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I now have comprehensive, authoritative content from multiple surgical and urology textbooks. Let me compile the full learning material.Here is the comprehensive surgical learning material covering all requested topics, synthesized from Campbell-Walsh Urology, Sabiston Textbook of Surgery, Schwartz's Principles of Surgery, Robbins Pathology, Smith & Tanagho's General Urology, and Mulholland & Greenfield's Surgery.

COMPREHENSIVE SURGICAL LEARNING MATERIAL

Urology & Urogenital Surgery


SECTION 1: EXAMINATION AND INVESTIGATION OF THE UROGENITAL SYSTEM

History-Taking

A focused urological history must address:
  • Voiding symptoms: Divided into obstructive (storage) and irritative (voiding) lower urinary tract symptoms (LUTS)
    • Obstructive LUTS: Incomplete emptying, urinary frequency (>every 2 hours), intermittency, weak stream, straining (Valsalva voiding)
    • Irritative LUTS: Urgency, urge incontinence, dysuria, nocturia
  • Pain: Flank pain suggests renal/ureteric pathology; suprapubic pain suggests bladder or urethral pathology; perineal pain suggests prostate pathology; scrotal/testicular pain is often acute and requires urgent evaluation
  • Haematuria: Timing in the stream (initial, terminal, or throughout)
  • Sexual function: Erectile function, libido, ejaculation
  • Prior pelvic/urologic surgery, catheterizations, or STIs

Physical Examination

  • Inspection: Penile abnormalities (phimosis, hypospadias, skin lesions), scrotal asymmetry
  • Palpation: Kidneys (bimanual ballottement), bladder (suprapubic), testicles (consistency, tenderness, masses), epididymis
  • Digital Rectal Examination (DRE): Size, consistency, symmetry of the prostate; a hard, nodular prostate raises concern for carcinoma; a smooth, symmetrically enlarged prostate suggests BPH; a tender, boggy prostate indicates prostatitis
  • Transillumination: Used to differentiate hydrocele (transilluminates) from solid testicular mass

Investigations

InvestigationIndication
Urinalysis + microscopyHaematuria, infection, proteinuria
Urine cultureUTI workup
PSA (prostate-specific antigen)Prostate cancer screening/monitoring
Serum creatinine/eGFRRenal function
Serum AFP, β-hCG, LDHTesticular tumor markers
Testosterone, FSH, LH, prolactinHypogonadism, infertility, ED
Renal ultrasoundHydronephrosis, masses, stones
CT urogram (CTU)Gold standard for upper tract evaluation, haematuria
Retrograde urethrogramUrethral stricture disease
CystoscopyBladder lesions, haematuria evaluation
UrodynamicsComplex voiding dysfunction
Doppler scrotal USSTesticular torsion, varicocele
TRUS (transrectal US)Prostate biopsy guidance
MAG3 renogramUPJ obstruction (functional)
Sources: Campbell Walsh Wein Urology; Sabiston Textbook of Surgery

SECTION 2: HAEMATURIA

Definition & Classification

  • Gross haematuria: Visible blood in urine — always warrants full evaluation
  • Microscopic haematuria: ≥3 RBCs/hpf on microscopy (note: dipstick alone is insufficient — it may give false positives with myoglobin or hemoglobin)
  • Pseudohaematuria: Red/brown urine without true RBCs — caused by certain foods (beets), medications (rifampicin), or dehydration

Timing in the Urinary Stream

TimingSource
Initial stream haematuriaUrethra or prostate
Terminal haematuriaBladder neck
Throughout streamUpper tract (kidney, ureter) or bladder
Clot shape also helps: vermiform (worm-like) clots originate from the upper tract; cuboid clots from the bladder.

Causes

Upper tract:
  • Renal cell carcinoma
  • Transitional cell carcinoma (urothelial) of the renal pelvis/ureter
  • Nephrolithiasis
  • IgA nephropathy, glomerulonephritis
  • Trauma
  • Renal infarction
Lower tract:
  • Bladder cancer (most common cause of gross haematuria in patients >50 years)
  • Bladder stones
  • Cystitis (bacterial, radiation-induced, drug-induced)
  • BPH
  • Urethral stricture/trauma

Risk Factors for Underlying Malignancy

  • Age >40
  • Male sex
  • Smoking history
  • Industrial chemical/dye exposure (aromatic amines)
  • Chronic cyclophosphamide therapy
  • Pelvic irradiation
  • Analgesic abuse (phenacetin)

Investigation Algorithm (AUA Guidelines)

  1. Exclude: UTI (especially in young women), recent urological manipulation, nephrological disease
  2. Urine cytology
  3. Cystoscopy + CT urogram for all patients with gross haematuria and for microscopic haematuria with risk factors
  4. Urine culture if infection suspected
Source: Campbell Walsh Wein Urology, block 1

SECTION 3: EXTERNAL HERNIAS AND HYDROCOELES

Inguinal Hernias

Anatomy & Embryology

The processus vaginalis is the peritoneal extension that descends alongside the testis during embryonic descent. Normally, it obliterates after testicular descent. Failure of obliteration leads to:
  • Patent processus vaginalis → indirect inguinal hernia or communicating hydrocele
  • Incidence of patent processus vaginalis: 80–94% in neonatal autopsy; 20–30% in adults

Types of Inguinal Hernias in Children

TypeIncidenceAnatomical origin
Indirect (congenital)~99%Lateral to inferior epigastric vessels; descends in spermatic cord
Direct~0.5%Medial to inferior epigastric vessels; through posterior wall of canal
Femoral<0.5%Medial to femoral vein, below inguinal ligament
  • Key: Only indirect hernias and hydroceles enter the scrotum; femoral hernias never do
  • Male:Female ratio = 5–10:1; right-sided predominance (3:1) due to later right testicular descent
  • Incarceration risk is highest in the first 6 months of life

Clinical Presentation

  • Painless reducible bulge in the inguinal region or scrotum
  • Bulge may appear with straining, crying, or Valsalva
  • Incarcerated hernia: Tender, irreducible bulge + signs of bowel obstruction
  • Strangulated hernia: Ischaemic bowel; surgical emergency

Surgery

  • Inguinal hernia repair is the most common elective pediatric surgical procedure
  • In children: High ligation of the hernia sac (herniotomy) through an inguinal approach
  • In adults: Tension-free mesh repair (Lichtenstein technique) is standard
  • Laparoscopic approaches allow simultaneous evaluation of the contralateral internal ring

Hydrocoele

Definition

A collection of fluid between the layers of the tunica vaginalis.

Types

TypeCharacteristics
Communicating (neonatal/childhood)Patent processus vaginalis; fluid fluctuates with position and activity
Non-communicating (isolated)Obliterated processus; delayed fluid absorption; resolves spontaneously in most infants
Hydrocele of the cord (encysted)Fluid along spermatic cord
Secondary (reactive)Inflammatory, traumatic, or tumour-related

Management

  • Neonatal/childhood: Observe until age 2 years for spontaneous resolution
  • If persistent after age 2, or adult-onset: Surgical repair (excision of tunica vaginalis or Lord's procedure)
  • Adults: Always evaluate for underlying testicular pathology (USS)
Sources: Campbell Walsh Wein Urology block 20; Mulholland & Greenfield's Surgery block 20; Sabiston block 28

SECTION 4: OBSTRUCTIVE UROPATHY, CATHETERS AND CATHETERIZATION

Obstructive Uropathy

Definition

Any process causing impaired outflow of urine from the kidney to the urethral meatus.

Causes (by level)

LevelCause
UrethraPosterior urethral valves (males), urethral stricture, meatal stenosis, phimosis
Bladder neck/prostateBPH, prostate cancer, prostatitis, bladder neck contracture
BladderNeurogenic bladder, bladder tumour
UreterCalculi, transitional cell carcinoma, external compression (tumour, retroperitoneal fibrosis, lymphoma), stricture
Ureteropelvic junctionCongenital UPJ obstruction, crossing vessel
PregnancyPhysiological ureteric compression by gravid uterus
FunctionalNeurogenic (spinal cord injury, diabetic autonomic neuropathy)

Pathophysiology

  • Obstruction → ↑ intraluminal pressure → transmitted to collecting system → hydronephrosis
  • Continued glomerular filtration → filtrate reabsorbed by interstitium/lymphatics
  • Medullary blood flow compromised → initial tubular dysfunction (impaired concentrating ability) → then ↓ GFR
  • Prolonged obstruction → interstitial fibrosis and permanent renal atrophy

Morphology of Hydronephrosis

  • Early: Dilation of pelvis and calyces with interstitial inflammation
  • Late: Cortical tubular atrophy, blunting of pyramid apices, marked interstitial fibrosis
  • End-stage: Kidney reduced to thin-walled cystic structure

Clinical Features

  • May be silent (chronic, insidious) or present with flank pain, urinary retention, UTI, haematuria
  • Bilateral obstruction → anuria, acute kidney injury
  • Chronic incomplete obstruction → polyuria/polydipsia (tubular concentrating defect)

Investigations

  • Renal ultrasound: First-line — shows hydronephrosis
  • CT KUB: Best for stones; CT urogram for full evaluation
  • MAG3 renogram: Gold standard for functional obstruction (UPJ)
  • Retrograde pyelography: Most sensitive for ureteral lesions

Management

  • Relief of obstruction: Urethral or suprapubic catheter (lower tract), nephrostomy tube or ureteral stent (upper tract)
  • Definitive: Treat underlying cause (stone removal, pyeloplasty, stricture repair, TURP)

Urinary Catheterization

Indications

  • Acute urinary retention
  • Monitoring urine output (critically ill/peri-operative)
  • Neurogenic bladder
  • Haematuria with clots (catheter irrigation)
  • Pre/peri-operative
  • Urethral instillation of medication (BCG for bladder cancer)

Types of Urinary Catheters

TypeUse
Foley (2-way)Standard indwelling catheter
3-way FoleyBladder irrigation (e.g., post-TURP haematuria)
Coudé-tipCurved tip for men with BPH or urethral obstruction
Suprapubic catheterLong-term drainage; preferred for urethral trauma/stricture
Intermittent self-catheterisationNeurogenic bladder, long-term management

Complications of Catheterisation

  • UTI / catheter-associated UTI (CAUTI) — most common; risk increases with duration
  • Urethral trauma / false passage — especially with forceful insertion
  • Haematuria — traumatic
  • Paraphimosis — if foreskin not reduced after procedure
  • Bladder spasm — due to balloon irritation
  • Long-term: Urethral stricture, bladder calculi, periurethral abscess
Sources: Robbins Pathology block 10; Comprehensive Clinical Nephrology; Smith & Tanagho's Urology block 5

SECTION 5: ACUTE SCROTUM

Definition

Acute onset of pain and/or swelling in the scrotum — a urological emergency until testicular torsion is excluded.

Differential Diagnosis

ConditionAgeKey Features
Testicular torsionNeonates; adolescents/young adultsSudden severe pain; high-riding testis; absent cremasteric reflex
Torsion of appendix testisPrepubertal (10–14 years)Gradual onset; "blue dot sign"
Epididymo-orchitisPost-pubertal, adultsGradual onset; dysuria; pyuria; + cremasteric reflex
Incarcerated inguinal herniaInfants, elderlyInguinal mass; vomiting; bowel obstruction
Idiopathic scrotal oedemaYoung boysBilateral oedema, not tender
Trauma / haematoceleAny ageClear history of injury

Testicular Torsion — Detailed

Mechanism

  • Extravaginal torsion: Neonates — twisting of spermatic cord outside tunica vaginalis; usually in utero (prenatal) or within first 30 days (postnatal)
  • Intravaginal torsion: Adolescents/adults — bell-clapper deformity (absent normal posterior fixation of tunica vaginalis to scrotal wall); anomaly present bilaterally

Clinical Features

  • Sudden, severe unilateral scrotal pain (may radiate to the abdomen)
  • Nausea and vomiting
  • High-riding testis (cremasteric muscle contraction shortens cord)
  • Absent cremasteric reflex
  • Horizontal lie of the testis
  • Oedema and erythema developing over hours

Diagnosis

  • Clinical diagnosis is sufficient — do not delay surgery for imaging if torsion is highly suspected
  • Doppler USS: Absence of testicular blood flow confirms torsion (sensitivity ~90%); its absence should not delay surgery
  • Radionuclide scan: Most specific but impractical in acute setting

Management — Salvage Rates

Duration of torsionSalvage rate
<6 hours~90%
6–12 hours~50%
12–24 hours~10%
>24 hours<5%
  • Emergency surgical scrotal exploration via midline raphe incision
  • Detorsion → assess viability → orchidopexy (3-point fixation) if viable; orchiectomy if non-viable
  • Contralateral orchidopexy always performed in adolescents/adults (bilateral anatomical defect)
  • In neonates: Prenatal torsion → urgent orchidopexy of contralateral testis; postnatal torsion → urgent exploration of both testes

Torsion vs Epididymo-orchitis

FeatureTorsionEpididymo-orchitis
OnsetSuddenGradual
Cremasteric reflexAbsentPresent
Urinary symptomsAbsentOften present
Prehn's signPain ↑ with elevationPain ↓ with elevation
Doppler USSAbsent flow↑ flow
TreatmentEmergency surgeryAntibiotics
Sources: Sabiston Textbook of Surgery block 28 & 30; Campbell Walsh Wein Urology block 8; Schwartz's Principles of Surgery

SECTION 6: CONGENITAL ABNORMALITIES OF THE GENITOURINARY TRACT

Cryptorchidism (Undescended Testis / Vacant Scrotum)

Definition

Failure of one or both testes to complete their normal descent into the scrotum by birth.

Classification

  • True cryptorchidism: Testis arrested along normal descent path (abdominal, inguinal, prescrotal)
  • Ectopic testis: Testis deviated from normal descent path (perineal, femoral, pubopenile)
  • Retractile testis: Normal testis that retracts due to hyperactive cremasteric reflex — not a true undescended testis

Incidence

  • ~3–4% at birth; ~1% at 1 year (many descend spontaneously in first few months)
  • Higher incidence in premature infants

Complications

  • Infertility: Undescended testis exposed to higher body temperature → germinal cell damage; bilateral cryptorchidism → azoospermia if untreated
  • Malignancy: Risk of testicular cancer increased (especially seminoma); orchidopexy does not reduce malignancy risk but facilitates earlier detection
  • Testicular torsion: Higher risk in intra-abdominal testes
  • Inguinal hernia: Patent processus vaginalis almost always present

Management

  • Surgical treatment (orchidopexy) recommended at 6–18 months of age
  • Hormonal therapy (hCG or GnRH) is an option but has limited efficacy and is not widely used
  • Orchiectomy for post-pubertal unilateral undescended testis (due to malignancy risk and poor fertility potential)

Posterior Urethral Valves (PUV)

  • Most common obstructive urethral lesion in male infants/newborns
  • Mucosal folds in the distal prostatic urethra causing variable degrees of obstruction during voiding
  • Clinical features: Poor/dribbling urinary stream, recurrent UTI, failure to thrive, bilateral hydronephrosis (palpable abdominal masses)
  • Lab findings: Azotemia, impaired concentrating ability, anaemia (if chronic infection)
  • Imaging: VCUG (voiding cysturethrogram) — gold standard; shows dilated posterior urethra
  • Treatment: Cystoscopic valve ablation; nephrostomy drainage if severe obstruction

Uretero-Pelvic Junction (UPJ) Obstruction

  • Most common congenital anomaly of the ureter
  • Intrinsic (atretic ureteral segment) or extrinsic (crossing vessel — aberrant renal artery branch)
  • Presents with: Flank pain exacerbated by high fluid intake (Dietl's crisis), recurrent UTI, hydronephrosis on imaging
  • Gold standard investigation: MAG3 Lasix renogram (t½ >20 min = obstruction)
  • Treatment: Dismembered pyeloplasty (Anderson-Hynes) — >90% success; can be done laparoscopically or robotically

Hypospadias

  • Opening of the urethral meatus on the ventral surface of the penis (rather than the tip)
  • Associated with chordee (penile curvature), foreskin abnormality
  • Types: Glanular (50%), penile shaft (30%), penoscrotal/perineal (20%)
  • Treatment: Surgical repair before 18 months of age; avoid circumcision (foreskin used for repair)

Vesico-Ureteric Reflux (VUR)

  • Retrograde flow of urine from bladder into ureters
  • Risk of pyelonephritis and renal scarring
  • Graded I–V (Grade V = gross dilation with intrarenal reflux)
  • Managed with prophylactic antibiotics and/or endoscopic injection (bulking agents) or ureteral reimplantation

SECTION 7: BENIGN PROSTATIC HYPERPLASIA (BPH)

Epidemiology

  • Affects ~50% of men at age 60 and 90% by the 8th decade
  • One of the most common conditions managed by urologists

Pathogenesis

  • Stromal and glandular proliferation of the transition zone of the prostate
  • Mediated by dihydrotestosterone (DHT): testosterone → DHT via 5α-reductase type 2 in the prostate
  • DHT binds nuclear androgen receptors → stimulates stromal proliferation + inhibits epithelial apoptosis
  • Oestrogen (↑ relative to falling testosterone with age) acts synergistically with DHT
  • DHT is 10× more potent than testosterone; BPH does not occur in castrated males or those with 5α-reductase deficiency

Morphology

  • Prostate weight increases 3–5 fold (60–100 g or more)
  • Hyperplastic nodules compress the urethra to a slit-like orifice
  • Microscopically: Variable proportions of proliferating glands and fibromuscular stroma
  • Glands lined by tall columnar cells with peripheral flattened basal cells (contrasting with carcinoma)
  • Corpora amylacea (laminated proteinaceous secretory material) in glandular lumina

Symptoms — LUTS

  • Storage symptoms: Urgency, frequency, nocturia, urge incontinence
  • Voiding symptoms: Weak stream, hesitancy, intermittency, straining
  • Post-voiding symptoms: Incomplete emptying, terminal dribbling
  • Note: Prostate volume poorly correlates with symptom severity

Complications

  • Urinary retention (acute or chronic)
  • Bladder hypertrophy → detrusor instability
  • Residual urine → recurrent UTI, bladder stones
  • Upper tract obstructive uropathy
  • Renal failure (bilateral obstruction)

Assessment

  • IPSS (International Prostate Symptom Score): Validated symptom questionnaire
  • DRE: Smooth, symmetrical, rubbery enlargement
  • PSA: Elevated in BPH (~0.1–0.3 ng/mL per gram of benign tissue); must exclude carcinoma
  • Post-void residual (PVR) volume
  • Urinary flow rate (Qmax <10 mL/s = significant obstruction)
  • Renal function if bilateral obstruction suspected

Treatment

Conservative

  • Lifestyle modifications: Fluid restriction (evening), avoid caffeine/alcohol, bladder training, double voiding

Medical

Drug classMechanismDrug examplesKey side effects
α₁-blockersRelax smooth muscle in bladder neck, prostate, urethraTamsulosin, doxazosin, terazosinOrthostatic hypotension, retrograde ejaculation, rhinitis
5α-reductase inhibitorsBlock testosterone → DHT conversion; ↓ prostate volume by ~25%Finasteride (type 2), dutasteride (types 1+2)Sexual dysfunction, ↓ PSA by ~50% (important for screening)
Combination therapyAdditive effect for larger prostatesα-blocker + 5-ARIAs above
Antimuscarinics / β₃ agonistsFor storage LUTS/OAB componentSolifenacin, mirabegronDry mouth, urinary retention

Surgical

ProcedureIndication/Notes
TURP (transurethral resection of prostate)Gold standard; uses electrocautery loop; risk: TUR syndrome (dilutional hyponatraemia from glycine irrigation — nausea, bradycardia, hypertension, pulmonary oedema)
Bipolar TURP / Laser (HoLEP, PVP)Uses normal saline irrigation → eliminates TUR syndrome risk; shorter catheter time; comparable efficacy
Open/robotic simple prostatectomyReserved for very large prostates (>100 g) or when concomitant bladder surgery needed
Urethral stent / catheterTemporary relief in poor surgical candidates
Sources: Sabiston Textbook of Surgery block 30; Schwartz's Principles of Surgery block 19; Robbins & Kumar Basic Pathology block 6

SECTION 8: CANCER OF THE PROSTATE

Epidemiology

  • Most common cancer in men (in the United States, 3 of the 12 most common cancers are urological)
  • Risk increases with age; rare before 50 years
  • Higher incidence in Black men; positive family history increases risk

Pathology

  • ~95% are adenocarcinoma arising from the peripheral zone (contrasting with BPH, which originates in the transition zone)
  • Microscopic features: Malignant glands lack the peripheral basal cell layer seen in BPH
  • Graded by the Gleason score: Based on glandular architecture
    • Gleason pattern 1–5 (1 = well-differentiated, 5 = anaplastic)
    • Gleason score = primary + secondary pattern (e.g., 3+4=7)
    • Contemporary reporting uses Grade Groups 1–5 (Grade Group 1 = Gleason ≤6; Grade Group 5 = Gleason 9–10)

Clinical Features

  • Early: Often asymptomatic; detected on PSA screening or DRE
  • LUTS: If central/transition zone involvement (less common); prostate cancer more typically in peripheral zone
  • Advanced/metastatic: Bone pain (osteoblastic metastases to axial skeleton — spine, pelvis), pathological fractures, haematuria, lower limb oedema (lymphatic obstruction), spinal cord compression

PSA

  • Glycoprotein produced exclusively by prostatic epithelium
  • Normal <4.0 ng/mL; however, PSA is prostate-specific, not cancer-specific
  • PSA elevated in: BPH, prostatitis, post-DRE/ejaculation, catheterisation, and cancer
  • PSA density (PSA/prostate volume), PSA velocity (rate of rise), and free:total PSA ratio (lower ratio = higher cancer risk) improve specificity

Staging

TNM System (abbreviated):
  • T1: Clinically inapparent (found on biopsy or TURP specimen)
  • T2: Palpable or visible, confined to prostate
  • T3: Extends beyond prostate capsule / seminal vesicle invasion
  • T4: Fixed, invades adjacent structures (bladder, rectum)
  • N+: Regional lymph node involvement
  • M1: Distant metastasis (bone most common → osteoblastic lesions on bone scan)

Diagnosis

  1. PSA + DRE
  2. TRUS-guided prostate biopsy (12-core systematic biopsy ± targeted biopsy)
  3. MRI of the prostate (multiparametric MRI — mpMRI): Identifies suspicious lesions (PI-RADS scoring); increasingly used before biopsy
  4. Bone scan: If PSA >20, Gleason ≥8, T3/T4, or symptomatic
  5. CT abdomen/pelvis: Lymph node staging in intermediate/high-risk disease

Treatment

StageOptions
Localised (T1–T2), low-riskActive surveillance; radical prostatectomy; external beam radiotherapy (EBRT); brachytherapy
Localised, intermediate/high-riskRadical prostatectomy ± lymph node dissection; EBRT + androgen deprivation therapy (ADT)
Locally advanced (T3–T4)EBRT + prolonged ADT; radical prostatectomy in selected patients
MetastaticADT (LHRH agonist/antagonist ± antiandrogen); chemotherapy (docetaxel); novel AR pathway inhibitors (enzalutamide, abiraterone)
Castration-resistant prostate cancerDocetaxel, cabazitaxel, enzalutamide, abiraterone, Ra-223 for bone mets

Androgen Deprivation Therapy (ADT)

  • LHRH agonists (leuprolide, goserelin): Initial testosterone flare → then castration levels
  • LHRH antagonists (degarelix): Immediate testosterone suppression, no flare
  • Side effects: Hot flushes, erectile dysfunction, osteoporosis, metabolic syndrome, cardiovascular risk
Sources: Sabiston Textbook of Surgery block 30; Robbins & Kumar Basic Pathology block 6; Campbell Walsh Wein Urology

SECTION 9: URETHRAL STRICTURES

Definition

An area of scarring/fibrosis causing concentric narrowing of the urethra, impeding urine flow.

Anatomy

The male urethra from proximal to distal:
  1. Prostatic urethra
  2. Membranous urethra
  3. Bulbar urethra (most common site of strictures)
  4. Penile urethra
  5. Fossa navicularis (distal penile)

Aetiology

CauseProportion
Iatrogenic (catheterization, cystoscopy, TURP, hypospadias repair)~33%
Trauma (straddle injury, pelvic fractures — posterior urethra)~19%
Inflammatory (gonococcal urethritis, lichen sclerosus)~15%
Idiopathic~33%

Clinical Features

  • Weak or split urinary stream
  • Incomplete bladder emptying
  • Urinary frequency, urgency
  • Recurrent UTI
  • Urinary retention (severe)

Investigations

  • Uroflowmetry: Reduced Qmax; plateau-shaped flow curve
  • Retrograde urethrogram (RUG): Gold standard — defines location, length, and severity of stricture
  • Voiding cysturethrogram (VCUG): Defines proximal extent
  • Cystoscopy + urethroscopy: Direct visualisation

Management

Endoscopic (First-line)

  • Urethral dilation: Mechanical stretching; success rate ~30% for a single attempt; drops to ~13% for repeat procedures
  • Direct vision internal urethrotomy (DVIU): Incision of stricture under direct vision with a urethrotome; comparable to dilation; success depends on stricture length and location

Surgical Reconstruction (Urethroplasty)

Indicated after failed endoscopic treatment (recommend only one endoscopic attempt before referral):
TechniqueIndication
Anastomotic urethroplasty (excision and primary anastomosis, EPA)Short bulbar strictures (<2 cm); membranous strictures
Buccal mucosa graft urethroplastyLonger strictures; ventral or dorsal onlay
Penile skin flap urethroplastyAnterior strictures; alternative to buccal mucosa
Perineal urethrostomyPalliative; complex strictures unsuitable for reconstruction
  • Urethroplasty has superior long-term success (~85–90%) compared to endoscopic treatment
Sources: Schwartz's Principles of Surgery block 19; Smith & Tanagho's General Urology block 6; Campbell Walsh Wein Urology block 21

SECTION 10: ERECTILE DYSFUNCTION

Definition

The persistent inability to attain and/or maintain a penile erection sufficient for satisfactory sexual performance.

Physiology of Erection

  • Complex neurovascular event involving the parasympathetic nervous system (S2–S4), sympathetic NS, and somatic NS
  • Sexual stimulation → release of nitric oxide (NO) from nerve endings and endothelium → activates guanylyl cyclase → ↑ cGMP → smooth muscle relaxation → increased arterial inflow to corpus cavernosum → venous occlusion (veno-occlusive mechanism) → erection
  • Detumescence: Sympathetic stimulation → ↑ cAMP breakdown → smooth muscle contraction

Aetiology

CategoryCauses
Vascular (most common)Atherosclerosis, hypertension, dyslipidaemia, diabetes, smoking, peripheral vascular disease
NeurologicalSpinal cord injury, multiple sclerosis, radical prostatectomy, pelvic surgery, diabetic neuropathy
EndocrineHypogonadism (↓ testosterone), hyperprolactinaemia, hypothyroidism, Cushing's syndrome
PsychogenicPerformance anxiety, depression, relationship issues, PTSD
Drug-inducedAntihypertensives (β-blockers, thiazides), antidepressants (SSRIs), antipsychotics, antiandrogens
StructuralPeyronie's disease (fibrotic plaques in tunica albuginea), priapism-related fibrosis
Important: ED is an early marker for cardiovascular disease — particularly in younger men (<60 years); ED may precede coronary artery disease by 3–5 years.

Evaluation

  • Full sexual, medical, and psychosocial history
  • Physical exam: Secondary sexual characteristics, genitalia, vascular/neurological exam
  • Validated questionnaire: International Index of Erectile Function (IIEF)
  • Investigations: Fasting morning testosterone, LH, FSH, prolactin, fasting lipids, HbA1c, fasting glucose
  • Specialised: Penile duplex Doppler USS (vascular assessment); biothesiometry (neurological)

Management

Lifestyle

  • Weight loss, regular exercise, smoking cessation, alcohol reduction — independently improve erectile function

Medical

TreatmentMechanismNotes
PDE5 inhibitors (sildenafil, tadalafil, vardenafil, avanafil)Block PDE5 → ↑ cGMP → smooth muscle relaxationFirst-line; contraindicated with nitrates (severe hypotension); avoid in severe cardiovascular disease
Testosterone replacementTreats hypogonadismEffective only when low testosterone is the cause; multiple formulations (IM, transdermal, oral)
Intracavernosal injection (alprostadil — PGE₁)Direct smooth muscle relaxationUsed when PDE5i fail; risk of priapism
Intraurethral suppository (MUSE)Transurethral alprostadilLess effective than injection
Vacuum erection deviceMechanical; creates negative pressureNon-pharmacological; useful for post-surgical ED
Psychotherapy/sex therapyPsychogenic EDOften combined with medical therapy

Surgical

  • Inflatable penile prosthesis (IPP): Gold standard surgical treatment; 3-piece system (paired cylinders + scrotal pump + reservoir); satisfaction rates >90%
  • Malleable (semi-rigid) prosthesis: Simpler; lower mechanical failure rate; less natural erection quality
  • Penile arterial revascularisation: Inferior epigastric artery pedicle flap; limited to young men with traumatic arterial injury; controversial
Sources: Sabiston Textbook of Surgery block 30; Campbell Walsh Wein Urology

SECTION 11: CANCERS OF THE KIDNEY

Renal Cell Carcinoma (RCC)

Epidemiology

  • Represents 80–85% of all primary renal malignancies
  • 2–3% of all adult cancers; ~65,000 cases/year in the USA
  • Male:female ratio = 2:1; peak incidence 6th–7th decade
  • Risk factors: Smoking (doubles risk), hypertension, obesity, cadmium exposure, acquired polycystic kidney disease (30-fold increased risk in dialysis patients)

Molecular Classification

TypeFrequencyGeneticsHistology
Clear cell RCC65%VHL gene loss (3p25) → ↑ HIF → ↑ VEGF (angiogenesis)Clear cytoplasm; highly vascular
Papillary RCC10–15%MET gene activation (7q) — activating mutations or copy number gainPapillary architecture; often multifocal/bilateral
Chromophobe RCC5%Multiple chromosome lossesEosinophilic cytoplasm; best prognosis
Oncocytoma~5%BenignMahogany brown; central stellate scar
Collecting duct carcinomaRareVery aggressive
Wilms tumour (nephroblastoma)ChildrenWT1 gene mutationSee paediatric section

Clinical Features

Classic triad (now seen in <5% of patients):
  • Flank pain
  • Gross haematuria
  • Palpable abdominal mass
Current reality: >50% discovered incidentally on imaging for other complaints; 30% present with metastatic disease.
Paraneoplastic syndromes (important distinguishing feature):
  • Polycythaemia (ectopic EPO production)
  • Hypercalcaemia (PTHrP or bony metastases)
  • Stauffer syndrome (non-metastatic hepatic dysfunction)
  • Hypertension (ectopic renin)
  • Feminisation/masculinisation (ectopic gonadotropins)
  • Amyloidosis
Tumour extends into renal vein and IVC in ~25% of cases (critical surgical consideration)

Staging (AJCC/TNM)

StageDescription
T1a≤4 cm, confined to kidney
T1b4–7 cm, confined to kidney
T2>7 cm, confined to kidney
T3Renal vein/IVC invasion or adrenal/perinephric fat invasion within Gerota's fascia
T4Beyond Gerota's fascia

Treatment

StageTreatment
T1a (≤4 cm)Partial nephrectomy (nephron-sparing) — preferred; or ablation (cryotherapy/RFA)
T1b–T2Radical nephrectomy (laparoscopic or open); partial nephrectomy if technically feasible
T3–T4Radical nephrectomy ± IVC thrombectomy (requires cardiopulmonary bypass if above diaphragm)
MetastaticCytoreductive nephrectomy + systemic therapy

Systemic therapy for metastatic RCC

  • Targeted therapy (1st line): VEGF/VEGFR inhibitors (sunitinib, pazopanib, cabozantinib), mTOR inhibitors (everolimus)
  • Immunotherapy: Anti-PD-1/PD-L1 checkpoint inhibitors (nivolumab, pembrolizumab); combination IO therapy now preferred in most patients
  • RCC is resistant to cytotoxic chemotherapy
Sources: Robbins & Kumar Basic Pathology block 5; Sabiston Textbook of Surgery block 30; Campbell Walsh Wein Urology

SECTION 12: UROGENITAL TRAUMA

Background

  • 10–15% of all abdominal and pelvic trauma involves the genitourinary system
  • Isolated urological injuries are uncommon; associated abdominal/pelvic injuries common
  • Initial: Haemodynamic stabilisation → then advanced imaging
  • Early urological consultation is essential

Renal Trauma

Mechanism

  • Blunt trauma (~80%): MVA, falls, sports; deceleration injuries → intimal tears in renal vasculature
  • Penetrating trauma (~20%): Knife/gunshot wounds

Classification (AAST Renal Injury Scale)

GradeDescription
IContusion/non-expanding subcapsular haematoma
IINon-expanding perirenal haematoma; cortical laceration <1 cm; no urinary extravasation
IIICortical laceration >1 cm; no collecting system involvement or urinary extravasation
IVLaceration through cortex + medulla + collecting system; vascular injury (main renal artery/vein)
VShattered kidney; complete renal vascular avulsion

Diagnosis

  • Gross haematuria with abdominal trauma → renal imaging indicated
  • Microscopic haematuria with haemodynamic shock → also image
  • CT with IV contrast + delayed phase = gold standard for staging renal injuries

Management

  • Grade I–III: Conservative — bed rest, monitoring, serial imaging; angioembolisation for persistent haemorrhage
  • Grade IV: Usually non-operative; embolisation for active haemorrhage; stent for urinary extravasation
  • Grade V: Surgical exploration; attempt renorrhaphy or partial/total nephrectomy

Ureteral Trauma

  • Usually iatrogenic (pelvic surgery, ureteroscopy, gynaecological procedures)
  • Presentation: Fever, flank pain, urinary fistula, ileus post-surgery
  • Diagnosis: CT urogram; retrograde pyelography (most sensitive)
  • Management: Stable → direct surgical repair over ureteral stent; unstable → intraoperative tagging + nephrostomy + delayed repair

Bladder Trauma

  • 1–2% of blunt abdominal trauma; 83–95% associated with pelvic fractures
  • Gross haematuria present in 75–100% of cases
  • Types:
    • Extraperitoneal rupture (most common): Due to pelvic bone fragments; managed conservatively with catheter drainage (2–3 weeks)
    • Intraperitoneal rupture: Dome of bladder (weak point); due to blunt force on full bladder; requires surgical repair
  • Diagnosis: Retrograde cystography (CT cystogram) — gold standard; must fill bladder adequately (300–400 mL)

Urethral Trauma

  • Posterior urethral injury: Associated with pelvic fractures; disruption at the bulbomembranous junction
    • Presentation: Blood at urethral meatus, perineal bruising, inability to void, "high-riding" prostate on DRE
    • Do not attempt urethral catheterisation before imaging — risk of converting partial to complete tear
    • Management: Primary realignment over a catheter vs suprapubic cystostomy and delayed urethroplasty
  • Anterior urethral injury: Bulbar urethra most common; due to straddle injury
    • Urine/blood extravasates within Colles' fascia → butterfly-shaped perineal bruising
    • Management: Suprapubic catheter + delayed urethroplasty

Genital Trauma

  • Penile fracture: Rupture of tunica albuginea during erect penile trauma; "cracking sound" + immediate detumescence + haematoma; surgical emergency — immediate surgical repair
  • Testicular rupture: From direct blunt trauma; USS-guided; requires surgical exploration and repair (or orchiectomy if non-viable)
  • Scrotal avulsion injuries: Manage with debridement and closure; testicles remarkably resistant to infection
Sources: Sabiston Textbook of Surgery block 8; Campbell Walsh Wein Urology block 49

SECTION 13: TESTICULAR TUMOURS

Epidemiology

  • Most common solid malignancy in males aged 15–40 years
  • Bimodal distribution: ~2 years of age (yolk sac tumour) and puberty/young adulthood (seminoma/NSGCT)
  • Risk factors: Cryptorchidism (most important), testicular atrophy, Klinefelter syndrome, positive family history, contralateral GCT

Classification

Testicular Tumours
├── Germ Cell Tumours (>95%)
│   ├── Seminoma (~50%)
│   └── Non-seminomatous GCT (NSGCT) (~50%)
│       ├── Embryonal carcinoma
│       ├── Yolk sac tumour (endodermal sinus tumour)
│       ├── Choriocarcinoma
│       ├── Teratoma (mature, immature)
│       └── Mixed (most common NSGCT)
└── Non-Germ Cell (Stromal) Tumours (<5%)
    ├── Leydig cell tumour
    └── Sertoli cell tumour

Tumour Markers

MarkerElevated inNotes
AFP (α-fetoprotein)Yolk sac tumour, embryonal carcinoma, mixed GCTNOT elevated in pure seminoma or choriocarcinoma
β-hCGChoriocarcinoma, embryonal carcinoma; mildly in seminoma
LDHMarker of tumour bulk
PLAP (placental alkaline phosphatase)SeminomaLess clinically used
Key rule: Elevated AFP with a "seminoma" on histology → reclassify as NSGCT and treat accordingly.

Clinical Features

  • Painless scrotal mass — most common presentation; often discovered incidentally
  • Dull ache or heaviness in the scrotum
  • Approximately 10% present with acute pain (haemorrhage into tumour)
  • Gynaecomastia (in β-hCG-producing tumours)
  • Back/flank pain (retroperitoneal lymph node metastasis)

Diagnosis

  1. Scrotal USS with Doppler: First imaging; intratesticular solid hypoechoic mass = cancer until proved otherwise
  2. Tumour markers: AFP, β-hCG, LDH (before and after orchiectomy)
  3. CT chest/abdomen/pelvis: Staging for retroperitoneal lymphadenopathy and distant metastases
  4. Radical inguinal orchiectomy: Both diagnostic AND therapeutic — always inguinal approach (not scrotal, to avoid disturbing lymphatic drainage)

Staging

StageDescription
Stage IConfined to testis, no lymph node involvement, markers normalise post-orchiectomy
Stage IIRetroperitoneal lymph node involvement
Stage IIIDistant metastases (lung, liver, brain, bone) or persistent marker elevation

Seminoma — Treatment

StageTreatment
Stage ISurveillance (preferred) OR carboplatin x1 cycle OR para-aortic radiotherapy
Stage IIA/BRadiotherapy (para-aortic + ipsilateral iliac) OR BEP chemotherapy
Stage IIC/IIIBEP chemotherapy (bleomycin + etoposide + cisplatin)

NSGCT — Treatment

StageTreatment
Clinical Stage I, low riskSurveillance
Clinical Stage I, high risk (IVI or EC predominance)RPLND or 1×BEP
Stage II–IIIBEP chemotherapy ± RPLND for residual mass
Prognostic factors for CS I NSGCT (risk of occult metastasis ~20–30%):
  • Lymphovascular invasion (LVI): OR 5.2
  • Embryonal carcinoma predominance: OR 2.8
  • MIB-1 staining >70%: OR 4.7

5-Year Survival

  • Stage I: ~99%
  • Stage II: ~95%
  • Stage III: ~70–80% (with good-risk markers) → ~50% (poor-risk)
Sources: Sabiston Textbook of Surgery block 28 & 30; Campbell Walsh Wein Urology block 42; Schwartz's Principles of Surgery

SECTION 14: CANCER OF THE BLADDER

Epidemiology

  • 9th most common cancer worldwide; predominantly in men (M:F = 3–4:1)
  • Peak incidence 50–80 years
  • USA: ~90% urothelial carcinoma; ~5% squamous cell carcinoma (SCC); <2% adenocarcinoma

Risk Factors

  • Cigarette smoking (strongest risk factor; 2–4× increased risk; accounts for ~50%)
  • Aromatic amines / aniline dyes (occupational: rubber, paint, dye industries)
  • Cyclophosphamide chemotherapy (haemorrhagic cystitis + long-term malignancy risk)
  • Pelvic radiation
  • Chronic schistosomiasis (Schistosoma haematobium) → SCC (endemic in East Africa, Middle East)
  • Chronic indwelling catheters → SCC
  • Phenacetin abuse

Pathology

Urothelial (Transitional Cell) Carcinoma

Two distinct molecular pathways:
Pathway 1 — Papillary (low-grade) tumours:
  • FGFR3 mutations, RAS mutations, PI3K activation
  • Frequently recur but rarely invade muscle (~20%)
Pathway 2 — Carcinoma in Situ (CIS) → invasive:
  • TP53 and RB gene mutations
  • Flat lesion; high-grade; aggressive; progresses to muscle invasion

Morphological grades

  • Non-invasive (Ta/Tis): Papillary or flat, within urothelium
  • Invasive (T1–T4): Progressive muscular invasion

Clinical Features

  • Painless gross haematuria — cardinal symptom (>80%)
  • Irritative LUTS (urgency, frequency, dysuria) — especially with CIS
  • Advanced: Pelvic pain, ureteric obstruction, lower limb oedema

Investigations

  1. Urine cytology: High sensitivity for high-grade/CIS; low sensitivity for low-grade
  2. Cystoscopy: Gold standard; white light ± narrow-band imaging (NBI) or photodynamic diagnosis (PDD)
  3. TURBT (transurethral resection of bladder tumour): Diagnostic + therapeutic
  4. CT urogram: Upper tract evaluation + staging
  5. MRI (VIRADS system): Muscle invasion assessment

Staging (TNM)

StageDescription
TaNon-invasive papillary carcinoma
TisCarcinoma in situ (flat, high-grade)
T1Invasion of lamina propria (subepithelial connective tissue)
T2a/bSuperficial/deep muscle invasion
T3Perivesical fat invasion
T4Adjacent organ invasion (prostate, uterus, vagina, bowel)
Key clinical divide: Non-muscle-invasive (NMIBC: Ta, T1, Tis) vs muscle-invasive (MIBC: ≥T2)

Treatment

Non-Muscle Invasive Bladder Cancer (NMIBC)

  1. TURBT — complete resection; second-look TURBT for high-grade T1 tumours
  2. Intravesical therapy:
    • BCG (Bacillus Calmette-Guérin): Gold standard for high-risk NMIBC; immunotherapy; reduces recurrence and progression
    • Mitomycin C (MMC): Chemotherapy; single peri-operative instillation for low/intermediate risk
  3. Follow-up cystoscopy: Mandatory surveillance

Muscle-Invasive Bladder Cancer (MIBC)

  1. Neoadjuvant cisplatin-based chemotherapy (MVAC or GC) → then surgery (preferred)
  2. Radical cystectomy with urinary diversion:
    • Male: Removal of bladder, prostate, seminal vesicles
    • Female: Bladder, uterus, anterior vagina, urethra
    • Urinary diversion: Ileal conduit (urostomy), continent orthotopic neobladder (Studer), continent cutaneous reservoir
  3. Bladder-sparing trimodality therapy: TURBT + concurrent chemoradiation (for selected patients)

Metastatic Bladder Cancer

  • Platinum-based chemotherapy: MVAC (methotrexate + vinblastine + doxorubicin + cisplatin) or GC (gemcitabine + cisplatin)
  • Checkpoint inhibitors: Pembrolizumab, atezolizumab (PD-1/PD-L1)
  • Enfortumab vedotin + pembrolizumab: New standard first-line for platinum-ineligible patients
Sources: Robbins & Kumar Basic Pathology block 6; Campbell Walsh Wein Urology block 84; Smith & Tanagho's General Urology

QUICK REFERENCE SUMMARY TABLE

TopicKey Fact
Most common cause of gross haematuria in >50 yearsBladder cancer
Bell-clapper deformityCause of intravaginal testicular torsion in adolescents
Salvage rate with torsion <6 hours~90%
BPH pathogenesis key mediatorDHT via 5α-reductase
5α-RI effect on PSAReduces PSA by ~50%
TUR syndrome causeGlycine irrigation (dilutional hyponatraemia)
Most common site of urethral strictureBulbar urethra
RCC associated with VHL geneClear cell RCC
Classic RCC paraneoplasticPolycythaemia, hypercalcaemia, Stauffer syndrome
Most common renal trauma mechanismBlunt (~80%)
Extraperitoneal bladder rupture managementConservative (catheter drainage)
Intraperitoneal bladder rupture managementSurgical repair
Do not catheterise ifBlood at urethral meatus after pelvic trauma
Testicular cancer marker ruleElevated AFP = NOT pure seminoma
Risk of occult metastasis in CS I NSGCT20–30%
Strongest risk factor for bladder cancerCigarette smoking
BCG useHigh-risk non-muscle-invasive bladder cancer
Cryptorchidism complicationMalignancy (seminoma most common) + infertility
Orchidopexy ideal age6–18 months
ED as cardiovascular markerMay precede CAD by 3–5 years
PDE5 inhibitor contraindicationConcurrent nitrate use (severe hypotension)

*Sources: Campbell Walsh Wein Urology (9780323546423) | Sabiston Textbook of Surgery (9780443124341) | Schwartz's Principles of Surgery (9781259835346) | Robbins & Kumar Basic Pathology (9780323790185) | Robbins, Cotran & Kumar Pathologic Basis of Disease (9780443264528) | Smith & Tanagho's General Urology (9781259834332) | Mulholland & Greenfield's Surgery (9781975143169)*Your credits are exhausted. Your daily credits reset tomorrow, or you can purchase a top-up for more.
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