URO - Urological Cancers Flashcards

1
Q

Prostate Cancer

Pathophysiology
Clinical Features
PSA Testing
Initial Investigations

A

1.) Pathophysiology
- the majority are adenocarcinomas (95%), arise from the peripheral zone (75%), and are often multifocal
- acinar adenocarcinoma: originates in glandular cells lining the prostate gland (most common)
- ductal adenocarcinoma: originates in cells that line the ducts of the prostate gland (metastasise faster)
- risk factors: ↑age, obesity, afro-Caribbean, FH, BRCA2/1 gene,

3.) Clinical Features
- localised prostate cancer is often asymptomatic as it’s often in the periphery so doesn’t cause obstructive sx
- LUTS, dysuria, haematuria, haematospermia,
- incontinence, pelvic/suprapubic pain, rectal tenesmus
- lethargy, weight loss, ↓appetite, bone pain (mets)
- DRE: asymmetry, nodularity, fixed irregular mass, with loss of median sulcus

4.) PSA Testing - PSA is an enzyme produced by normal and malignant prostate epithelial cells
- normal level: <3 (50-59yrs), <4 (60-69), <5 (70+)
- has poor sensitivity and specificity as it can also be raised in: BPH, prostatitis, UTI, ejaculation, vigorous exercise, retention, urinary tract instrumentation
- PSA test should be delayed: >1mth after UTI tx, >48hrs after ejaculation, >48hrs after vigorous exercise

4.) Initial Investigations - suspected cancer is based on symptoms, abnormal DRE, ↑PSA, FH + other risk factors
- 1°multiparametric MRI - Likert score of 3+/5 suggests ↑risk of prostate cancer so a biopsy is required
- 2°TRUS biopsy: invasive procedure w/ complications inc pain, fever, sepsis, bleeding/haematuria
- biopsy produces a Gleason score

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2
Q

Management of Prostate Cancer

Staging of Prostate Cancer
Low Risk Disease
Intermediate/High Risk Disease
Metastatic Disease
Castrate-Resistant Disease

A

1.) Staging of Prostate Cancer - risk stratification is based on the PSA, Gleason score, and the tumour size
- Gleason score: 2-10, 2 grades on a scale of 1-5, most dominant grade written first (4+3 is worse than 3+4)
- imaging: staging CT (CT-CAP) and PET scan for intermediate or high risk disease
- T1/T2: localised prostate cancer
- T3/T4: locally advanced prostate cancer

2.) Low-Risk Disease - PSA<10, Gleason <6, T1-T2a
- active surveillance: assessing for progression with 3mthly PSA, 6-12mthly DRE, re-biopsy 1-3 yr intervals, radical treatments if evidence of disease progression
- watchful waiting: sx guided, the intent is not curative (reserved for older patients with ↓life expectancy)

3.) Intermediate/High Risk Disease: intermediate (PSA 10-20, G7, T2b), high (PSA >20, G8-10, T2c+)
- open/lap/robotic radical prostatectomy: side effects inc erectile dysfunction, stress incontinence
- external-beam radiotherapy and brachytherapy can be curative for localised prostate cancer
- intermediate can have surveillance or treatment

4.) Metastatic Disease - anti-androgen hormone ther…
- synthetic GnRH agonist (goserelin) or antagonists
- bicalutamide: non-steroidal, block androgen receptor
- abiraterone: androgen synthesis inhibitor
- bilateral orchidectomy: rapidly ↓testosterone levels
- chemotherapy: docetaxel, cabazitaxel (if relapsed)

5.) Castrate-Resistant - hormone-relapsed disease
- further chemotherapy, corticosteroids

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3
Q

Bladder Cancer

Classification
Risk Factors
Clinical Features
Investigations

A

1.) Classification
- urothelial carcinoma (TCC, >90%), SCC, adenocarcinoma, sarcoma
- non-muscle invasive (70-80%), muscle invasive,
locally advanced or metastatic bladder cancer

2.) Risk Factors
- ↑age, smoking, schistosomiasis (SCC), radiation, aromatic hydrocarbons (industrial dyes or rubbers)

3.) Clinical Features
- majority present with painless visible haematuria
- other symptoms: non-visible haematuria, recurrent UTIs, LUTS,
- clinical exam often unremarkable in early disease
- advanced: pelvic pain, systemic symptoms
- 2WW referral criteria:
- >45 w/ unexplained visible haematuria without persistent or recurring UTIs
- >60 w/ unexplained non-visible haematuria + dysuria OR ↑WCC

4.) Investigations
- urgent cystoscopy (rigid more definitive)
- biopsy and potential resection (TURBT)
- imaging required if muscle invasive: staging CT

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4
Q

Management of Bladder Cancer

Non-Muscle Invasive
Muscle Invasive
Locally Advanced or Metastatic

A

1.) Non-Muscle Invasive
- TURBT +/- intravesical therapy (bCG/Mitomycin C)
- regular surveillance (cytology and cystoscopy) due to high recurrence rate (70% within 3 years)

2.) Muscle Invasive
- radical cystectomy +/- neoadjuvant chemo (cisplatin)
- urinary diversion required after cystectomy via:
- ileal conduit w/ urostomy or neobladder reconstruction from bowel (↑risk of adenocarcinoma)

3.) Locally Advanced or Metastatic
- chemo: cisplatin or carboplatin+gemcitabine based
- manage sx through MDT, discuss palliative options

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5
Q

Renal Cancer (RCC)

Pathophysiology
Risk Factors
Clinical Features

A

1.) Pathophysiology
- RCC most common, others include: TCC (urothelial), SCC (chronic irritation), nephroblastoma (children)
- RCC is adenocarcinoma of the renal cortex arising from mainly the PCT and upper pole of the kidney, most common type is clear cell RCC
- can spread to adrenals, renal vein, IVC, (direct), lymph nodes, bones, liver, brain, lung (haematogenous)

2.) Risk Factors
- smoking, dialysis, HTN, obesity, industrial exposure to carcinogens e.g. cadmium, lead, aromatic hydrocarbons
- anatomical variants: polycystic/horseshoe kidneys
- genetic: Hippel-Lindau disease, BAP1 mutant disease, tuberous sclerosis

3.) Clinical Features
- classic triad: haematuria, flank pain, flank mass (don’t always have all 3)
- others: pyrexia of unknown origin, lethargy, weight loss, left varicocoele
- respiratory sx: 75% of RCC spread to the lungs (cannonball mets)
- if symptomatic, usually already at stage 4 disease
- paraneoplastic syndromes –> polycythemia (EPO), hypercalcaemia (PTH), HTN (renin)
- Stauffer syndrome: paraneoplastic hepatic dysfunction syndrome causing RUQ pain, nausea, cholestatic jaundice (↑ALP), hepatosplenomegaly

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6
Q

Investigations and Management of Renal Cancer (RCC)

Investigations
Management of Localised Disease
Management of Metastatic Disease
Prognosis

A

1.) Investigations
- routine bloods (inc calcium), urinalysis (NVH)
- CT-CAP pre and post IV contrast (gold), staging CT
- biopsy of renal lesions: clear cells

2.) Management of Localised Disease
- partial or radical nephrectomy (+uretectomy)
- radiofrequency ablation or cryotherapy if not suitable or fit enough for surgery
- RCC is usually resistant to radiotherapy and chemo
- surveillance if patients are unfit or low life expectancy

3.) Management of Metastatic Disease
- nephrectomy + immunotherapy (chemo is ineffective)
- metastasectomy, biologic agents

  1. Prognosis - 70% at 3yrs post-nephrectomy
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7
Q

Testicular Cancer

Risk Factors
Clinical Features
Investigations
Management

A

1.) Risk Factors
- cryptorchidism (4-10x), previous malignancy, FH
- Klinefelter’s syndrome
- demographic: 20-40yrs, Caucasian, north European

2.) Clinical Features
- unilateral painless testicular lump/mass
- mass is irregular, firm, fixed, does not transilluminate
- can present with gynaecomastia (due to excess beta-hCG and/or oestrogen)
- evidence of mets: weight loss, back pain, SOB, palpate supraclavicular lymph nodes

3.) Investigations
- tumour markers: PLAP, ß-hCG, AFP, LDH
- scrotal USS, staging CT w/ contrast
- biopsy not performed to prevent seeding of cancer

4.) Management - depends on tumour subtype, disease stage, and risk scoring
- surgery, radiotherapy, chemotherapy
- surgery: inguinal radical orchidectomy (enter through inguinal region to remove spermatic cord, to prevent spread to other lymph [para-aortic] nodes)
- semen analysis and cryopreservation offered

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8
Q

Types of Testicular Tumours

Broad Classsifications
Seminomatous (inc tumour markers)
Non-Seminomatous (inc tumour markers)
Sex-Cord Stromal
Other

A

Classifications- germ cell (95%) vs non-germ cell
- germ cell: seminomatous or non-seminomatous
- non germ cell: sex cord stromal or other

1.) Seminomatous (SGCT)
- good prognosis, remain localised until quite late
- tumour markers: placental alkaline phosphatase (PLAP), ß-hCG (only 15%), serum gamma-GT (30%), LDH (non-specific)

2.) Non-Seminomatous (NSGCT)
- worse prognosis, metastasise early
- yolk sac tumours + teratomas: AFP
- choriocarcinoma (ß-hCG), embryonal carcinoma
- tumour markers: AFP, ß-hCG, LDH (non-specific)

3.) Sex-Cord Stromal - usually benign
- leydig cell tumours, sertoli cell tumours
- secretes androgens and oestrogens respectively

4.) Other - lymphoma (older men), mets (very rare)

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