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Genitourinary > GU Cancers - Prostate, Bladder, Testicular, Renal > Flashcards

GU Cancers - Prostate, Bladder, Testicular, Renal Flashcards

1
Q

What is the function of the prostate?

A

The prostate secretes proteolytic enzymes into the semen, which break down clotting factors in the ejaculate.

Produces seminal fluid to sustain semen.

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2
Q

Which anatomical zone of the prostate does prostate cancer commonly affect?

A

The peripheral zone.

Transitional in BPH.

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3
Q

What is PSA?

A

A glycoprotein secreted by the prostate into the blood stream.

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4
Q

Give examples of 3 times when PSA may be high.

A
  1. Prostate cancer
  2. BPH
  3. Exercise
  4. Post ejaculation
  5. Infection - prostatitis
  6. UTI
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5
Q

What kind of cancer is prostate cancer normally?

A

Adenocarcinoma

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6
Q

Where can prostate cancer commonly metastasise to?

A

Lymph nodes and bone.

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7
Q

Describe the clinical presentation of prostate cancer.

A
  1. Urine retention
  2. Pain
    - Lower abdominal
    - Specifically: back pain - because of metastasis
  3. LUTS e.g. frequency, post-void dribbling, nocturia, hesitancy
  4. Asymetrical hard, lumpy prostate with loss of median sulcus
    weight loss, etc
  5. Haematuria
    - More likely prostate cancer
    - Less likely see it in BPH
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8
Q

investigations for prostate cancer.

A
  1. Serum PSA - non specific
  2. Multiparametric MRI
    - 1st line investigation for suspected localised prostate cancer.
  3. Trans-rectal ultrasound (TRUS) & biopsy
    - DIAGNOSTIC
  4. Urine biomarkers
    - E.g. PCA3 or gene fusion protein
  5. DRE
    - Hard, irregular, craggy
  6. Endorectal coil MRI
    - To locally stage tumour
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9
Q

How is prostate cancer graded & staged?

A

Gleasson score to grade (higher is worse)
TMN to stage

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10
Q

What are the 5 gleasson stages?

A

1 - well formed uniformly distributed
2 - mostly well formed with minor poorly formed
3 - mostly poorly formed with minor well formed
4 - poorly formed glands
5 - necrosis, cords, nests, sheets

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11
Q

Describe the treatment for prostate carcinoma.

A
  1. Radical prostatectomy or radiotherapy.
  2. For metastatic disease, remove the androgenic drive e.g. bilateral orchidectomy.
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12
Q

What is a key complication of external beam radiotherapy?

A

A key complication of external beam radiotherapy is proctitis (inflammation in the rectum) caused by radiation affecting the rectum.

Proctitis can cause pain, altered bowel habit, rectal bleeding and discharge.

Prednisolone suppositories can help reduce inflammation.

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13
Q

What is the treatment for localised prostate cancer?

A
  1. Active surveillance
    - IF >70yrs and low risk
  2. Radical prostatectomy if <70yrs - excellent disease free survival
  3. External beam radiotherapy + hormone therapy
    - Alternative to surgery
  4. Brachytherapy
    - Implantation of radioactive material targeted at tumours
  5. Hormone therapy
    - Temporarily delays tumour progression
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14
Q

Give 2 advantages and 1 disadvantage of radical treatment for localised prostate cancer.

A
  • Curative.
  • Reduced patient anxiety.
  • Can have adverse effects.
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15
Q

What is the treatment for metastatic prostate cancer?

A

Hormone therapy

Androgen deprivation:
1. Orchidectomy (removal of testes)
2. LHRH agonists e.g. SC GOSERELIN or SC LEUPRORELIN
3. Androgen receptor blockers e.g. BICALUTAMIDE

Analgesia
Treat hypercalcaemia
Radiotherapy for bone metastases/spinal cord compression

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16
Q

Give 2 advantages and 2 disadvantages of screening in prostate cancer.

A
  • Screening can lead to early diagnosis/early treatment and so cure or effective palliation.
  • Uncertain natural history.
  • Screening leads to over diagnosis and treatment.
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17
Q

What are the side effects of androgen receptor blockers?

A

Androgen receptor blockers e.g. BICALUTAMIDE:
- Side effects; weakness, nausea, hot flushes, weight
changes

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18
Q

What are the side effects of hormone therapy?

A

Side effects of hormone therapy include:

Hot flushes
Sexual dysfunction
Gynaecomastia
Fatigue
Osteoporosis

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19
Q

What nerves innervate the bladder?

A

Sympathetic - relax detrusor - inferior hypogastric
Parasymp - contracts detrusor - pelvic
Somatic - sphincter - pudendal

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20
Q

Where might a transitional cell carcinoma arise?

A
  1. Bladder (50%).
  2. Ureter.
  3. Renal pelvis.
  4. Urethra.
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21
Q

Describe the epidemiology of TCCs.

A
  1. M:F = 3:1.
  2. Age > 40 y/o.
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22
Q

Give 4 symptoms of transitional cell carcinoma.

A
  1. PAINLESS HAEMATURIA.
  2. Dysuria.
  3. Recurrent UTIs.
  4. Raised WBC on FBC.
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23
Q

Give 5 investigations that you might do in someone who you suspect has transitional cell carcinoma.

A
  1. Urine dipstick.
  2. Blood tests
    - Urinary tumour marker = fibrin.
  3. Flexible cystoscopy with biopsy = diagnostic.
  4. Imaging of upper urinary tract e.g. CT IVU (IV Urogram)
    - For staging = diagnostic!
  5. TURBT.
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24
Q

Give 2 potential risks of flexible cystoscopy.

A
  1. UTI’s.
  2. Problems passing urine.
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25
Q

Why would you want to image the upper urinary tract of someone with transitional cell carcinoma?

A

You image the UUT to confirm that there is no other TCC elsewhere in the urinary tract.

CT IVU, USS and XR can be used.

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26
Q

Why might you do a trans-urethral resection of bladder tumour (TURBT) in someone with TCC?

A

For histological and staging analysis.

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27
Q

What staging system is used for TCC?

A

TNM staging.

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28
Q

Describe the treatment for non-muscle invasive bladder cancer (CIS, Ta, T1).

A
  1. TURBT
    - Surgical resection.
  2. Chemotherapy
    - To reduce the risk of recurrence and progression to muscle invasion.
    - MITOMYCIN, DOXORUBICIN and CISPLATIN
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29
Q

Describe the treatment for localised muscle invasive bladder cancer (T2, T3).

A
  1. Radical cystectomy = gold standard
    - Bladder removal
  2. +/- neo-adjuvant chemotherapy.
  3. Radical radiotherapy if not fit/unwilling to undergo cystectomy.
  • Radical cystectomy (bladder removal) - GOLD STANDARD:
  • Post-op chemotherapy: M-VAC; METHOTREXATE, VINBLASTINE,
    ADRIAMYCIN and CISPLATIN
  • Radical radiotherapy - if not fit for surgery
  • Chemotherapy:
  • CMV - CISPLATIN, METHOTREXATE, VINBLASTINE
30
Q

Describe the treatment for T4 TCC (invasion beyond the bladder).

A
  1. Palliative chemo/radiotherapy.
  2. Chronic catheterisation for pain.
31
Q

Name a helminth that can cause SQUAMOUS cell carcinoma of the bladder.

A

Schistosomiasis.

32
Q

What is the most common bladder cancer?

A

Transitional cell carcinoma (TCCs)

33
Q

Give 3 risk factors for TCCs.

A
  1. Smoking
  2. Occupation:
    - PAH (polycyclic aromatic hydrocarbons)
    - Hairdressers (use dyes), dye + rubber factory, Sulphur
  3. Schistosomiasis
    - Causes SQUAMOUS cell carcinoma of the bladder in countries with a high prevalence of the infection
  4. Increasing age
  5. Male gender
  6. FHx
34
Q

What is the tumour marker for bladder cancer?

A

Fibrin

35
Q

Why is it important to consider the patient’s occupation during their presentation?

A

TOP TIP:
The typical presentation to look out for in your exams is a retired dye factory worker with painless haematuria.

Whenever an exam question mentions a patient’s occupation, it is almost certainly relevant and will tell you the diagnosis.

E.G.
Dye factory workers get transitional cell carcinoma of the bladder. Patients with asbestos exposure get mesothelioma.
Outdoor workers with significant sun exposure get skin cancer.

36
Q

Describe the TNM staging system used for bladder cancer.

A

The TNM staging system is used for bladder cancer, rating the T (tumour), N (lymph node) and M (metastasis) stages.

There is a clear distinction between:
- Non-muscle-invasive bladder cancer (not invading the muscle layer of the bladder)
- Muscle-invasive bladder cancer (invading the muscle and beyond)

Non-muscle-invasive bladder cancer includes:
1. Tis/carcinoma in situ: cancer cells only affect the urothelium and are flat
2. Ta: cancer only affecting the urothelium and projecting into the bladder
3. T1: cancer invading the connective tissue layer beyond the urothelium, but not the muscle layer

Invasive bladder cancer includes T2 – 4 and any lymph node or metastatic spread.

37
Q

What are the most commons site of metastasis for bladder cancer?

A

Most common sites of metastasis = lymph nodes, bones, lung, liver

38
Q

Where does testicular cancer arise from?

A

Testicular cancer arises from the germ cells in the testes.
Germ cells are cells that produce gametes (sperm in males).

There are other, rare tumours in the testes, such as non-germ cell tumours and secondary metastases.

39
Q

What are the 2 types of testicular cancer?

A
  1. Seminomas
  2. Non-seminomas (mostly teratomas)
40
Q

Describe the epidemiology of testicular cancer.

A

Most common cancer in younger males aged 15-44 yrs

41
Q

Give 3 risk factors for testicular cancer.

A
  1. Undescended testes
  2. Male infertility
  3. Family history
  4. Increased height
  5. Infant hernia
42
Q

Describe the clinical presentation of testicular cancer. Give 3 symptoms.

A
  1. Painless lump on testicle
  2. Testicular pain and/or abdominal pain
  3. Hydrocele
  4. Cough and dyspnoea - indicative of lung metastases
  5. Back pain - indicative of para-aortic lymph node metastasis
  6. Abdominal mass

Gynecomastia

43
Q

Describe the painless lump found on the testicle.

A

The lump will be:

Non-tender (or even reduced sensation)
Arising from testicle
Hard
Irregular
Not fluctuant
No transillumination

44
Q

Diagnosis of testicular cancer.

A
  1. Scrotal Ultrasound:
    * To differentiate between masses in the body of the testes and other intrascrotal swellings
  2. Biopsy and histology
  3. Serum tumour markers:
    1) Alpha-fetoprotein (AFP)
    2) Beta subunit of human chorionic gonadotrophin (B-hCG)

= Raised AFP & B-hCG in teratomas
= B-hCG in minority of those with seminomas
= AFP is not elevated in those with pure seminomas

  1. Chest X-ray & CT
    - To assess tumour staging
45
Q

What are the 2 serum tumour markers for testicular cancer?

A
  1. Alpha fetoprotein
  2. Beta subunit of hCG
46
Q

Describe the findings of AFP + B-hCG in teratomas and seminomas.

A
  • Raised AFP & B-hCG in teratomas
  • B-hCG in minority of those with seminomas
  • AFP is not elevated in those with pure seminomas
47
Q

What staging system is used for testicular cancer?

A

Royal Marsden Staging System:

Stage 1 – isolated to the testicle
Stage 2 – spread to the retroperitoneal lymph nodes
Stage 3 – spread to the lymph nodes above the diaphragm
Stage 4 – metastasised to other organs

48
Q

Management of testicular cancer.

A
  1. Surgery: Radical orchidectomy (removal of testes) via inguinal approach
  2. Radiotherapy:
    - Seminomas with metastases below diaphragm - only treated with radiotherapy
  3. Chemotherapy:
    - More widespread tumours are treated with chemotherapy
    - Teratomas treated with chemotherapy
  4. Sperm storage/banking offered
49
Q

Give some long term side effects of treatment of testicular cancer.

A
  1. Infertility
  2. Hypogonadism (testosterone replacement may be required)
  3. Peripheral neuropathy
  4. Hearing loss
  5. Lasting kidney, liver or heart damage
  6. Increased risk of cancer in the future
50
Q

What is renal cell carcinoma (RCC)?

A

Renal cell carcinoma (RCC) is the most common type of kidney tumour.

Also known as Hypernephroma and Grawitz tumour.

51
Q

Renal cell carcinoma is what kind of cancer?

A

Adenocarcinoma

52
Q

Where does RCC arise from?

A

Arises from the Proximal Convoluted Tubular Epithelium

53
Q

Describe the epidemiology of RCC.

A
  1. Incidence increases in those > 60 y/o.
  2. Males > females.
  3. Most common renal tumour in adults.
54
Q

What are the 3 most common types of RCC?

A
  1. Clear cell (around 80%)
  2. Papillary (around 15%)
  3. Chromophobe (around 5%)
55
Q

Give 3 risk factors for RCC.

A
  1. Smoking.
  2. Obesity.
  3. Hypertension!! and Hyperlipidaemia
  4. Chronic kidney disease, End Stage Renal failure & haemodialysis (15% develop RCC).
  5. Polycystic kidneys.
  6. Von Hippel-Lindau Disease.
  7. Age
56
Q

What is the most common type of RCC?

A

Clear cell

57
Q

Name and describe an inherited renal disease that can cause RCC.

A

Von Hippel Lindau disease.

An Autosomal dominant disease.

There is a loss of the tumour suppressor gene VHL, which is encoded for on chromosome 3.
Lots of benign cysts grow, some of which may develop into cancer.

58
Q

What are the 3 classic signs of RCC?

A
  1. Haematuria.
  2. Vague loin/flank pain.
  3. Abdominal mass (palpable on examination)
  4. Non-specific symptoms of cancer (e.g. weight loss, fatigue, anorexia, night sweats)
59
Q

Why do people with RCC rarely present with symptoms of the disease?

A

Often asymptomatic and discovered incidentally

The signs of RCC are now rare.

People with the disease are detected incidentally through imaging for something else before they show any symptoms.

60
Q

Name 3 places that RCC might metastasise to.

A
  1. Lymph nodes.
  2. Lungs.
    - ‘Cannonball metastases’ = clearly-defined circular opacities scattered throughout the lung fields on CXR.
  3. Bones.
  4. Liver.
  5. Adrenals

Renal cell carcinoma tends to spread to the tissues around the kidney, within Gerota’s fascia. It often spreads to the renal vein, then to the inferior vena cava.

  • Spread may be direct (renal vein), via lymph or haematogenous (bone, liver, lung)
61
Q

What is varicocele?

A

An abnormal enlargement of the pampiniform venous plexus in the scrotum.

62
Q

Why might RCC cause left sided varicocele?

A

If the renal tumour obstructs where the gonadal vein drains into, the renal vein blood can back up and so you may see left sided varicocele.

63
Q

What are the 4 paraneoplastic syndromes associated with RCC?

A
  1. Polycythaemia
    – Due to secretion of unregulated erythropoietin (EPO)
  2. Hypercalcaemia
    – Due to secretion of a hormone that mimics the action of parathyroid hormone (PTH-like molecule)
  3. Hypertension
    – Due to various factors, including increased renin secretion, polycythaemia and physical compression
  4. Stauffer’s syndrome
    – Abnormal liver function tests (raised ALT, AST, ALP and bilirubin) without liver metastasis
64
Q

3 common paraneoplastic syndromes related to RCC?

A

Renin = Hypertension
EPO = Polycythaemia
PTH-like molecule = Hypercalcaemia

65
Q

Stauffer’s syndrome is a triad of:

A
  1. Deranged LFT
  2. Hypoglycaemia
  3. Fever

(Stauffer’s syndrome is a paraneoplastic syndrome associated with RCC)

66
Q

What investigations might you do in someone with RCC?

A
  1. Ultrasound.
    * To distinguish simple cyst from complex cyst or tumour
  2. Bloods:
    * FBC - detect polycythaemia and anaemia due to EPO decrease
    * ESR may be raised
    * Liver biochemistry may be abnormal
    *U+E
  3. CT chest and abdomen with contrast:
    * More sensitive than ultrasound in detecting a renal mass and will show involvement of the renal vein of inferior vena cava, if present
    * Using contrast demonstrates kidney function since in normal kidney should see it being taken up and excreted well
  4. Bone scan for boney metastases
    - Only if there are signs or serum Ca2+ raised
  5. Renal biopsy
    * Get histology to identify tumour
  6. MRI
    - For tumour staging
67
Q

What staging system is used for RCC?

A

TNM staging system and number system (Stage 1 - Stage 4)

68
Q

What is the treatment for localised renal cell carcinoma?

A
  1. Surgical excision
    - Radical Nephrectomy (remove kidney) unless tumours are bilateral (present on both kidneys)
    * If bilateral involvement then: partial nephrectomy
  2. Ablative techniques
    - Used in patients with significant comorbidities, who would not tolerate surgery
    - Can harm kidney function
    1) Arterial embolisation = cutting off the blood supply to the affected kidney
    2) Percutaneous cryotherapy = injecting liquid nitrogen to freeze and kill the tumour cells
    3) Radiofrequency ablation = putting a needle in the tumour and using an electrical current to kill the tumour cells
69
Q

What is the treatment for metastatic renal cell carcinoma?

A
  • Metastatic or locally advanced:
  • Interleukin-2 & Interferon alpha - produce remission in 20%
  • Biological angio-genesis targeted therapy:
  • SUNITINIB, BEVACIZUMAB and SORAFENIB
  • TEMSIROLIMUS (mTOR inhibitor) - found to improve survival more than interferon
  • Last 2 options given if patients do not respond to 1st
70
Q

Differential diagnosis of RCC.

A

Transitional cell carcinoma.
Wilms’ tumour.
Renal oncocytoma.
Leiomyosarcoma.

71
Q

What is an oncocytoma?

A

Benign kidney mass in the collecting duct.

72
Q

What is Wilms’ tumour? Describe its main clinical presentation, diagnosis and treatment.

A

Definition:
- Childhood tumour of the primitive renal tubules and mesenchymal cells

Epidemiology:
- Seen within the first 3 years of life - it is the chief abdominal malignancy in children

Clinical presentation:
* Presents as an abdominal mass and less commonly with haematuria

Investigation:
* Diagnosis is established by ultrasound, CT and MRI

Treatment:
* Treated with a combination of nephrectomy, radiotherapy and chemotherapy

Genitourinary (17 decks)

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