abnormal attachment. Inguinal hernia: Patent processus vaginalis present in ~90% of cryptorchid testes.

Management

Hormonal therapy (hCG or GnRH) is not recommended by AUA/EAU guidelines due to low success rates and lack of long-term benefit. Orchiopexy is the treatment of choice and should be performed between 6 and 18 months of age (AUA guideline: referral by 6 months, surgery by 18 months). For palpable testes: inguinal orchiopexy (inguinal incision, mobilization of testis and cord, closure of processus vaginalis, fixation of testis in a sub-dartos pouch in the scrotum). For nonpalpable testes: diagnostic laparoscopy is the first step — if testis is found intra-abdominally and viable, either single-stage or two-stage Fowler-Stephens orchiopexy (stage 1: ligate testicular vessels laparoscopically; stage 2: 6 months later, bring testis to scrotum on a pedicle of vas deferens and its artery + gubernacular collaterals). If testis is absent or nubbins found, orchiectomy of remnant.

Orchiopexy should be completed by 12-18 months of age to optimize fertility and cancer risk reduction. Every 6-month delay beyond 1 year of age results in progressive germ cell loss. A retractile testis (one that can be manipulated into the scrotum and stays temporarily) does not require surgery but should be monitored annually because ~30% of retractile testes become ascending (acquired cryptorchidism) requiring orchiopexy.

Inguinal Hernia & Hydrocele in Children

An indirect inguinal hernia in children results from a patent processus vaginalis. It presents as a groin bulge that appears with crying/straining and is reducible. Unlike adult hernias, pediatric inguinal hernias do not resolve spontaneously and carry a risk of incarceration — all pediatric inguinal hernias require surgical repair. Repair: inguinal hernia repair with high ligation of the processus vaginalis (no mesh in children). A communicating hydrocele results from a narrow patent processus vaginalis that allows peritoneal fluid (but not abdominal contents) to surround the testis — size fluctuates with activity/position. Communicating hydroceles in children < 12-24 months may resolve spontaneously; if persistent beyond 12-24 months, surgical repair (same as hernia repair — ligation of processus vaginalis). A non-communicating (simple) hydrocele in adults is managed with observation if asymptomatic; aspiration is temporary; hydrocelectomy if bothersome.

Diagram showing normal testicular descent and cryptorchidism
Figure 21 — Cryptorchidism. The testis may arrest at any point along the path of descent from the abdomen through the inguinal canal to the scrotum. Orchiopexy should be performed by 12-18 months of age. Source: Wikimedia Commons. Public domain.

20 Vesicoureteral Reflux

Overview

Vesicoureteral reflux (VUR) is the retrograde flow of urine from the bladder into the ureter and renal collecting system. It is the most common urologic abnormality in children, affecting ~1% of the general pediatric population and ~30-40% of children who present with UTI. VUR predisposes to recurrent pyelonephritis and reflux nephropathy (renal scarring), which can lead to hypertension and chronic kidney disease.

Classification

VUR is classified by voiding cystourethrogram (VCUG) into 5 grades (International Reflux Study):

GradeDescriptionSpontaneous Resolution Rate
IReflux into ureter only (does not reach renal pelvis)~80%
IIReflux into renal pelvis and calyces without dilation~60-80%
IIIMild dilation of ureter and renal pelvis; mild calyceal blunting~50%
IVModerate dilation; tortuous ureter; moderate calyceal blunting~10-20%
VSevere dilation and tortuosity; papillary impression lost; gross intrarenal reflux< 5%

Management

Medical (conservative) management: Low-grade VUR (I-III) in young children has high spontaneous resolution rates. Continuous antibiotic prophylaxis (CAP) with low-dose trimethoprim or nitrofurantoin reduces recurrent UTI. The RIVUR trial showed that CAP reduces UTI recurrence by ~50% in children with VUR but does not prevent renal scarring.

Surgical management is indicated for: high-grade VUR (IV-V), breakthrough UTIs on prophylaxis, persistent VUR, non-compliance with medical management, and renal scarring with ongoing reflux. Options: (1) Endoscopic injection (STING/Deflux) — injection of dextranomer/hyaluronic acid (Deflux) at the ureteral orifice; outpatient procedure; success rate ~70-80% for grades I-III, lower for higher grades; may require repeat injection. (2) Open ureteral reimplantation — the gold standard with ~95-98% success rate; the ureter is reimplanted into the bladder with a longer submucosal tunnel (5:1 tunnel length-to-diameter ratio) to create a flap-valve mechanism (Cohen cross-trigonal or Lich-Gregoir extravesical technique). (3) Robotic-assisted reimplantation is emerging with comparable success rates.

Diagram showing grades I through V of vesicoureteral reflux
Figure 14 — VUR Grading (I-V). Progressive grades of vesicoureteral reflux from ureter-only reflux (Grade I) to severe dilation with loss of papillary impressions (Grade V). Source: Wikimedia Commons. Public domain.

Renal Scarring & Reflux Nephropathy

Reflux nephropathy is renal scarring resulting from VUR-associated pyelonephritis, particularly in young children (< 5 years). It is the most common cause of hypertension in children and the leading urologic cause of end-stage renal disease in children. Risk factors for scarring: high-grade VUR (IV-V), recurrent febrile UTIs, delayed treatment, younger age at first UTI, and intrarenal reflux. DMSA (dimercaptosuccinic acid) renal scan is the gold standard for detecting renal scarring — more sensitive than ultrasound. Prevention of scarring requires prompt treatment of febrile UTIs (antibiotics within 72 hours of fever onset) and prevention of recurrent UTIs through antibiotic prophylaxis or surgical correction of VUR.

The combination of high-grade VUR (Grade IV-V) and febrile UTI in a child under 5 years carries the highest risk of renal scarring and long-term renal damage. These children benefit most from definitive surgical correction (ureteral reimplantation) rather than prolonged medical management. All children with febrile UTI should undergo renal/bladder ultrasound, and VCUG should be considered, particularly in children under 2 years or those with recurrent UTI.

RIVUR Trial Investigators. "Antimicrobial prophylaxis for children with vesicoureteral reflux." N Engl J Med. 2014;370(25):2367-2376. PMID: 24795142

21 Hypospadias & Congenital Anomalies

Hypospadias

Hypospadias is a congenital anomaly in which the urethral meatus opens on the ventral surface of the penis, proximal to the normal glanular position. Incidence: ~1 in 200-300 live male births — one of the most common congenital anomalies. Classification by meatal position: distal/anterior (~70% — glanular, coronal, distal shaft), middle/midshaft (~15%), and proximal/posterior (~15% — penoscrotal, scrotal, perineal). Associated findings: ventral curvature (chordee) in ~10-50%, hooded/incomplete foreskin (dorsal hood), and undescended testis (especially in proximal forms — evaluate for DSD if bilateral UDT + hypospadias).

Repair Principles

Repair is recommended at 6-18 months of age. Goals: straight penis, slit-like meatus at the tip of the glans, conical glans shape, and functional urethra with a good stream. The most commonly used technique is the TIP (tubularized incised plate) repair (Snodgrass) — relaxing midline incision of the urethral plate allows tubularization into a neourethra; used for distal and many midshaft hypospadias with excellent cosmetic and functional results. For proximal hypospadias or those with severe chordee: two-stage repair (first stage: chordee correction and placement of buccal mucosal or preputial skin graft; second stage: tubularization of the neourethral plate at 6+ months). Circumcision must NOT be performed before hypospadias repair — the prepuce may be needed as tissue for reconstruction.

Posterior Urethral Valves (PUV)

Posterior urethral valves (PUV) are the most common cause of congenital lower urinary tract obstruction in males. Type I valves (most common, ~95%) are mucosal folds extending from the verumontanum to the membranous urethra. Presentation: prenatal hydronephrosis and oligohydramnios (severe cases → pulmonary hypoplasia), postnatal urinary retention, poor stream, UTI, renal insufficiency. Diagnosis: VCUG showing dilated posterior urethra with a "keyhole" sign. Treatment: primary valve ablation (endoscopic incision) once the infant is stable; vesicostomy if the infant is too small for endoscopic instruments. Despite treatment, ~30-40% develop end-stage renal disease due to renal dysplasia and the "valve bladder" (chronic high-pressure detrusor changes with poor compliance).

Epispadias & Bladder Exstrophy

Bladder exstrophy is a rare (1:30,000-50,000 births) midline closure defect where the bladder is open and exposed on the anterior abdominal wall. Associated with epispadias (dorsally displaced urethral meatus), pubic diastasis, and inguinal hernias. Management requires staged reconstruction: primary closure of the bladder and abdominal wall (ideally within 72 hours of birth), epispadias repair, and later bladder neck reconstruction for continence. The exstrophy-epispadias complex carries a lifelong risk of malignancy (adenocarcinoma).

Ureterocele & Ectopic Ureter

A ureterocele is a cystic dilation of the intravesical submucosal ureter, most commonly associated with the upper pole moiety of a duplex collecting system. Classified as intravesical (orthotopic) or ectopic (extends to the bladder neck or urethra). Presents in children with UTI, obstruction, or prenatal hydronephrosis. On ultrasound, appears as a thin-walled cystic structure within the bladder ("cobra head" sign on IVP). Treatment depends on size and obstruction: endoscopic puncture/incision, upper pole heminephroureterectomy for a non-functioning moiety, or ureterocele excision with reimplantation.

An ectopic ureter inserts at a location other than the normal trigonal position. In the Weigert-Meyer rule for duplex systems: the upper pole ureter inserts medially and inferiorly (more prone to obstruction/ureterocele), while the lower pole ureter inserts laterally and superiorly (more prone to reflux). In girls, an ectopic ureter may insert below the external sphincter (into the vagina or vestibule) — presenting with continuous urinary dribbling despite normal voiding. In boys, ectopic ureters always insert above the external sphincter (into the prostatic urethra, seminal vesicles, or vas deferens) and do not cause incontinence.

Classification of hypospadias by meatal position
Figure 18 — Hypospadias Classification. Classification by meatal position: glanular, coronal, distal shaft, midshaft, proximal shaft, penoscrotal, scrotal, and perineal. Distal forms account for approximately 70% of cases. Source: Wikimedia Commons. Public domain.

22 Fournier Gangrene, Priapism & Paraphimosis

Fournier Gangrene

Emergency Fournier gangrene is a life-threatening necrotizing fasciitis of the perineum and external genitalia. It is a polymicrobial infection (aerobic + anaerobic organisms: E. coli, Bacteroides, Streptococcus, Staphylococcus, Clostridium) involving the superficial fascia (Colles, dartos, Buck, Scarpa). Sources: perianal (30-50%), urogenital (20-40%), cutaneous (20%). Risk factors: diabetes mellitus (most common), immunosuppression, alcoholism, obesity, chronic kidney disease.

Presentation: rapidly progressive perineal/scrotal pain, swelling, erythema extending beyond the apparent margin, crepitus (subcutaneous gas), systemic toxicity (fever, tachycardia, sepsis). Management: (1) aggressive surgical debridement — the cornerstone of treatment; wide excision of all necrotic tissue; often requires multiple returns to the OR (planned "second look" at 24-48 hours); (2) broad-spectrum IV antibiotics (vancomycin + piperacillin-tazobactam + clindamycin or a carbapenem); (3) resuscitation and ICU care. Testes are typically spared (separate blood supply from the testicular artery) and can be placed in subcutaneous thigh pouches. Wound management: negative pressure wound therapy (wound VAC) followed by delayed primary closure, skin grafting, or flap reconstruction. Mortality: 20-40% despite treatment — higher with delayed debridement.

Fournier gangrene mortality directly correlates with time to surgical debridement. The clinical appearance underestimates the extent of subcutaneous necrosis — the "tip of the iceberg" phenomenon. Always debride widely beyond the apparent margins of involved tissue. CT imaging can help delineate the extent of fascial involvement and identify gas in soft tissues, but should never delay surgical intervention.

Priapism

Emergency Priapism is a persistent penile erection unrelated to sexual stimulation lasting > 4 hours. Two main types:

FeatureIschemic (Low-Flow) — EMERGENCYNonischemic (High-Flow)
MechanismVeno-occlusive: blood trapped in corpora cavernosaArterial: unregulated cavernosal arterial inflow (usually post-traumatic)
PainPainful, rigidPainless, partially rigid
Blood gasDark blood; pO2 < 30, pCO2 > 60, pH < 7.25 (ischemic)Bright red blood; arterial gas values
CausesSickle cell disease (most common in children), medications (PDE5 inhibitors, intracavernosal injections, trazodone, antipsychotics), idiopathicPerineal/penile trauma (straddle injury) → cavernosal artery pseudoaneurysm/fistula
ManagementURGENT: corporal aspiration with 16-18G needle → injection of phenylephrine (100-500 mcg every 3-5 min) → if refractory (> 72 hrs), surgical shunt (distal: Winter percutaneous, T-shunt; proximal: Quackels; last resort: penile prosthesis)Non-urgent: observation (many resolve); selective arterial embolization if persistent
SequelaeSmooth muscle necrosis & fibrosis → ED if untreated > 24-48 hrsED rare

Paraphimosis

Emergency Paraphimosis is the inability to reduce a retracted foreskin back over the glans penis, causing a constricting band at the coronal sulcus. This leads to venous congestion, edema of the glans, and if untreated, arterial compromise and gangrene. Most common cause: failure to replace the foreskin after catheterization or examination. Management: (1) manual reduction — apply steady circumferential pressure to the edematous glans for 5-10 minutes (ice/osmotic agents like granulated sugar can reduce edema), then push the glans back through the phimotic ring while pulling the foreskin forward; (2) if manual reduction fails: dorsal slit (incision of the constricting band under local anesthesia) to release the constriction; (3) elective circumcision after edema resolves to prevent recurrence.

Erectile Dysfunction

Erectile dysfunction (ED) is the inability to achieve or maintain an erection sufficient for satisfactory sexual performance. Prevalence increases with age (~40% of men at age 40, ~70% at age 70). Etiology is often multifactorial: vascular (most common — atherosclerosis of penile arteries; shared risk factors with cardiovascular disease), neurogenic (diabetes, spinal cord injury, post-radical prostatectomy), hormonal (hypogonadism), medication-related (antihypertensives, SSRIs, anti-androgens), psychogenic, and structural (Peyronie disease).

Evaluation: sexual history, IIEF-5 questionnaire, focused physical exam, fasting glucose/HbA1c, lipid panel, morning testosterone. Treatment: First-line: PDE5 inhibitors — sildenafil (Viagra, 25-100 mg), tadalafil (Cialis, 5-20 mg — also daily 5 mg for BPH/ED), vardenafil (Levitra), avanafil (Stendra). Contraindicated with nitrates (severe hypotension). Second-line: Intracavernosal injection therapy (alprostadil, trimix — PGE1 + phentolamine + papaverine), vacuum erection devices, intraurethral alprostadil (MUSE). Third-line: Penile prosthesis implantation — inflatable 3-piece (AMS 700, Coloplast Titan) provides the most natural erection; malleable/semi-rigid rods are simpler. Patient satisfaction rates exceed 90% with inflatable prostheses.

Peyronie Disease

Peyronie disease is an acquired fibrotic disorder of the tunica albuginea causing penile curvature, pain, and potential ED. Prevalence ~3-9% of adult men. Two phases: acute/inflammatory phase (first 6-12 months — pain, evolving curvature, plaque formation) and chronic/stable phase (pain resolves, curvature stabilizes). Treatment during stable phase: intralesional collagenase (Xiaflex) for curvature 30-90 degrees (FDA-approved); surgical correction for refractory cases — plication (Nesbit, 16-dot) for curvature < 60-70 degrees with adequate length, or plaque incision/excision with grafting for severe curvature or short penis. Penile prosthesis for concurrent ED.

Cross-section of the penis showing corpora cavernosa involved in priapism
Figure 15 — Penile Cross-Section Relevant to Priapism. The corpora cavernosa are the erectile bodies involved in priapism. Corporal aspiration and phenylephrine injection target these structures. Source: Wikimedia Commons. Public domain.

23 Classification Systems

Gleason / ISUP Grading (Prostate Cancer)

ISUP Grade GroupGleason ScorePattern Description
13+3 = 6Well-formed individual glands
23+4 = 7Predominantly well-formed glands with a lesser component of poorly formed/fused/cribriform glands
34+3 = 7Predominantly poorly formed/fused/cribriform glands with a lesser component of well-formed glands
48 (4+4, 3+5, 5+3)Only poorly formed/fused/cribriform glands, or lacking gland formation with or without well-formed glands
59-10 (4+5, 5+4, 5+5)Lacking gland formation (sheets, cords, single cells, comedonecrosis) with or without poorly formed glands

TNM Staging — Kidney Cancer (AJCC 8th Edition)

T StageDescription
T1a≤ 4 cm, confined to kidney
T1b> 4 cm but ≤ 7 cm, confined to kidney
T2a> 7 cm but ≤ 10 cm, confined to kidney
T2b> 10 cm, confined to kidney
T3aExtends into renal vein or perinephric/renal sinus fat, not beyond Gerota fascia
T3bExtends into IVC below diaphragm
T3cExtends into IVC above diaphragm or invades IVC wall
T4Extends beyond Gerota fascia or into ipsilateral adrenal

TNM Staging — Testicular Cancer (AJCC 8th Edition)

T StageDescription
pT1 (Seminoma)Any size, limited to testis without lymphovascular invasion (LVI)
pT1 (NSGCT)Limited to testis without LVI; may invade rete testis, epididymis, tunica albuginea
pT2LVI present, or involvement of hilar soft tissue, epididymis, or penetrates tunica vaginalis
pT3Invades spermatic cord
pT4Invades scrotum

Bosniak Classification (Renal Cysts) — Summary

CategoryManagementMalignancy Risk
I — Simple cystBenign, no follow-up< 1%
II — Minimally complexBenign, no follow-up< 5%
IIF — Mildly complex, needs follow-upFollow-up imaging5-15%
III — IndeterminateSurgery or active surveillance40-60%
IV — Clearly malignantSurgery> 80%

AUA Symptom Score (IPSS)

Score RangeSeverityImplication
0-7MildWatchful waiting acceptable if not bothersome
8-19ModerateConsider medical therapy
20-35SevereMedical or surgical therapy recommended

VUR Grading (International Reflux Study)

GradeDescription
IReflux into non-dilated ureter only
IIReflux into renal pelvis and calyces, no dilation, normal calyceal fornices
IIIMild to moderate dilation of ureter, renal pelvis, and calyces; minimal calyceal blunting
IVModerate dilation and tortuosity of ureter; moderate dilation of pelvis and calyces; complete obliteration of sharp calyceal angles
VGross dilation and tortuosity of ureter, pelvis, and calyces; papillary impressions no longer visible; intrarenal reflux

Stone Composition & Crystal Morphology

Stone TypeCrystal ShapeX-Ray AppearanceUrine pH
Calcium oxalate monohydrateDumbbell/ovalRadiopaqueAny
Calcium oxalate dihydrateBipyramidal envelopeRadiopaqueAny
Calcium phosphate (apatite)AmorphousRadiopaque> 6.5
Uric acidRhomboid/rosetteRadiolucent< 5.5
Struvite (MAP)Coffin-lidRadiopaque> 7.2
CystineHexagonalSemi-opaque< 6.5

PI-RADS v2.1 (Prostate MRI)

ScoreAssessmentLikelihood of Clinically Significant Cancer
1Very lowClinically significant cancer highly unlikely
2LowClinically significant cancer unlikely
3IntermediateEquivocal — clinically significant cancer possible
4HighClinically significant cancer likely
5Very highClinically significant cancer highly likely

Clavien-Dindo Classification of Surgical Complications

GradeDefinitionExamples in Urology
IAny deviation from normal postoperative course; no pharmacologic/surgical/endoscopic/radiologic intervention neededWound infection treated at bedside, ileus resolving with conservative measures
IIRequiring pharmacologic treatment, blood transfusion, or TPNBlood transfusion after PCNL, antibiotics for UTI, DVT requiring anticoagulation
IIIaRequiring surgical/endoscopic/radiologic intervention — NOT under general anesthesiaUreteral stent placement for urinoma, percutaneous drainage of abscess
IIIbRequiring intervention under general anesthesiaReoperation for bleeding, repair of ureteral injury
IVaSingle organ dysfunction (including dialysis)Acute renal failure requiring dialysis, respiratory failure requiring intubation
IVbMulti-organ dysfunctionSeptic shock with multi-organ failure
VDeathAny cause

R.E.N.A.L. Nephrometry Score (Renal Tumor Complexity)

The R.E.N.A.L. nephrometry score standardizes description of renal tumor complexity to guide surgical planning (partial vs radical nephrectomy):

Component1 Point2 Points3 Points
R — Radius (maximal diameter)≤ 4 cm> 4 to < 7 cm≥ 7 cm
E — Exophytic/endophytic≥ 50% exophytic< 50% exophyticEntirely endophytic
N — Nearness to collecting system/sinus (mm)≥ 7 mm> 4 to < 7 mm≤ 4 mm
A — Anterior/Posteriora = anterior, p = posterior, x = neither (suffix, not scored)
L — Location relative to polar linesEntirely above/below polar lineCrosses a polar line> 50% across polar line or crosses axial renal midline, or entirely between polar lines

Total score: 4-6 = low complexity, 7-9 = moderate complexity, 10-12 = high complexity. Higher complexity scores correlate with longer ischemia times, higher complication rates, and greater likelihood of requiring radical nephrectomy.

Urinary Tract Infection — Classification & Management

TypeDefinitionManagement
Uncomplicated cystitisLower UTI in a non-pregnant, pre-menopausal woman with normal urinary tractNitrofurantoin 5 days, TMP-SMX 3 days, or fosfomycin single dose
Uncomplicated pyelonephritisUpper UTI without complicating factorsOral fluoroquinolone 5-7 days or TMP-SMX 14 days; IV if unable to tolerate oral
Complicated UTIUTI with structural/functional abnormality (stones, obstruction, catheter, neurogenic bladder, male sex, pregnancy, immunosuppression)Broader spectrum antibiotics (fluoroquinolone, cephalosporin, or carbapenem), longer course (7-14 days); address underlying cause
Catheter-associated UTI (CAUTI)UTI in patient with indwelling catheter or within 48h of removalRemove or replace catheter; treat only if symptomatic; 7 days if symptoms resolve promptly
Recurrent UTI≥ 2 infections in 6 months or ≥ 3 in 12 monthsEvaluate for structural cause; low-dose prophylaxis (nitrofurantoin, TMP-SMX); vaginal estrogen in postmenopausal women; D-mannose
Emphysematous pyelonephritisNecrotizing infection with gas in renal parenchyma; associated with diabetesEmergency — IV antibiotics + percutaneous drainage or nephrectomy for severe cases; mortality 20-40%

24 Medications Master Table

Alpha-Adrenergic Blockers (BPH / MET)

DrugSelectivityDoseKey Notes
TamsulosinAlpha-1A selective0.4 mg dailyMost commonly prescribed; less orthostatic hypotension; IFIS risk; also used for MET
AlfuzosinAlpha-1 (uroselective)10 mg daily (ER)Once daily; contraindicated with CYP3A4 inhibitors
SilodosinAlpha-1A (most selective)8 mg dailyHighest rate of retrograde ejaculation (~28%)
DoxazosinNon-selective alpha-11-8 mg dailyMore orthostatic hypotension; also treats hypertension
TerazosinNon-selective alpha-11-10 mg dailyRequires dose titration; orthostatic hypotension

5-Alpha Reductase Inhibitors

DrugMechanismDoseKey Notes
FinasterideType 2 5-AR inhibitor5 mg dailyReduces prostate volume ~20-30%; PSA reduced ~50%; effect in 6-12 months
DutasterideType 1 & 2 5-AR inhibitor0.5 mg dailyDual inhibition; similar clinical outcomes to finasteride; long half-life (5 weeks)

Antimuscarinics (OAB)

DrugSelectivityDoseKey Notes
OxybutyninNon-selective M5 mg BID-TID (IR), patch, gelMost anticholinergic side effects; transdermal form has fewer side effects; avoid in elderly
TolterodineNon-selective M2 mg BID (IR) or 4 mg daily (ER)Better tolerated than oxybutynin; ER preferred
SolifenacinM3 selective5-10 mg dailyOnce daily; less dry mouth than oxybutynin
DarifenacinM3 selective7.5-15 mg dailyMinimal CNS effects (less crosses BBB); good for elderly
TrospiumNon-selective M20 mg BIDQuaternary amine — does NOT cross BBB; safest for cognition in elderly
FesoterodineNon-selective M4-8 mg dailyActive metabolite of tolterodine

Beta-3 Agonists (OAB)

DrugDoseKey Notes
Mirabegron25-50 mg dailyNo anticholinergic side effects; may raise BP slightly; can combine with antimuscarinics
Vibegron75 mg dailyNo CYP2D6 inhibition (fewer drug interactions than mirabegron)

Androgen Deprivation Therapy

DrugClassRouteKey Notes
LeuprolideGnRH agonistIM/SC (1, 3, 4, 6 month depot)Initial testosterone flare — co-administer anti-androgen × 2-4 wks
GoserelinGnRH agonistSC implant (1, 3 month)Similar to leuprolide
DegarelixGnRH antagonistSC monthlyNo testosterone flare; injection site reactions
RelugolixOral GnRH antagonist120 mg PO dailyNo flare; lower CV risk vs leuprolide (HERO trial); oral convenience
EnzalutamideAR antagonist (2nd gen)160 mg PO dailyFor mCRPC and mHSPC; seizure risk; drug interactions
AbirateroneCYP17 inhibitor1000 mg PO daily + prednisone 5 mg BIDBlocks adrenal/intratumoral androgen synthesis; monitor LFTs, electrolytes, BP
ApalutamideAR antagonist240 mg PO dailyFor nmCRPC and mHSPC; rash common
DarolutamideAR antagonist600 mg PO BIDFor nmCRPC and mHSPC; minimal CNS side effects; low drug interaction risk

Chemotherapy (Urologic Malignancies)

RegimenIndicationKey Toxicities
BEP (bleomycin, etoposide, cisplatin)Metastatic GCT (testicular cancer)Bleomycin pulmonary toxicity (limit total dose; PFTs); cisplatin nephrotoxicity, neuropathy, ototoxicity
Gemcitabine/Cisplatin (GC)Metastatic urothelial carcinoma, neoadjuvant bladder cancerMyelosuppression, nephrotoxicity; similar efficacy to MVAC with less toxicity
MVAC (methotrexate, vinblastine, adriamycin, cisplatin)Metastatic urothelial carcinomaSignificant myelosuppression, mucositis; dose-dense MVAC with GCSF preferred
DocetaxelmCRPC (first-line chemo), mHSPCNeutropenia, neuropathy, fluid retention
CabazitaxelmCRPC (post-docetaxel)Myelosuppression (neutropenia)

Medical Expulsive Therapy & Stone Prevention

DrugIndicationMechanism/Notes
Tamsulosin 0.4 mg dailyDistal ureteral stones 5-10 mmAlpha-blocker; relaxes ureteral smooth muscle
Potassium citrateHypocitraturia, uric acid stones, RTA stonesAlkalinizes urine; binds calcium; increases citrate excretion
Hydrochlorothiazide 25-50 mgHypercalciuria (calcium stones)Enhances renal calcium reabsorption
Allopurinol 300 mg dailyHyperuricosuria, uric acid stonesXanthine oxidase inhibitor; reduces uric acid production
TioproninCystine stonesThiol agent — chelates cystine, increases solubility
Acetohydroxamic acid (AHA)Struvite stones (adjunct)Urease inhibitor; prevents struvite crystallization

Erectile Dysfunction Medications

DrugOnsetDurationKey Features
Sildenafil (Viagra)30-60 min4-6 hrsTake on empty stomach; avoid with high-fat meals; original PDE5i
Tadalafil (Cialis)30-60 min24-36 hrsLongest duration; 5 mg daily dosing for BPH + ED; food-independent
Vardenafil (Levitra)30-60 min4-6 hrsAvoid with QT-prolonging drugs; ODT form available
Avanafil (Stendra)15-30 min6 hrsFastest onset; most selective PDE5i; fewer visual side effects

All PDE5 inhibitors are absolutely contraindicated with nitrates (nitroglycerin, isosorbide mononitrate/dinitrate) — risk of severe, refractory hypotension. Relative caution with alpha-blockers (orthostatic hypotension). Common side effects: headache, flushing, dyspepsia, nasal congestion, visual disturbances (blue tinge with sildenafil — PDE6 cross-reactivity), and myalgias (tadalafil — PDE11 cross-reactivity).

Intracavernosal Injection Therapy

AgentMechanismNotes
Alprostadil (PGE1)Direct smooth muscle relaxation via cAMPFDA-approved; injection or intraurethral (MUSE); penile pain in ~30%
Trimix (PGE1 + phentolamine + papaverine)Triple mechanism: cAMP, alpha-blockade, PDE inhibitionMost effective injectable; compounded; lower pain than alprostadil alone
PapaverineNon-selective PDE inhibitorRarely used alone; risk of priapism and fibrosis

25 Imaging & Diagnostics

CT Urogram

The CT urogram is the gold standard for evaluating hematuria and the upper urinary tract. It consists of three phases: non-contrast (detects stones, calcifications), nephrographic (enhancing renal masses), and delayed/excretory (opacifies the collecting system, ureters, and bladder — detects urothelial lesions). Sensitivity for ureteral stones ~97%; sensitivity for renal masses ~95%; sensitivity for UTUC ~96%.

Renal Ultrasound

Renal ultrasound is the first-line imaging for hydronephrosis, renal cysts (Bosniak I-II), pediatric evaluation, pregnant patients with suspected stones, and transplant kidney assessment. Advantages: no radiation, no contrast, portable, real-time. Limitations: operator-dependent, poor sensitivity for small ureteral stones (< 5 mm), cannot reliably characterize solid renal masses. Scrotal ultrasound with color Doppler is the first-line imaging for testicular masses and acute scrotum.

MRI Prostate (mpMRI)

Multiparametric MRI (mpMRI) of the prostate uses T2-weighted, diffusion-weighted (DWI/ADC), and dynamic contrast-enhanced (DCE) sequences. The PI-RADS v2.1 scoring system (1-5) standardizes reporting. mpMRI is used for: (1) pre-biopsy risk stratification — PI-RADS 1-2 has a high negative predictive value for clinically significant cancer (may avoid biopsy); (2) targeted biopsy guidance (MRI-TRUS fusion biopsy) for PI-RADS ≥ 3 lesions; (3) active surveillance monitoring; (4) local staging (extracapsular extension, SV invasion). The PRECISION trial showed that MRI-targeted biopsy detected more clinically significant cancers and fewer insignificant cancers compared to standard systematic biopsy.

Voiding Cystourethrogram (VCUG)

VCUG is the gold standard for diagnosing and grading VUR. Fluoroscopic imaging during bladder filling and voiding with contrast. Also evaluates: posterior urethral valves (dilated posterior urethra), bladder diverticula, and urethral abnormalities. In pediatric patients, a nuclear cystogram (radionuclide cystography) can be used for VUR surveillance with lower radiation dose.

Cystoscopy

Cystoscopy (flexible or rigid) allows direct visualization of the urethra and bladder. Indications: hematuria evaluation, bladder tumor surveillance, foreign body removal, stent placement/removal, and therapeutic interventions (TURBT, Botox injection). Flexible cystoscopy is performed in the office under local anesthesia (lidocaine gel). Blue-light (photodynamic) cystoscopy using hexaminolevulinate (HAL) improves detection of CIS and flat urothelial lesions compared to white-light cystoscopy.

Urodynamic Studies (UDS)

Urodynamics is the functional study of the lower urinary tract. Components: (1) Uroflowmetry — non-invasive measurement of flow rate; (2) Filling cystometry — measures intravesical pressure, compliance, capacity, and detects involuntary detrusor contractions during filling; (3) Pressure-flow study (voiding cystometry) — measures detrusor pressure during voiding to differentiate BOO from detrusor underactivity; (4) EMG — assesses pelvic floor/sphincter activity; (5) Video-urodynamics — combines UDS with fluoroscopy for anatomic correlation (gold standard for neurogenic bladder). Key parameters: detrusor pressure at Qmax (PdetQmax) > 40 cm H2O with Qmax < 12 mL/s = obstructed (Abrams-Griffiths nomogram).

Diuretic Renography (MAG3 Scan)

MAG3 diuretic renography uses Tc-99m-MAG3 radionuclide with furosemide administration to assess differential renal function and drainage. Key parameters: differential function (< 40% indicates significant impairment of the affected kidney), T½ (half-time of radionuclide washout after furosemide) — T½ < 10 min = non-obstructed, 10-20 min = indeterminate, > 20 min = obstructed. Primary indication: evaluation of UPJ obstruction and hydronephrosis to differentiate true obstruction from non-obstructive dilation.

PSMA PET-CT

PSMA PET-CT (prostate-specific membrane antigen positron emission tomography) uses radiolabeled tracers (Ga-68 PSMA-11 or F-18 piflufolastat/DCFPyL) that bind to PSMA expressed on prostate cancer cells. It has dramatically improved the detection of recurrent and metastatic prostate cancer, with sensitivity far exceeding conventional imaging (CT, bone scan, MRI). Indications: biochemical recurrence after definitive therapy (detects recurrence at PSA levels as low as 0.2 ng/mL), initial staging of high-risk or unfavorable intermediate-risk prostate cancer, and identification of PSMA-expressing tumors eligible for Lu-177-PSMA-617 radioligand therapy. PSMA PET-CT has been shown to change management in > 50% of patients with BCR.

Angiomyolipoma (AML)

Angiomyolipoma is the most common benign renal tumor. It contains fat, smooth muscle, and blood vessels. Classic AMLs are identified by the presence of macroscopic fat on CT (pathognomonic — HU < -10). Most are sporadic (80%, typically solitary, in women 40-60). Twenty percent occur in association with tuberous sclerosis complex (TSC) — bilateral, multiple, and presenting at a younger age. AMLs > 4 cm or symptomatic (hemorrhage) may require treatment: selective arterial embolization (first-line for acute hemorrhage), partial nephrectomy, or mTOR inhibitors (everolimus — for TSC-associated AMLs). Fat-poor AMLs can mimic RCC on imaging and may require biopsy or excision.

Renal Trauma

Renal trauma is classified by the AAST (American Association for the Surgery of Trauma) grading system:

GradeDescriptionManagement
ISubcapsular hematoma, non-expanding; contusion without lacerationConservative: bed rest, serial hematocrit, imaging follow-up
IIPerirenal hematoma confined to retroperitoneum; cortical laceration < 1 cm depth, no collecting system involvementConservative
IIICortical laceration > 1 cm depth, no collecting system involvement or urinary extravasationConservative; selective angioembolization if active bleeding
IVLaceration into collecting system with urinary extravasation; renal artery/vein injury with contained hemorrhage; segmental infarctionConservative if hemodynamically stable; ureteral stent for persistent urinoma; angioembolization for vascular injury
VShattered kidney; renal hilar avulsion; devascularized kidneySurgical exploration; nephrectomy often required for hilar avulsion; attempt repair if possible

Key principle: >95% of blunt renal injuries (Grades I-IV) can be managed non-operatively with observation, bed rest, and serial imaging. Indications for surgical exploration: hemodynamic instability not responding to resuscitation, expanding/pulsatile perirenal hematoma found during laparotomy, and Grade V hilar injury. Always attempt to confirm two functioning kidneys before performing nephrectomy (one-shot IVP or contralateral kidney palpation at surgery).

CT scan showing renal laceration with perirenal hematoma after blunt trauma
Figure 20 — Renal Trauma on CT. CT with IV contrast showing renal laceration with perirenal hematoma. CT is the imaging standard for evaluating renal trauma in hemodynamically stable patients. Source: Wikimedia Commons. Public domain.
MRI of the prostate showing multiparametric sequences
Figure 16 — Multiparametric MRI of the Prostate. T2-weighted and diffusion-weighted imaging help identify suspicious lesions scored using the PI-RADS system to guide biopsy decisions. Source: Wikimedia Commons. Public domain.

Varicocele

Varicocele is abnormal dilation of the pampiniform venous plexus within the spermatic cord, present in ~15% of the general male population and ~35-40% of men with primary infertility. Left-sided varicoceles are far more common (~90%) due to the longer course and perpendicular drainage of the left gonadal vein into the left renal vein. On examination, a varicocele feels like a "bag of worms" that distends with Valsalva and decompresses in the supine position. Grading: Grade I (palpable only with Valsalva), Grade II (palpable without Valsalva), Grade III (visible through scrotal skin).

Indications for varicocele repair: palpable varicocele + abnormal semen parameters + couple trying to conceive, or adolescent with testicular growth arrest (> 2 mL or 20% asymmetry). Repair options: microsurgical subinguinal varicocelectomy (gold standard — lowest recurrence ~1%, lowest hydrocele rate ~0.5%), inguinal varicocelectomy, laparoscopic varicocelectomy, and percutaneous embolization (interventional radiology). Semen parameters improve in ~60-70% of men after repair; spontaneous pregnancy rates increase by ~30-40%.

Ultrasound image of varicocele showing dilated pampiniform plexus veins
Figure 19 — Varicocele. Dilated pampiniform venous plexus veins within the spermatic cord. Left-sided predominance is due to the perpendicular drainage of the left gonadal vein into the left renal vein. Source: Wikimedia Commons. Public domain.

Male Infertility — Evaluation Overview

Male factor contributes to ~50% of couple infertility. Evaluation: semen analysis (× 2, 2-7 days abstinence) — WHO 2021 reference values: volume ≥ 1.4 mL, concentration ≥ 16 million/mL, total motility ≥ 42%, progressive motility ≥ 30%, normal morphology ≥ 4% (strict Kruger criteria). Azoospermia (no sperm in ejaculate) is classified as obstructive (normal FSH, normal testis volume — causes: vasectomy, ejaculatory duct obstruction, congenital bilateral absence of vas deferens/CBAVD associated with CFTR mutations) or non-obstructive (elevated FSH, small testes — causes: Klinefelter syndrome 47,XXY, Y-chromosome microdeletions, cryptorchidism, chemotherapy/radiation). Hormonal evaluation: FSH, LH, testosterone, prolactin. Genetic testing: karyotype and Y-microdeletion analysis for severe oligospermia (< 5 million/mL) or non-obstructive azoospermia.

Microsurgical testicular sperm extraction (micro-TESE) is the gold standard for sperm retrieval in non-obstructive azoospermia — identifies enlarged seminiferous tubules (more likely to contain spermatogenesis) under the operating microscope; sperm retrieval rate ~50%. Retrieved sperm are used for intracytoplasmic sperm injection (ICSI). Vasectomy reversal (vasovasostomy or vasoepididymostomy) has patency rates of 85-97% for vasovasostomy and 60-85% for vasoepididymostomy; success decreases with obstructive interval > 15 years.

Kasivisvanathan V et al. "MRI-targeted or standard biopsy for prostate-cancer diagnosis." N Engl J Med. 2018;378(19):1767-1777. PMID: 29552975 (PRECISION Trial)

26 Abbreviations Master List

AbbreviationMeaning
ADTAndrogen deprivation therapy
AFPAlpha-fetoprotein
ARAndrogen receptor
AUAAmerican Urological Association
AUSArtificial urinary sphincter
BCGBacillus Calmette-Guérin
BEPBleomycin, etoposide, cisplatin
BMGBuccal mucosal graft
BOOBladder outlet obstruction
BPHBenign prostatic hyperplasia
CICClean intermittent catheterization
CISCarcinoma in situ
CKDChronic kidney disease
CRPCCastration-resistant prostate cancer
CTComputed tomography
DCEDynamic contrast-enhanced (MRI)
DJDouble-J (ureteral stent)
DLPPDetrusor leak point pressure
DREDigital rectal examination
DSDDetrusor-sphincter dyssynergia
DVIUDirect vision internal urethrotomy
DWIDiffusion-weighted imaging
EBRTExternal beam radiation therapy
EDErectile dysfunction
EPAExcision and primary anastomosis
GCTGerm cell tumor
GFRGlomerular filtration rate
GnRHGonadotropin-releasing hormone
hCGHuman chorionic gonadotropin
HoLEPHolmium laser enucleation of prostate
HPFHigh-power field
ICIImmune checkpoint inhibitor
IFISIntraoperative floppy iris syndrome
IGCCCGInternational Germ Cell Cancer Collaborative Group
IMRTIntensity-modulated radiation therapy
IPSSInternational Prostate Symptom Score
ISDIntrinsic sphincter deficiency
ISUPInternational Society of Urological Pathology
IVCInferior vena cava
LDHLactate dehydrogenase
LUTSLower urinary tract symptoms
MAPMagnesium ammonium phosphate (struvite)
METMedical expulsive therapy
MIBCMuscle-invasive bladder cancer
mpMRIMultiparametric MRI
mRCCMetastatic renal cell carcinoma
MVACMethotrexate, vinblastine, adriamycin, cisplatin
NMIBCNon-muscle-invasive bladder cancer
NSGCTNonseminomatous germ cell tumor
NVBNeurovascular bundle
OABOveractive bladder
PCNLPercutaneous nephrolithotomy
PCNPercutaneous nephrostomy
PDE5Phosphodiesterase type 5
PFMTPelvic floor muscle training
PI-RADSProstate Imaging — Reporting and Data System
PSAProstate-specific antigen
PTNSPercutaneous tibial nerve stimulation
PUVPosterior urethral valves
PVRPost-void residual
RAASRenin-angiotensin-aldosterone system
RARPRobot-assisted radical prostatectomy
RCCRenal cell carcinoma
RNURadical nephroureterectomy
RPRadical prostatectomy
RPLNDRetroperitoneal lymph node dissection
RTARenal tubular acidosis
RUGRetrograde urethrogram
SBRTStereotactic body radiation therapy
SNMSacral neuromodulation
SUIStress urinary incontinence
SWLShock wave lithotripsy
TCCTransitional cell carcinoma
TIPTubularized incised plate
TKITyrosine kinase inhibitor
TNMTumor-Node-Metastasis (staging)
TURBTTransurethral resection of bladder tumor
TURPTransurethral resection of prostate
UDSUrodynamic studies
UPJUreteropelvic junction
URSUreteroscopy
UTUCUpper tract urothelial carcinoma
UUIUrgency urinary incontinence
UVJUreterovesical junction
VCUGVoiding cystourethrogram
VHLVon Hippel-Lindau
VURVesicoureteral reflux
5-ARI5-alpha reductase inhibitor
ADAutonomic dysreflexia
ADCApparent diffusion coefficient (MRI)
AMLAngiomyolipoma
BRCABreast cancer gene
CAUTICatheter-associated urinary tract infection
CBAVDCongenital bilateral absence of vas deferens
CFTRCystic fibrosis transmembrane conductance regulator
CTComputed tomography
DSDDisorders of sex development / Detrusor-sphincter dyssynergia
GCNISGerm cell neoplasia in situ
HRRHomologous recombination repair
ICSIIntracytoplasmic sperm injection
IMDCInternational Metastatic RCC Database Consortium
LVILymphovascular invasion
MAG3Mercaptoacetyltriglycine (renal scan)
mHSPCMetastatic hormone-sensitive prostate cancer
mTORMechanistic target of rapamycin
MUSMidurethral sling
PARPPoly (ADP-ribose) polymerase
PDE5iPhosphodiesterase type 5 inhibitor
PSMAProstate-specific membrane antigen
PULProstatic urethral lift (UroLift)
PVPPhotoselective vaporization of prostate
RENALRadius, Exophytic, Nearness, Anterior/posterior, Location (nephrometry)
SCISpinal cord injury
SRMSmall renal mass
SRTSalvage radiation therapy
TESETesticular sperm extraction
TSCTuberous sclerosis complex
TWOCTrial without catheter
UASUreteral access sheath
VACVacuum-assisted closure (wound therapy)
VEGFVascular endothelial growth factor
WHOWorld Health Organization

Landmark Trials in Urology

TrialTopicKey Finding
ProtecT (2016)Localized prostate cancerNo difference in prostate-cancer-specific mortality at 10 years between active monitoring, radical prostatectomy, and EBRT
PRECISION (2018)Prostate biopsyMRI-targeted biopsy detected more clinically significant cancers and fewer insignificant cancers than systematic biopsy
CHAARTED (2015)mHSPCADT + docetaxel improved OS by 13.6 months vs ADT alone in high-volume mHSPC
LATITUDE (2017)mHSPCADT + abiraterone/prednisone significantly improved OS in newly diagnosed high-risk mHSPC
CheckMate 214 (2018)Metastatic RCCIpilimumab + nivolumab improved OS vs sunitinib in intermediate/poor-risk mRCC
KEYNOTE-426 (2019)Metastatic RCCPembrolizumab + axitinib improved OS and PFS vs sunitinib across all IMDC risk groups
MTOPS (2003)BPHCombination doxazosin + finasteride superior to monotherapy in reducing BPH clinical progression
CombAT (2010)BPHDutasteride + tamsulosin superior to monotherapy in men with enlarged prostates (> 30 mL)
RIVUR (2014)Pediatric VURAntibiotic prophylaxis reduced UTI recurrence by ~50% in children with VUR but did not prevent scarring
SWOG 8794 (2009)Adjuvant RT after RPAdjuvant RT after RP for pT3 prostate cancer improved biochemical recurrence-free survival
EV-302/KEYNOTE-A39 (2023)Metastatic urothelialEnfortumab vedotin + pembrolizumab became new standard first-line for metastatic urothelial carcinoma
HERO (2020)ADT for prostate cancerOral relugolix achieved testosterone suppression with lower cardiovascular event rate vs leuprolide
CARMENA (2018)Cytoreductive nephrectomy in mRCCSunitinib alone was non-inferior to cytoreductive nephrectomy + sunitinib in IMDC intermediate/poor-risk mRCC
JAVELIN Bladder 100 (2020)Maintenance immunotherapy in urothelial carcinomaAvelumab maintenance after platinum-based chemo improved OS in advanced urothelial carcinoma

Urologic Emergencies — Quick Reference

EmergencyKey Time WindowImmediate Action
Testicular torsionSalvage within 6 hoursEmergent scrotal exploration, detorsion, bilateral orchiopexy
Fournier gangreneHours (mortality rises with delay)Broad-spectrum IV antibiotics + emergent surgical debridement
Ischemic priapismIntervene within 4-6 hoursCorporal aspiration + phenylephrine injection
ParaphimosisUrgent (risk of ischemic necrosis)Manual reduction; dorsal slit if unsuccessful
Infected obstructed kidneyUrgent (sepsis risk)IV antibiotics + ureteral stent or percutaneous nephrostomy
Autonomic dysreflexiaMinutes (hypertensive crisis)Sit up, identify trigger (usually bladder distension), catheterize, antihypertensives
Bilateral ureteral obstructionUrgent (renal failure)Emergent decompression (stents or nephrostomy tubes bilaterally)
Renal trauma Grade VImmediate (hemorrhage)Surgical exploration if hemodynamically unstable; angioembolization if stable