Fellowship of the Royal College of Surgeons (FRCS) Urology Syllabus

How does penile squamous cell carcinoma typically spread, and what is the significance of the inguinal lymph nodes?

It spreads via lymphatics first to the superficial and deep inguinal lymph nodes, then to pelvic nodes. Inguinal lymph node status is the single most important prognostic factor; palpable or high-risk nodes warrant inguinal lymphadenectomy.

State the chemical composition of the most common urinary tract stone and the urinary conditions that favour its formation.

Calcium oxalate is the most common stone (~70-80%). Formation is favoured by hypercalciuria, hyperoxaluria, hypocitraturia, and low urine volume. Calcium oxalate stones form across a wide pH range and are radio-opaque.

Which urinary stones are radiolucent on plain X-ray (KUB), and how are they best imaged?

Pure uric acid stones, xanthine stones, and indinavir (drug) stones are radiolucent on plain KUB. They are best visualised on non-contrast CT (CT-KUB) or ultrasound; uric acid stones are visible on CT despite being radiolucent on plain film.

Which stone type is associated with urease-producing organisms, and what is the classic stone morphology?

Struvite (magnesium ammonium phosphate) stones, also called infection/triple-phosphate stones, are associated with urease-producing organisms such as Proteus, Klebsiella, and Pseudomonas. They form in alkaline urine and classically produce large staghorn calculi.

How does urease promote struvite stone formation? Give the relevant chemical reaction.

Urease hydrolyses urea, raising urine pH and generating ammonium, which precipitates magnesium ammonium phosphate. The reaction is: $$\ce{CO(NH2)2 + 2H2O ->[urease] 2NH3 + CO2}$$ The ammonia raises pH ($\ce{NH3 + H2O -> NH4+ + OH-}$), promoting precipitation.

What metabolic abnormality causes cystine stones, and what is the characteristic crystal appearance?

Cystinuria, an autosomal recessive defect in renal tubular reabsorption of dibasic amino acids (COLA: cystine, ornithine, lysine, arginine), causes cystine stones. The characteristic crystals are hexagonal. Treatment includes hyperhydration, urinary alkalinisation, and thiol agents (e.g. penicillamine, tiopronin).

What is the imaging investigation of choice for acute renal/ureteric colic, and why?

Non-contrast CT of the kidneys, ureters and bladder (CT-KUB) is the gold standard. It is highly sensitive and specific, detects nearly all stone types (including radiolucent uric acid), provides stone size/location/density, and identifies alternative diagnoses, all without contrast.

What is the first-line analgesia for acute ureteric colic, and why is it preferred over opioids?

NSAIDs (e.g. intramuscular/PR diclofenac) are first-line because they reduce ureteric smooth muscle tone and glomerular afferent prostaglandin-mediated pressure, providing superior and more durable analgesia with less nausea than opioids. Opioids are used if NSAIDs are contraindicated.

What stone size threshold generally favours conservative management with likely spontaneous passage of a ureteric stone?

Stones $<5\ \text{mm}$ have a high likelihood (~70-90%) of spontaneous passage and are usually managed conservatively. Stones $>10\ \text{mm}$ rarely pass spontaneously and usually require intervention; 5-10 mm stones are intermediate, and medical expulsive therapy may be trialled.

What is medical expulsive therapy (MET) for ureteric stones, and which drug class is used?

MET uses an alpha-blocker (e.g. tamsulosin) to relax distal ureteric smooth muscle and facilitate passage of ureteric stones, particularly distal stones 5-10 mm. It is offered alongside analgesia during a trial of conservative management.

What are the indications for emergency/urgent intervention in a patient with an obstructing ureteric stone?

Infection proximal to an obstructing stone (obstructed infected system/pyonephrosis with sepsis), acute kidney injury, obstruction of a solitary or transplanted kidney, bilateral obstruction, and uncontrolled pain/vomiting. An infected obstructed system requires emergency decompression.

How is an obstructed, infected kidney (pyonephrosis) decompressed, and what is the management principle?

Emergency decompression by percutaneous nephrostomy or retrograde ureteric (JJ) stent, plus IV antibiotics and resuscitation. The principle is 'drain and treat sepsis first'; definitive stone treatment is deferred until the infection has resolved.

What are the main treatment modalities for surgical stone management, and what stone factors guide choice?

Extracorporeal shock wave lithotripsy (ESWL), ureteroscopy with laser lithotripsy (URS/RIRS), and percutaneous nephrolithotomy (PCNL). Choice depends on stone size, location, composition/density, and patient anatomy; PCNL is preferred for large (>2 cm) renal/staghorn stones.

What is the size threshold above which percutaneous nephrolithotomy (PCNL) is generally preferred over ESWL for renal stones?

PCNL is generally preferred for renal stones larger than $2\ \text{cm}$ (and for staghorn calculi and lower-pole stones >1.5 cm or hard stones), as it offers the highest stone-free rates for large stone burdens.

Name three contraindications to extracorporeal shock wave lithotripsy (ESWL).

Pregnancy, uncontrolled bleeding diathesis/anticoagulation, untreated urinary tract infection, distal obstruction below the stone, and abdominal aortic aneurysm. Hard stones (e.g. cystine, calcium oxalate monohydrate) and very large/dense stones respond poorly. Any three are acceptable.

Define obstructive uropathy and distinguish it from obstructive nephropathy.

Obstructive uropathy is structural or functional obstruction to urinary flow anywhere along the urinary tract, which may cause hydronephrosis. Obstructive nephropathy is the resulting parenchymal kidney damage/functional impairment caused by that obstruction.

What are the two main options for upper urinary tract drainage in obstruction, and how do you choose between them?

Retrograde ureteric (JJ) stent placed cystoscopically, or antegrade percutaneous nephrostomy. Nephrostomy is preferred in pyonephrosis/sepsis (better drainage, can be placed under local anaesthetic) and when retrograde access fails; stents are useful for longer-term internal drainage.

What is post-obstructive diuresis, and how should it be managed?

After relief of bilateral or solitary-kidney obstruction, a marked diuresis can occur due to retained solutes, tubular dysfunction, and accumulated fluid. Management is close monitoring of urine output, weight, and electrolytes, with judicious fluid/electrolyte replacement (typically replacing ~50-75% of losses) to avoid hypovolaemia and electrolyte disturbance.

What is the pathophysiology of benign prostatic enlargement causing lower urinary tract symptoms (LUTS)?

Age- and androgen (dihydrotestosterone)-driven hyperplasia of the transition zone causes a static component (mechanical obstruction by enlarged tissue) and a dynamic component (alpha-1 adrenergic smooth muscle tone in prostate/bladder neck), producing bladder outlet obstruction and secondary detrusor changes, leading to voiding and storage LUTS.

Contrast the two main drug classes for BPH/LUTS in terms of mechanism and onset of action.

Alpha-1 blockers (e.g. tamsulosin) relax prostatic/bladder neck smooth muscle (dynamic component) with rapid symptom relief within days. 5-alpha-reductase inhibitors (e.g. finasteride) block conversion of testosterone to dihydrotestosterone, shrinking the gland (static component) over months, and reduce the risk of retention/surgery in large glands.

What is the gold-standard surgical treatment for bladder outlet obstruction due to BPH, and name a serious metabolic complication of the traditional technique.

Transurethral resection of the prostate (TURP) is the gold standard. With monopolar TURP using hypotonic glycine irrigation, absorption can cause TUR syndrome (dilutional hyponatraemia, fluid overload, confusion, visual disturbance). Bipolar TURP uses normal saline and largely avoids this.

Classify urinary incontinence into its main types and give the defining feature of each.

Stress incontinence: leakage on raised intra-abdominal pressure (cough/exertion) due to sphincter/urethral support weakness. Urgency incontinence: leakage preceded by urgency, due to detrusor overactivity. Mixed: both. Overflow: leakage from chronic retention/bladder outlet obstruction. Continuous: usually fistula or ectopic ureter.

What is the role of urodynamics, and what does a cystometrogram measure?

Urodynamics objectively assesses bladder storage and voiding function before invasive treatment or in complex/refractory cases. Cystometry measures detrusor pressure (subtracting abdominal/rectal pressure from vesical pressure: $P_{det} = P_{ves} - P_{abd}$), bladder capacity, compliance, sensation, presence of detrusor overactivity, and the pressure-flow voiding relationship.

What is first-line management for stress urinary incontinence and for urgency (overactive bladder) incontinence?

Stress incontinence: pelvic floor muscle training (supervised, ≥3 months) first-line; surgery (e.g. colposuspension, autologous sling) if it fails. Urgency/OAB: bladder training plus lifestyle measures first-line; then antimuscarinics (e.g. solifenacin) or a beta-3 agonist (mirabegron).

What is a neurogenic bladder, and how do suprapontine/upper motor neuron lesions typically differ from lower motor neuron (sacral) lesions?

A neurogenic bladder is bladder dysfunction from neurological disease. Suprasacral/UMN lesions typically cause detrusor overactivity often with detrusor-sphincter dyssynergia (spastic, high-pressure, small-capacity bladder). Lower motor neuron/sacral (e.g. cauda equina) lesions cause an areflexic, flaccid bladder with retention and overflow.

Why is detrusor-sphincter dyssynergia in neurogenic bladder dangerous, and what is the management goal?

Simultaneous detrusor contraction against a closed external sphincter generates high intravesical storage/voiding pressures, risking vesicoureteric reflux, hydronephrosis, and renal failure. The management goal is to maintain low-pressure storage and complete emptying, often using clean intermittent self-catheterisation plus antimuscarinics/botulinum toxin.

What is the first-line oral drug class for erectile dysfunction, its mechanism, and a key contraindication?

Phosphodiesterase-5 (PDE-5) inhibitors (e.g. sildenafil, tadalafil) are first-line. They inhibit PDE-5, increasing cyclic GMP and prolonging nitric oxide-mediated cavernosal smooth muscle relaxation and penile blood flow. They are contraindicated with nitrates (risk of profound hypotension).

What is the underlying mechanism of an erection, and which vascular and neural elements mediate it?

Parasympathetic (S2-S4, nervi erigentes) release of nitric oxide raises cavernosal cyclic GMP, relaxing smooth muscle and increasing arterial inflow; engorgement of the corpora compresses subtunical venules (veno-occlusive mechanism), trapping blood. Erectile dysfunction is most commonly of vascular (endothelial) origin and is a marker of cardiovascular disease.

Define acute urinary retention and contrast it with chronic retention in terms of presentation.

Acute urinary retention is the sudden, painful inability to pass urine with a palpable, tender, distended bladder, relieved by catheterisation. Chronic retention is gradual, typically painless with a large-capacity bladder, often presenting with overflow incontinence and a risk of high-pressure retention causing hydronephrosis and renal impairment.

What is high-pressure chronic urinary retention, and why must it be recognised?

It is chronic retention with raised intravesical pressure causing bilateral hydronephrosis and obstructive (post-renal) acute-on-chronic kidney injury, often with nocturnal enuresis. It must be recognised because catheterisation can precipitate marked post-obstructive diuresis and decompression haematuria, requiring fluid monitoring and admission.

Describe the grading system for blunt renal trauma and the general management principle.

The AAST renal injury scale grades I-V (I = contusion/subcapsular haematoma; V = shattered kidney or renal pedicle avulsion). Most blunt renal injuries (grades I-III, and many IV) are managed non-operatively/conservatively in haemodynamically stable patients; haemodynamic instability or expanding/pulsatile haematoma is the main indication for renal exploration.

In suspected urethral injury (e.g. pelvic fracture), what clinical signs should prompt urethrography before catheterisation, and why?

Blood at the urethral meatus, a high-riding/non-palpable prostate, perineal/scrotal bruising, and inability to void should prompt retrograde urethrography. Blind urethral catheterisation is avoided as it may convert a partial urethral tear into a complete disruption.

What is the classic mechanism and the imaging investigation of choice for bladder rupture, and how do intra- vs extraperitoneal ruptures differ in management?

Bladder rupture follows blunt trauma to a full bladder or pelvic fracture; CT cystography (or retrograde cystography) is the investigation of choice. Extraperitoneal rupture is usually managed conservatively with catheter drainage; intraperitoneal rupture requires surgical repair.

What is testicular torsion, what is the typical age peak, and the critical time window for salvage?

Testicular torsion is twisting of the spermatic cord causing testicular ischaemia, classically due to a 'bell-clapper' deformity. The peak incidence is in adolescence (around puberty). It is a surgical emergency; testicular salvage rates are high if detorsion occurs within $6\ \text{hours}$ and fall rapidly thereafter.

What clinical signs help distinguish testicular torsion from epididymo-orchitis?

Torsion: sudden severe pain, high-riding testis with a horizontal lie, absent cremasteric reflex, and pain NOT relieved by elevation (negative Prehn sign). Epididymo-orchitis: more gradual onset, present cremasteric reflex, and pain relieved by elevation (positive Prehn sign). When torsion is suspected, urgent scrotal exploration is mandatory and should not be delayed for imaging.

What is the surgical management of confirmed testicular torsion?

Emergency scrotal exploration with detorsion and bilateral orchidopexy (fixation) — the contralateral testis is also fixed because the predisposing bell-clapper deformity is usually bilateral. A non-viable testis is removed (orchidectomy).

List the differential diagnoses of the acute scrotum and the must-not-miss diagnosis.

Testicular torsion (must-not-miss), torsion of a testicular/epididymal appendage (appendix testis — 'blue dot sign'), epididymo-orchitis, incarcerated/strangulated inguinal hernia, idiopathic scrotal oedema, trauma/haematocele, and Fournier gangrene. Torsion must be excluded first.

What is Fournier gangrene, and what is its management?

Fournier gangrene is a rapidly progressive necrotising fasciitis of the perineal, genital, and perianal regions, often polymicrobial, more common in diabetics and the immunocompromised. Management is urgent aggressive surgical debridement, broad-spectrum IV antibiotics, and resuscitation; it carries a high mortality.

What is the most common uropathogen causing uncomplicated urinary tract infection, and what defines a complicated UTI?

Escherichia coli causes ~75-85% of uncomplicated UTIs. A complicated UTI occurs with a functional/structural abnormality (obstruction, stones, catheter, neurogenic bladder), in men, pregnancy, immunocompromise, or when involving the upper tract (pyelonephritis), and carries a higher risk of treatment failure and sepsis.

Define urosepsis and outline its initial management priorities.

Urosepsis is sepsis (life-threatening organ dysfunction from a dysregulated host response to infection) arising from a urinary tract source. Initial management follows the Sepsis Six: take blood cultures, lactate, and urine output monitoring; give oxygen, IV broad-spectrum antibiotics, and IV fluids. Crucially, any obstructed/infected system must be urgently decompressed (source control).

In urinary tract infection, distinguish asymptomatic bacteriuria from a symptomatic UTI, and when should asymptomatic bacteriuria be treated?

Asymptomatic bacteriuria is significant bacteriuria without urinary symptoms; symptomatic UTI requires symptoms (dysuria, frequency, loin pain, etc.) plus bacteriuria. Asymptomatic bacteriuria is generally NOT treated except in pregnancy and before urological procedures that breach the mucosa, where treatment reduces complications.

Define visible (macroscopic) and non-visible (microscopic) haematuria, and what threshold defines significant non-visible haematuria on dipstick?

Visible haematuria is blood visible to the naked eye in urine. Non-visible haematuria is detected only on testing; significant non-visible haematuria is generally ≥1+ blood on urine dipstick (after excluding transient causes such as UTI, menstruation, and vigorous exercise). Both warrant assessment to exclude malignancy.

Outline the standard investigation pathway for a patient with painless visible haematuria.

Urgent (2-week-wait) referral for urological assessment comprising: flexible cystoscopy to evaluate the bladder/urethra, and upper tract imaging — CT urogram is the investigation of choice for visible haematuria (ultrasound for non-visible). Urine cytology may supplement assessment. Painless visible haematuria is bladder cancer until proven otherwise.

What features distinguish a glomerular (nephrological) cause of haematuria from a urological cause?

Glomerular haematuria suggests dysmorphic red cells, red cell casts, significant proteinuria, hypertension, and impaired renal function, prompting nephrology referral. Urological haematuria typically has isomorphic red cells, may produce clots, and lacks casts/significant proteinuria, prompting cystoscopy and upper tract imaging.