GC183 Common Urological Malignancies And Their Presentations - Nov 7
Common urological malignancies—including renal cell carcinoma, bladder cancer, prostate cancer, and testicular cancer—are neoplasms of the genitourinary tract that typically present with hematuria, pelvic symptoms, lower urinary tract obstruction, or scrotal masses depending on the site of origin.
Common Urological Malignancies and Their Presentations
This lecture by Dr. CF Tsang (Consultant Urologist, QMH) covers the major urological cancers — renal cell carcinoma (RCC), bladder cancer, upper tract transitional cell carcinoma (TCC), and prostate cancer — unified by the presenting symptom of hematuria and the investigation pathway that follows. The lecture also addresses PSA as a screening and diagnostic tool for prostate cancer. [1]
The Big Idea: A patient walks in with blood in the urine. Your job is to (1) confirm it's real hematuria, (2) figure out where it's coming from (kidney → ureter → bladder → prostate → urethra), (3) determine whether it's benign or malignant, and (4) stage and manage accordingly. The unifying clinical axiom from this lecture is:
Painless gross hematuria = MALIGNANCY UNTIL PROVEN OTHERWISE [1]
Learning Objectives:
- Understand the approach to hematuria (visible vs. non-visible, painful vs. painless)
- Recognize conditions that mimic hematuria
- Know the causes of hematuria by anatomical site
- Understand the risk factors, pathology, staging, and treatment of RCC, bladder cancer, upper tract TCC, and prostate cancer
- Master PSA interpretation including ways to improve specificity
- Understand the Gleason grading system and prostate cancer risk groups
1. Hematuria — The Cardinal Presenting Symptom
Gross hematuria / visible hematuria — blood visible to the naked eye [1] Microscopic hematuria / non-visible hematuria — ≥ 3 RBC per high power field on urine microscopy [1]
Why these definitions matter: The distinction drives urgency. Gross painless hematuria demands urgent cancer workup. Microscopic hematuria has only a 1–3% risk of malignancy but still needs systematic evaluation, especially in patients with risk factors. [1]
Painless gross hematuria = MALIGNANCY UNTIL PROVEN OTHERWISE [1]
Painful gross hematuria → think infection [1]
Why? Malignant tumors bleed because they have friable, abnormal blood vessels that erode into the urinary tract lumen. These tumors typically don't cause pain until they invade surrounding structures or cause obstruction. Infections, on the other hand, cause mucosal inflammation → pain + hematuria together.
| Condition | Mechanism |
|---|---|
| Menstrual blood contamination | Female patients — always ask about timing relative to menses |
| Myoglobinuria / hemoglobinuria | Rhabdomyolysis / hemolysis — dipstick positive for "blood" but no RBCs on microscopy |
| Betanin (beetroot) | Food pigment turns urine red/pink |
| Rifampicin / Pyridium | Drug-induced urine discoloration (rifampicin → orange-red; pyridium → orange) |
Dipstick vs. Microscopy
Dipstick hematuria ≠ microscopic hematuria. All dipstick hematuria requires urine microscopy for confirmation. 20–70% of dipstick-positive urine has normal microscopic examination. [1] This is a common exam trap — the dipstick detects the peroxidase activity of hemoglobin (also triggered by myoglobin), so it gives false positives.
- ≥ 3 RBC per high power field on microscopy [1]
- Present in 2–30% of healthy people [1]
- Risk of malignancy: only 1–3% [1]
- Always confirm dipstick with formal microscopy
Risk-stratified evaluation (from the lecture algorithm slide): microscopic hematuria is not a single “always cystoscopy” rule. Intensity of workup scales with age/sex, smoking pack-years, degree of microscopic hematuria, prior gross hematuria, and other urothelial-cancer risk factors. [1]
| Risk band | Typical criteria on the slide | Initial pathway |
|---|---|---|
| Low / negligible | Women < 60 and men < 40; never-smoker or < 10 pack-years; 3–10 RBC/HPF on one UA; no additional urothelial risk factors | Repeat UA within 6 months |
| Intermediate | Women ≥ 60 or men 40–59; 10–30 pack-years; 11–25 RBC/HPF; ≥1 additional risk factor; or previously low-risk with persistent 3–25 RBC/HPF on repeat UA | Cystoscopy + renal US; urine cytology / validated urinary biomarkers may help decide about cystoscopy; if cystoscopy deferred, repeat UA within 12 months |
| High | Men ≥ 60 (women not high-risk by age alone); > 30 pack-years; > 25 RBC/HPF; history of gross hematuria; or additional risk factors plus a high-risk feature | Cystoscopy + axial upper-tract imaging |
Treat the table as the lecture's teaching scaffold for triage intensity — local pathways and full guideline footnotes still matter for edge cases. Gross painless hematuria remains a separate, urgent malignancy rule and is not downgraded by this microscopic algorithm. [1]
Hallmarks of nephrological causes of microscopic hematuria: [1]
- RBC casts — RBCs extravasated into the tubular lumen get trapped within solidified Tamm-Horsfall protein matrix
- Dysmorphic RBCs — RBCs with irregular shape and contours from passage through the defective glomerular basement membrane + osmotic injury in tubules
- Proteinuria
Nephrological causes: IgA nephropathy, Alport's syndrome, acute nephritic syndrome, Henoch-Schönlein purpura [1] [2]
Why this matters clinically: If you see dysmorphic RBCs + casts + proteinuria → this is a medical kidney problem, not a surgical one. Refer to nephrology, not urology. If RBCs are isomorphic (normal shape) without casts or proteinuria → urological workup needed.
| Site | Benign Causes | Malignant Causes |
|---|---|---|
| Kidney | Stone, AML, infection, trauma, polycystic kidney, nephrological/medical causes | Renal cell carcinoma |
| Ureter | Stone | TCC |
| Bladder | Infection, stone, irradiation cystitis | Bladder cancer |
| Prostate | BPH | Prostate cancer |
| Urethra | Infection | Urethral cancer |
Key history points: [1]
- Painless vs. painful — painless = malignancy until proven otherwise
- Exclude mimics — menstruation, drugs, foods, myoglobinuria
- Timing — early/whole/end stream (though unreliable in predicting location)
- Blood clots — presence suggests severe bleeding; may cause clot retention
- Associated symptoms — loin pain, fever, stone passage, constitutional symptoms (weight loss, appetite loss, night sweats)
- Risk factors for malignancy — smoking, occupation, chemical exposure, family history
- Drugs — antiplatelets, anticoagulants
Timing of Hematuria
Traditional teaching suggests initial hematuria = urethral, terminal = bladder neck/prostate, total = kidney/ureter/bladder. However, the lecture explicitly states timing is unreliable in predicting location [1]. Don't hang your diagnosis on this alone.
Three key components: [1]
- General examination — signs of anemia (pallor, tachycardia), cachexia (muscle wasting, temporal wasting)
- Abdominal examination — ballotable kidney (RCC), palpable pelvic mass (advanced bladder cancer)
- External genitalia + Digital rectal examination (DRE) — prostate assessment (size, consistency, nodularity, median groove, tenderness)
5. Investigations for Hematuria
- CBC — anemia from chronic bleeding or bone marrow infiltration
- RFT — renal function, especially if considering CT contrast [1]
| Test | Purpose |
|---|---|
| MSU C/ST | Rule out UTI |
| EMU for AFB smear and culture | Rule out renal/urinary TB |
| Fresh urine for cytology | Detect shed malignant urothelial cells (high specificity, low sensitivity for low-grade tumors; better for high-grade/CIS) |
| Modality | Pros | Cons |
|---|---|---|
| USG urinary system | Highly sensitive for renal mass; no radiation or contrast risk | Not sensitive for upper tract TCC or ureteric visualization |
| CT urogram (CTU) | Highly sensitive for renal mass AND upper tract TCC/ureteric tumors; arterial + venous + delayed urogram phases | Radiation and contrast risk |
| MR urogram | Similar sensitivity to CTU; no radiation | Higher cost; reserved for patients contraindicated for CT (e.g., pregnant patients) |
- Flexible cystoscopy — direct visualization of the bladder mucosa; gold standard for detecting bladder tumors [1]
6. Renal Cell Carcinoma (RCC)
Risk factors for RCC: [1]
- Smoking
- Obesity
- Hypertension
- Genetic predisposition: Family history and inherited syndromes — von Hippel-Lindau (VHL), Birt-Hogg-Dubé, hereditary papillary RCC, tuberous sclerosis
- Chronic kidney disease and acquired cystic kidney disease
Why VHL is high-yield: VHL is an autosomal dominant syndrome caused by mutation in the VHL tumor suppressor gene on chromosome 3p. The VHL protein normally targets HIF (hypoxia-inducible factor) for degradation. When VHL is lost → HIF accumulates → upregulation of VEGF, PDGF, and other growth factors → angiogenesis and tumor growth. This is why RCC in VHL is highly vascular and why anti-VEGF agents work in RCC treatment.
Presentations of RCC: [1]
- Incidental finding on imaging — most common presentation in modern practice
- Classic triad (rare): loin pain + hematuria + palpable abdominal mass
- Paraneoplastic syndromes:
- Hypercalcemia — most common paraneoplastic syndrome in RCC; caused by tumor secretion of PTHrP (parathyroid hormone-related protein)
- Polycythemia — ectopic production of erythropoietin
- Hypertension — ectopic renin secretion
- Fever, weight loss, cachexia — cytokine-mediated
- Nonmetastatic hepatic dysfunction (Stauffer's syndrome) — reversible hepatic dysfunction without liver metastases
- Venous thrombus: lower limb edema, left-side varicocele
Left-Side Varicocele — Must Know!
In men with new onset left-side varicocele, USG/CT is MANDATORY to rule out left RCC with tumor thrombus. [1]
Why left side specifically? The left testicular vein drains into the left renal vein (unlike the right, which drains directly into the IVC). A left RCC can invade the left renal vein → obstruct outflow of the left testicular vein → left varicocele. A new left varicocele that doesn't decompress when supine is a red flag for RCC.
What the venous-drainage diagram shows: right testicular vein → IVC; left testicular vein → left renal vein, with a dilated left pampiniform plexus labelled varicocele — the asymmetry of drainage is the entire clinical pearl. [1]
Understanding Stauffer's Syndrome: This is a paraneoplastic phenomenon where the liver shows cholestatic dysfunction (elevated ALP, bilirubin, transaminases) but has no metastatic deposits. The mechanism involves cytokine production (likely IL-6) by the tumor. It resolves after nephrectomy. [4]
| Subtype | Approx. incidence | Origin / key features (lecture table) |
|---|---|---|
| Clear cell RCC (ccRCC) | ~75% | Proximal tubule; clear cytoplasm (lipid/glycogen); VHL; most common / aggressive behaviour relative to indolent subtypes |
| Papillary RCC (pRCC) | ~15% | Distal tubule; classical Type 1 (often MET) vs Type 2 (larger eosinophilic cells, worse prognosis); WHO labels continue to evolve |
| Chromophobe RCC | ~5% | Distal intercalated cells; pale eosinophilic cytoplasm, prominent membranes; better prognosis than ccRCC |
| Collecting duct carcinoma | ~1% | Collecting ducts; rare, aggressive, poor prognosis |
| T Stage | Description |
|---|---|
| T1 | Tumor confined to kidney, ≤ 7 cm |
| T1a | ≤ 4 cm |
| T1b | > 4 cm and ≤ 7 cm |
| T2 | Tumor > 7 cm but still confined to kidney |
| T2a | > 7 to ≤ 10 cm |
| T2b | > 10 cm |
| T3 | Extends beyond kidney but NOT beyond Gerota's fascia |
| T3a | Invades renal vein or segmental branches, or perinephric/renal sinus fat, but not beyond Gerota's |
| T3b | Tumor extends into vena cava BELOW diaphragm |
| T3c | Tumor extends into vena cava ABOVE diaphragm or invades vena cava wall |
| T4 | Invades beyond Gerota's fascia, including contiguous spread to ipsilateral adrenal gland |
Why Gerota's fascia is important: Gerota's fascia is the fibrous layer that encapsulates the kidney and perinephric fat. As long as the tumor stays within Gerota's, it's still T3 (not T4). Once it breaches Gerota's → T4.
Why T3b/T3c matter: RCC has a notorious tendency to grow into the renal vein and IVC as a "tumor thrombus." This can extend all the way up to the right atrium (T3c). Remarkably, even with IVC involvement, patients can still be cured with radical nephrectomy + thrombectomy, sometimes requiring cardiopulmonary bypass.
| Setting | Treatment |
|---|---|
| T1 | Partial nephrectomy (nephron-sparing); alternatives: cryotherapy / RFA / watchful waiting for frail patients |
| T2 | Laparoscopic / open radical nephrectomy |
| T3 | Radical nephrectomy + thrombectomy |
| T4 | Radical nephrectomy ± adrenalectomy |
| Metastatic RCC | Immunotherapy: checkpoint inhibitors (pembrolizumab, nivolumab, ipilimumab) |
| Targeted therapy: TKIs (sunitinib, pazopanib), anti-VEGF (bevacizumab) | |
| Combination therapies |
Why partial nephrectomy for T1? Preserving nephrons is critical for long-term renal function. Studies show equivalent oncological outcomes for T1 tumors with partial vs. radical nephrectomy, but better renal function preservation → lower cardiovascular mortality long-term.
Why immunotherapy works in RCC: RCC is classically considered one of the most immunogenic solid tumors. Traditional chemotherapy has poor efficacy. The VHL/HIF pathway creates a highly vascular, inflamed tumor microenvironment that responds well to checkpoint blockade.
7. Bladder Cancer
Risk factors for bladder cancer: [1]
- Smoking — most important risk factor
- Occupational exposure: aromatic amines and chemicals in dye, rubber, leather, textile, and paint industries
- Chronic bladder irritation and infections: long-term catheter use and infections → SCC
- Schistosomiasis infection in endemic areas → SCC
Why schistosomiasis causes SCC (not TCC): S. haematobium eggs deposit in the bladder wall → chronic granulomatous inflammation → squamous metaplasia of the urothelium → SCC. This is important because in Western countries, 90% of bladder cancers are urothelial (TCC), but in schistosomiasis-endemic areas (e.g., Egypt), SCC predominates.
Bladder cancer symptoms: [1]
- Hematuria — most common presentation
- Lower urinary tract symptoms — frequency, urgency (irritative LUTS, especially with CIS)
- Pain — lower abdominal or pelvic (advanced disease)
- Constitutional symptoms — weight loss, fatigue (advanced/metastatic)
| Type | Frequency | Notes |
|---|---|---|
| Urothelial carcinoma (TCC) | ~90% | Most common type |
| Squamous cell carcinoma | ~3-5% | A/w chronic irritation, schistosomiasis; late presentation, poor prognosis |
| Adenocarcinoma | Rare | May arise from urachal remnant |
| Small cell carcinoma | Rare | Very aggressive |
| Sarcomatoid carcinoma | Rare | Aggressive, poor prognosis |
| T Stage | Description |
|---|---|
| Ta | Non-invasive papillary carcinoma — no invasion of lamina propria |
| Tis (CIS) | Flat, high-grade lesion — confined to urothelium |
| T1 | Invades lamina propria but NOT muscle |
| T2 | Invades muscularis propria |
| T2a | Superficial muscle (inner half) |
| T2b | Deep muscle (outer half) |
| T3 | Invades perivesical fat |
| T3a | Microscopic invasion |
| T3b | Macroscopic invasion |
| T4 | Invades surrounding organs |
| T4a | Prostate, uterus, or vagina |
| T4b | Pelvic wall or abdominal wall |
NMIBC vs. MIBC — The Critical Distinction
Non-muscle-invasive bladder cancer (NMIBC) = Ta, Tis, T1 — the cancer has NOT reached the detrusor muscle (muscularis propria). Management is endoscopic (TURBT) + intravesical therapy.
Muscle-invasive bladder cancer (MIBC) = ≥ T2 — the cancer HAS invaded the detrusor muscle. Management is radical cystectomy ± neoadjuvant chemotherapy.
This staging distinction completely changes the treatment paradigm. That's why the staging TURBT must include detrusor muscle in the specimen — otherwise you cannot accurately stage. [1]
WHO 2004 Classification: [1]
- PUNLMP — Papillary urothelial neoplasm of low malignant potential (very slow growing)
- Low-grade papillary urothelial carcinoma
- High-grade papillary urothelial carcinoma
Clinical Significance: [1]
- Low-grade tumors tend to recur but rarely progress to muscle invasion
- High-grade tumors and CIS have a higher risk of progression and metastasis
7.6 Treatment
Staging TURBT (transurethral resection of bladder tumor) + immediate post-op instillation of mitomycin C [1]
- Mitomycin C given within 24 hours post-TURBT to reduce tumor cell implantation and recurrence
Why immediate mitomycin C? During TURBT, viable tumor cells are shed into the bladder and can implant on the denuded urothelium. A single immediate dose of intravesical mitomycin C (a chemotherapy agent) kills these floating cells before they can implant. This reduces recurrence by ~40%.
Performed 4–6 weeks after initial staging TURBT [1] Indications:
- High-grade / CIS — significant risk of upstaging (i.e., the initial TURBT may have under-sampled, and the true stage is worse)
- Absence of detrusor muscle in initial TURBT specimen — without muscle in the specimen, you cannot rule out T2 disease
- Incomplete initial resection
Why BCG (Bacillus Calmette-Guérin)? BCG is a live attenuated strain of Mycobacterium bovis. When instilled into the bladder, it triggers a robust local immune response (T-cell mediated) that attacks residual cancer cells. BCG is one of the oldest and most effective forms of cancer immunotherapy.
Why neoadjuvant (before surgery)? Giving cisplatin-based chemotherapy before cystectomy has a proven survival benefit (~5% absolute improvement in 5-year survival). The tumor is still in place, has intact blood supply → better drug delivery. Also allows pathological assessment of chemosensitivity.
8. Upper Tract TCC
Upper tract TCC refers to urothelial carcinoma arising in the renal pelvis or ureter. It's the same cell type as bladder cancer (urothelial/transitional cell) — the entire urothelium from renal pelvis to bladder is a single "field" at risk.
Upper tract TCC symptoms: [1]
- Hematuria
- Loin pain
- Constitutional symptoms
Why you need cystoscopy too: Because the entire urothelium shares the same carcinogen exposure (field change), patients with upper tract TCC have a 15–50% risk of concurrent or subsequent bladder cancer. You must always check the bladder.
| T Stage | Description |
|---|---|
| Ta | Noninvasive papillary, confined to urothelium |
| Tis | Flat high-grade CIS |
| T1 | Invades subepithelial connective tissue (lamina propria) |
| T2 | Invades muscularis |
| T3 | Invades beyond muscularis — into peripelvic fat/renal parenchyma (pelvis) or periureteric fat (ureter) |
| T4 | Invades adjacent organs, pelvic/abdominal wall, or through kidney into perinephric fat |
Localized disease: [1]
- Radical nephroureterectomy (RNU) with bladder cuff excision
- + Adjuvant platinum-based chemotherapy (gemcitabine + cisplatin or carboplatin) for high-risk UTUC
Metastatic disease: [1]
- Checkpoint inhibitors (pembrolizumab, nivolumab)
- Enfortumab vedotin + pembrolizumab
Why remove the entire ureter + bladder cuff? Field change concept — the urothelium of the ureter is at risk of harboring disease. Leaving the ureteral stump risks tumor implantation and recurrence at the stump.
9. Prostate Cancer
Prostate cancer presentations: [1]
- Elevated PSA — often the first clue (most common modern presentation)
- LUTS — may coexist with BPH
- Hematuria
- Bone pain, constitutional symptoms — suggests metastatic disease
PSA is: [1]
- A glycoprotein enzyme produced by the prostate
- Function: liquefy semen, aiding sperm motility
Important: PSA is prostate-specific, NOT prostate cancer-specific. Many conditions elevate PSA.
Differential diagnosis of elevated PSA: [1]
- BPH
- Infection (UTI, prostatitis)
- Retention of urine
- Prostate cancer
- Recent ejaculation or catheterization
PSA as a Screening Tool: [1]
- Highly sensitive but NOT specific for prostate cancer
- Elevated PSA does not confirm cancer — many men with raised PSA have benign conditions
- A normal PSA does not fully exclude cancer
This is an extremely high-yield section for exams.
| Method | Definition / Concept | Key Thresholds |
|---|---|---|
| 1. PSA Density (PSAD) | PSA ÷ prostate volume | Higher PSAD → higher cancer likelihood (threshold ~0.15 ng/mL/mL) |
| 2. PSA Velocity (PSAV) | Rate of PSA increase over time (ng/mL/year) | PSA < 4: 0.35–0.4 ng/mL/year; PSA 4–10: 0.75 ng/mL/year |
| 3. Age-Adjusted PSA | Higher cutoffs for older men (prostate grows with age) | Age 40-49: 2.5; 50-59: 3.5; 60-69: 4.5; 70+: 6.5 ng/mL |
| 4. Free-to-Total PSA Ratio (%fPSA) | Lower free:total ratio → higher cancer risk | Useful when PSA 4–10 ng/mL (the "grey zone") |
| 5. Prostate Health Index (PHI) | Composite: total PSA + free PSA + [-2]proPSA | < 27: Low risk; 27–35: Intermediate; > 35: High risk |
Why %fPSA works: In cancer, PSA is more likely to be bound to serum proteins (alpha-1-antichymotrypsin). In BPH, more PSA circulates in free form. So a lower free-to-total ratio suggests cancer.
Benefits: May reduce prostate cancer mortality [1]
Harms: [1]
- False positives → anxiety, unnecessary biopsies
- Overdiagnosis and overtreatment of indolent cancers — many prostate cancers are slow-growing and would never cause clinical harm
- Complications from biopsy (sepsis, bleeding) and treatment (incontinence, erectile dysfunction)
EAU guideline 2025: Screening targets men aged 55–69 primarily, with risk stratification including family history, ethnicity, and genetic predispositions (e.g., BRCA mutations). Men at higher risk screened earlier and more intensively. [1]
Multiparametric MRI (mpMRI) of the prostate [1]
- Pre-biopsy MRI is now standard of care
- Uses T2-weighted + diffusion-weighted + dynamic contrast-enhanced sequences
- Reported using PI-RADS scoring (1–5): higher score = higher likelihood of clinically significant cancer
Prostate biopsy (usually MRI/USG fusion biopsy) [1] Indications:
- Elevated PSA with suspicious lesion on MRI
- Abnormal DRE
What the fusion-biopsy figure shows: an Artemis-style MRI/US workstation with workflow tabs Scan → Plan → Biopsy → Report, a live TRUS biopsy setup, and fusion-navigation panels outlining the prostate with colour-coded target levels (Level 1–5). The teaching point is targeted sampling of MRI-suspicious foci (plus systematic cores as per local protocol), not “blind sextant forever.” [1]
The Gleason grading system evaluates aggressiveness of prostate cancer based on microscopic architectural patterns. [1]
How it works:
- The pathologist identifies the two most predominant architectural patterns (grades 1–5)
- Primary (most common) + Secondary (second most common) = Total Gleason score
- Practically, scores range from 6 (3+3) to 10 (5+5) because grades 1-2 are rarely assigned [1]
| Gleason Score | Grade Group (ISUP) | Interpretation |
|---|---|---|
| ≤ 6 (3+3) | Group 1 | Low-grade |
| 3+4 = 7 | Group 2 | Intermediate — mostly pattern 3 (less aggressive) |
| 4+3 = 7 | Group 3 | Intermediate — mostly pattern 4 (MORE aggressive) |
| 8 | Group 4 | High-grade |
| 9–10 | Group 5 | High-grade |
3+4 vs. 4+3 — A Common Exam Discriminator
Both add up to 7, but 4+3 is significantly worse than 3+4 because pattern 4 predominates. Pattern 4 shows fused/cribriform glands with loss of normal architecture → more aggressive behavior. This distinction is important for treatment decisions — 4+3 may warrant more aggressive therapy. [1]
| T Stage | Description |
|---|---|
| T1 | Not palpable or visible by imaging |
| T1a | Found incidentally in ≤ 5% of resected tissue (e.g., TURP specimen) |
| T1b | Found incidentally in > 5% of resected tissue |
| T1c | Found by needle biopsy because of elevated PSA |
| T2 | Confined within the prostate |
| T2a | ≤ half of one lobe |
| T2b | > half of one lobe but not both |
| T2c | Both lobes |
| T3 | Extends through the prostatic capsule |
| T3a | Extracapsular extension |
| T3b | Invades seminal vesicles |
| T4 | Fixed or invades adjacent structures (bladder neck, external sphincter, rectum, levator muscles, pelvic wall) |
Prostate cancer risk groups (slide table; D’Amico-style categories used for imaging/treatment decisions) [1]:
| Risk group | PSA (ng/mL) | Grade group (Gleason score) | Clinical stage |
|---|---|---|---|
| Low risk | < 10 | 1 (≤ 6) | T1–T2a |
| Intermediate risk | 10–20 | 2 or 3 (7) | T2b |
| High risk | > 20 | 4 or 5 (8–10) | T2c–T3 |
Systemic imaging (bone scan, PSMA PET) indicated in: [1]
- High-risk group
- Intermediate-risk group with Gleason Score 4+3
Why PSMA PET is revolutionary: Prostate-specific membrane antigen (PSMA) is overexpressed on prostate cancer cells. Gallium-68 or Fluorine-18 labeled PSMA PET/CT can detect metastases with much higher sensitivity and specificity than conventional bone scan + CT, even at low PSA levels.
9.9 Treatment
| Clinical Scenario | Treatment |
|---|---|
| Old / frail patients | Watchful waiting |
| Low risk | Active surveillance |
| Intermediate to high risk | Radical prostatectomy (robotic) / Radiotherapy with adjuvant LHRHa |
| Feature | Watchful Waiting | Active Surveillance |
|---|---|---|
| Intent | Palliative — for old fragile patients | Curative — for young patients with low-risk disease |
| When to treat | Start hormonal treatment (ADT) when symptomatic or high PSA | Defer radical treatment; intervene if cancer progresses |
| Protocol | Less stringent monitoring | Stringent protocol: regular DRE, PSA, MRI, and biopsy |
Why active surveillance exists: Many low-risk prostate cancers (Gleason 3+3) grow so slowly that they will never cause harm during the patient's lifetime. Radical prostatectomy or radiotherapy carries significant morbidity (incontinence, erectile dysfunction). Active surveillance avoids treatment-related harms while monitoring for any signs of progression.
Rationale: Suppressing testosterone reduces prostate cancer growth (prostate cancer is androgen-dependent) [1]
| Type | Method |
|---|---|
| Surgical castration | Bilateral simple orchidectomy |
| Medical castration | LHRHa (3–6 monthly injection) — e.g., goserelin, leuprolide |
| LHRH antagonist (monthly injection) — e.g., degarelix |
Why LHRHa (agonist) works paradoxically: LHRHa initially causes a surge of LH and testosterone ("flare"), but continuous administration → downregulation of GnRH receptors → suppression of LH release → castrate-level testosterone. The initial flare can be dangerous in patients with extensive metastatic disease (can worsen bone pain, spinal cord compression) — hence an anti-androgen "cover" is given for the first 2–4 weeks, or an LHRH antagonist (no flare) is used instead.
The lecture mentions complications for each major procedure [1]:
| Procedure | Key Complications |
|---|---|
| Partial nephrectomy | Hemorrhage, urine leak, AKI, tumor recurrence at margin |
| Radical nephrectomy | Hemorrhage, injury to adjacent organs (spleen, bowel, pancreas), long-term CKD risk |
| TURBT | Bleeding, bladder perforation (intra- or extraperitoneal), TUR syndrome (rare with modern bipolar resectors), obturator nerve reflex |
| Radical cystectomy | Hemorrhage, uretero-ileal anastomotic leak, ileus, stoma complications, long-term metabolic issues (hyperchloremic metabolic acidosis with ileal conduit), sexual dysfunction |
| Radical prostatectomy | Urinary incontinence, erectile dysfunction, uretero-vesical anastomotic stricture, lymphocele, hemorrhage |
11. Integration with Related Topics
Unprovoked VTE → must screen for occult malignancy. Urological cancers (especially RCC) are one of the important cancers to consider. [5]
Prostate cancer is one of the most common cancers to metastasize to bone (typically osteoblastic/sclerotic rather than lytic). RCC metastases tend to be lytic. [7]
Prostate and RCC can cause malignant spinal cord compression. Management: dexamethasone 4mg IV Q6H + urgent neurosurgical/oncological referral for decompression/RT. [7]
Exam Intelligence
| Trap | Correct Thinking |
|---|---|
| Confusing dipstick hematuria with true microscopic hematuria | Dipstick positive → MUST confirm with microscopy; 20-70% are false positive |
| Attributing painless hematuria to UTI | Painless = malignancy until proven otherwise |
| Thinking Gleason 3+4 = 4+3 | 4+3 is worse — pattern 4 predominates |
| Assuming PSA is specific for prostate cancer | PSA is prostate-specific, not cancer-specific; BPH, prostatitis, retention all elevate it |
| Forgetting to scope the bladder in upper tract TCC | Field change — always do cystoscopy |
| Missing left varicocele as sign of left RCC | Left testicular vein drains into left renal vein → tumor thrombus can cause left varicocele |
| Equating watchful waiting with active surveillance | WW = palliative intent; AS = curative intent with stringent monitoring |
| Thinking T1 prostate cancer is palpable | T1 = NOT palpable or visible on imaging; T1c = found on biopsy for elevated PSA |
- RCC treatment paradigm: Surgery is king even in locally advanced disease. For metastatic RCC, immunotherapy + targeted therapy (NOT traditional chemotherapy — RCC is chemo-resistant)
- Bladder cancer: NMIBC → TURBT + BCG. MIBC → neoadjuvant chemo + radical cystectomy
- Prostate cancer: Low risk → active surveillance. Metastatic → ADT + novel hormonal agent ± chemo/RT based on volume
- SCC of bladder vs. TCC: SCC associated with schistosomiasis and chronic catheter/irritation; TCC associated with smoking and aromatic amines
High Yield Summary
-
Painless gross hematuria = malignancy until proven otherwise.
- Painful = infection.
-
Dipstick hematuria ≠ microscopic hematuria
- always confirm with microscopy (20–70% false positive).
-
Microscopic hematuria
- requires ≥ 3 RBC/HPF. Nephrological causes show dysmorphic RBCs, RBC casts, and proteinuria.
-
Hematuria workup
- Blood (CBC, RFT) + Urine (MSU C/ST, EMU AFB, cytology) + Upper tract (USG or CT urogram) + Lower tract (flexible cystoscopy).
-
RCC
- Incidental finding most common; classic triad rare. Paraneoplastic syndromes (hypercalcemia via PTHrP, polycythemia via EPO, hypertension via renin). New left varicocele → mandatory USG/CT to rule out RCC. T1 → partial nephrectomy; metastatic → immunotherapy + TKI.
-
Bladder cancer
- 90% urothelial/TCC.
- Smoking is #1 risk factor.
- SCC associated with schistosomiasis/chronic irritation.
- Staging TURBT + immediate mitomycin C.
- NMIBC → surveillance + BCG for high-risk.
- MIBC → neoadjuvant chemo + radical cystectomy.
-
Upper tract TCC
- Same urothelium as bladder (field change). Always do cystoscopy. Treatment: radical nephroureterectomy ± adjuvant chemo.
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Prostate cancer
- PSA is sensitive but not specific. Improve specificity with PSAD, PSAV, age-adjusted PSA, %fPSA, PHI. Gleason 4+3 worse than 3+4. Low risk → active surveillance. Metastatic → ADT + novel hormonal agent ± chemo/RT.
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Watchful waiting
- = palliative intent (elderly/frail). Active surveillance = curative intent (young, low-risk).
Active Recall - Common Urological Malignancies
[1] Lecture slides: GC 183. Common urological malignancies and their presentations - Nov 7.pdf [2] Senior notes: Block A - Glomerular and Tubulo-interstitial Diseases and Acute Kidney Injury.pdf [3] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (Ch. Urology - History and PE) [4] Senior notes: Block A - Confused and dehydrated_ hypercalcaemia; hypocalcaemia.pdf [5] Senior notes: Block A - Leg swelling and chest pain_ deep vein thrombosis; pulmonary embolism; Thrombophilia.pdf [6] Senior notes: Ryan Ho Endocrine.pdf (Section 2.2.3 Hypercalcemia of Malignancy) [7] Senior notes: Ryan Ho Neurology.pdf (Section 9.2 Spinal Cord Tumours) [11] Senior notes: Ryan Ho Respiratory.pdf (Section 3.6 Lung Cancer)
GC182 Chopped And Stabbed Wound In Gang Fight Nerves And Vascular Injury; Classification Of Injuries
Chopped and stabbed wounds sustained in gang fights involving nerve and vascular damage are classified based on wound mechanism (incised, stab, or chop), depth of penetration, and severity of neurovascular injury to guide medicolegal documentation and surgical management.
GC184 Erection And Erectile Dysfunction
Erection is the neurovascular process of penile engorgement mediated by parasympathetic-induced smooth muscle relaxation and increased blood flow, while erectile dysfunction is the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance.