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

Urology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Urology in Fellowship of the Royal College of Surgeons (FRCS), not a summary of it.

1. 1

   Urological Oncology

   5 topics

   • Renal cell carcinoma
     • Staging and nephron-sparing surgery
   • Urothelial cancer of bladder and upper tract
     • Non-muscle invasive bladder cancer
     • Muscle-invasive disease and cystectomy
   • Prostate cancer
     • PSA, screening and diagnosis
     • Active surveillance and radical treatment
   • Testicular cancer
   • Penile cancer
2. 2

   Stone Disease and Endourology

   4 topics

   • Urolithiasis pathophysiology and metabolic work-up
   • Management of ureteric colic
   • Surgical stone treatment
     • Ureteroscopy and lithotripsy
     • Percutaneous nephrolithotomy
   • Obstructive uropathy and drainage
3. 3

   Benign and Functional Urology

   4 topics

   • Benign prostatic enlargement and LUTS
     • Medical management
     • Surgical options including TURP
   • Urinary incontinence and urodynamics
   • Neurogenic bladder
   • Erectile dysfunction and andrology
4. 4

   Emergency and Reconstructive Urology

   5 topics

   • Acute urinary retention
   • Urological trauma
     • Renal and bladder injury
     • Urethral injury
   • Testicular torsion and the acute scrotum
   • Urinary tract infection and urosepsis
   • Haematuria assessment

Urology flashcards for Fellowship of the Royal College of Surgeons (FRCS)

24 of 64 cards from the Urology deck — real questions with worked answers.

1. What is the most common histological subtype of renal cell carcinoma (RCC), and which genetic alteration is characteristically associated with it?

   Clear cell RCC is the most common subtype (~75-80%). It is characteristically associated with loss/mutation of the VHL (von Hippel-Lindau) tumour suppressor gene on chromosome 3p, leading to HIF accumulation and upregulation of VEGF.

2. What is the classic triad of renal cell carcinoma, and how often does it present?

   The classic triad is flank pain, a palpable abdominal mass, and visible (gross) haematuria. It occurs in only about 10% of patients and usually signifies advanced disease; most RCCs today are detected incidentally on imaging.

3. Name three paraneoplastic syndromes associated with renal cell carcinoma.

   Hypercalcaemia (PTHrP), polycythaemia (ectopic erythropoietin), hypertension (renin), Stauffer syndrome (non-metastatic hepatic dysfunction), and hypercortisolism/Cushing-like states. Any three are acceptable.

4. What is the standard surgical management for a small (T1a, <4 cm) renal cell carcinoma confined to the kidney?

   Partial nephrectomy (nephron-sparing surgery) is the preferred standard for T1a tumours, preserving renal function while achieving oncological control. Radical nephrectomy is reserved for larger or more complex tumours.

5. In RCC, which structure does tumour characteristically invade to form a tumour thrombus, and why is this surgically important?

   RCC characteristically invades the renal vein and may extend as a tumour thrombus up the inferior vena cava (IVC), potentially reaching the right atrium. Its level (Mayo/Neves classification) dictates the surgical approach and the need for vascular/cardiac involvement.

6. What is the most common type of urothelial cancer of the bladder, and what is the strongest modifiable risk factor?

   Urothelial (transitional cell) carcinoma is the most common type (~90% in the West). Cigarette smoking is the strongest modifiable risk factor; occupational exposure to aromatic amines (beta-naphthylamine, benzidine) is also important.

7. How are bladder urothelial carcinomas divided by depth of invasion, and what is the key staging cut-off?

   They are divided into non-muscle-invasive bladder cancer (NMIBC: Ta, T1, and Tis/CIS) and muscle-invasive bladder cancer (MIBC: T2 and above). Invasion of the detrusor muscle (T2) is the critical cut-off separating the two groups and dictating radical treatment.

8. What is the standard initial treatment for non-muscle-invasive bladder cancer, and what adjuvant intravesical therapies are used?

   Transurethral resection of bladder tumour (TURBT) is the standard initial treatment. Adjuvant intravesical therapy includes a single immediate dose of mitomycin C for low-risk disease, and intravesical BCG immunotherapy for high-risk NMIBC and CIS.

9. What is the gold-standard treatment for muscle-invasive bladder cancer (T2-T4a, N0, M0)?

   Neoadjuvant cisplatin-based combination chemotherapy followed by radical cystectomy with pelvic lymph node dissection and urinary diversion (e.g. ileal conduit or neobladder). Radical radiotherapy with a radiosensitiser is the main bladder-preserving alternative.

10. What syndrome predisposes to upper tract urothelial carcinoma, and on which side of the GI/renal axis does it commonly cluster?

    Lynch syndrome (hereditary non-polyposis colorectal cancer, HNPCC) due to DNA mismatch repair gene mutations predisposes to upper tract urothelial carcinoma of the renal pelvis and ureter. Standard treatment for unifocal upper tract disease is radical nephroureterectomy with a bladder cuff.

11. Which zone of the prostate gives rise to most prostate cancers, and which zone is responsible for benign prostatic enlargement?

    About 70-75% of prostate cancers arise in the peripheral zone (palpable on DRE). Benign prostatic enlargement arises predominantly from the transition zone surrounding the urethra.

12. What is the Gleason grading system, and how does the ISUP Grade Group correspond to Gleason scores?

    Gleason grading assigns 1-5 to the two most prevalent architectural patterns; the two are summed. ISUP Grade Groups: GG1 = Gleason ≤6; GG2 = 3+4=7; GG3 = 4+3=7; GG4 = 8; GG5 = 9-10. Higher grade groups indicate more aggressive disease.

13. What is the PSA, and what is the conventional upper limit of normal often quoted for screening?

    PSA (prostate-specific antigen) is a serine protease/glycoprotein produced by prostatic epithelium. A commonly quoted threshold is $\text{PSA} > 4\ \text{ng/mL}$, though age-specific ranges, free/total ratio, and PSA density refine interpretation. It is organ-specific but not cancer-specific.

14. What imaging is now recommended before prostate biopsy, and how are its findings scored?

    Multiparametric MRI (mpMRI) of the prostate is recommended before biopsy. Lesions are scored using PI-RADS (Prostate Imaging Reporting and Data System) v2.1 from 1 to 5, where higher scores indicate greater likelihood of clinically significant cancer and direct targeted biopsy.

15. What is the mechanism of action of GnRH (LHRH) agonists in prostate cancer, and what important early adverse effect must be prevented?

    GnRH agonists cause continuous (non-pulsatile) GnRH receptor stimulation, leading to downregulation and suppression of LH and testosterone (medical castration). Initially they cause a testosterone 'flare'; an anti-androgen is co-administered to prevent flare-related tumour progression/spinal cord compression.

16. What are the two most common histological types of testicular germ cell tumours, and how do their tumour markers differ?

    Seminoma and non-seminomatous germ cell tumours (NSGCT). Seminomas may mildly raise hCG but never raise AFP. NSGCTs (e.g. yolk sac, choriocarcinoma, teratoma, embryonal) can raise AFP and/or hCG. A raised AFP indicates non-seminomatous elements.

17. List the three serum tumour markers used in testicular cancer and their associated tumour types.

    AFP (alpha-fetoprotein) — yolk sac tumour, embryonal (never pure seminoma); beta-hCG — choriocarcinoma, embryonal, and some seminomas; LDH — reflects tumour bulk/turnover. They are used for diagnosis, staging (S category), and monitoring response.

18. What is the correct surgical approach for a suspected testicular tumour, and what approach must be avoided?

    Radical inguinal orchidectomy with high ligation of the spermatic cord is the standard. A trans-scrotal approach/biopsy must be avoided because it risks altering lymphatic drainage and causing scrotal/inguinal tumour seeding.

19. What is the primary lymphatic drainage of the testis, and why is this clinically relevant?

    The testis drains to the para-aortic (retroperitoneal) lymph nodes at the level of the renal hila, following its embryological origin. The scrotal skin drains to inguinal nodes. This is why testicular cancer metastasises first to retroperitoneal nodes, not inguinal nodes.

20. What is the most common histological type of penile cancer, and which infection is a major risk factor?

    Squamous cell carcinoma is the most common penile cancer (~95%). Human papillomavirus (HPV) infection, particularly types 16 and 18, is a major risk factor; phimosis, chronic inflammation, smoking, and lack of circumcision also contribute.

21. 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.

22. 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.

23. 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.

24. 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.

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