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2A - Urinary System > Tumours of the Urinary System 1 (Prostate and Testicular Cancers) > Flashcards

Tumours of the Urinary System 1 (Prostate and Testicular Cancers) Flashcards

1
Q

What is the commonest cancer in men?

A

Prostate cancer

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2
Q

What is the incidence of prostate cancer?

A
  • 134/100000 men/year
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3
Q

How does the incidence of prostate cancer change with age?

A
  • Incidence increases with age
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4
Q

What are risk factors for prostate cancer?

A
  • Age
  • Race/ethnicity
  • Geography
  • Family history
    • First degree relative is 2x risk
    • HPC1, BRCA1 and 2
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5
Q

What genes are linked to prostate cancer?

A
  • HPC1, BRCA1 and 2
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6
Q

How does most prostate cancer present?

A
  • 80% of newly diagnosed prostate cancers are localised
  • Mostly asymptomatic (do not have cancer specific symptoms)
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7
Q

How is prostate cancer diagnosed?

A
  • Diagnosed through opportunistic PSA testing (not screening)
    • Diagnostic triad of PSA, digital rectal examination and TRUS-guided prostate biopsies
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8
Q

What are some localised prostate cancer presenting symptoms?

A
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9
Q

What is the presentation of metastatic prostate cancer?

A
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10
Q

Is prostate cancer screened for?

A

Screening is not done for prostate cancer, but ad-hoc PSA testing is:

  • Kallikrein serine protease (liquifies semen)
  • Produced by glands of prostate
  • Normal serum range is 0-4ug/mL
    • Levels change with age
      • <50 years, 2.5 is upper limit
      • 50-60 years 3.5 is upper limit
      • 60-70 years 4.5 is upper limit
      • 6.5 years 6.5 is upper limit
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11
Q

What is the normal serum range of Kallikrein serine protease?

A
  • Normal serum range is 0-4ug/mL
    • Levels change with age
      • <50 years, 2.5 is upper limit
      • 50-60 years 3.5 is upper limit
      • 60-70 years 4.5 is upper limit

6.5 years 6.5 is upper limit

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12
Q

What does PSA testing measure?

A

Kallikrein serine protease

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13
Q

Elevations in PSA can occur due to?

A
  • UTI
  • Chronic prostatitis
  • Instrumentation (catheterisation)
  • Physiological (ejaculation)
  • Recent urological procedure
  • BPH
  • Prostate cancer
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14
Q

What is the half life of PSA?

A

2.2 days

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15
Q

If repeated PSA tests are needed, how long should be waited before rechecking?

A

If repeat PSA needed, recheck in at least 3 weeks (ie 8 half lifes)

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16
Q

What is the probability of cancer based on PSA levels?

A
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17
Q

What is used to grade prostate cancers pathologically?

A

Gleason grading of prostate cancer:

  • Pathologist classifies grade of prostate cancer
  • Score 3 to 5 (well to poorly differentiated)
  • Summate to give Gleason SUM score
  • Useful prognostically and guides treatment
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18
Q

What are Gleason gradings converted into?

A

ISUP grade

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19
Q

For purposes of treatment and prognosis, it is useful to divide prostate cancer into 4 stages, what are these?

A
  • Localised stage
  • Locally advanced stage
  • Metastatic stage
  • Hormone refractory stage
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20
Q

What can staging of localised prostate cancer be done by?

A
  • Digital rectal examination (local staging)
  • PSA
  • Transrectal US guided biopsies
  • CT (regional and distant staging)
  • MRI (local staging)
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21
Q

What is the treatment of localised prostate cancer?

A
  • Radiotherapy
    • External-beam
    • Brachytherapy
  • Radical prostatectomy
    • Open
    • Laparoscopic
    • Robotic
  • Others under investigation
    • Cryotherapy
    • Thermotherapy
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22
Q

What is the treatment of locally advanced prostate cancer?

A
  • Watchful waiting
  • Hormone therapy followed by surgery
  • Hormone therapy followed by radiation
  • Hormone therapy alone
  • Intermitted hormone therapy (clinical research)
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23
Q

What are different types of hormonal treatment for prostate cancer?

A
  • Surgical castration
    • Ie bilateral orchidectomy
  • Chemical castration
    • Ie LHRH analogue or LHRH antagonists
      • LHRH analogues eventually downregulates androgen receptors by negative feedback
      • Tumour flare in first week of therapy, LHRH antagonists do not cause tumour flair
  • Anti-androgens
    • Inhibit androgen receptors
  • Oestrogens
    • Inhibits LHRH and testosterone secretion inactivates androgens and has direct cytotoxic effects on prostatic epithelial cells
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24
Q

What are examples of chemical castration?

A
  • Ie LHRH analogue or LHRH antagonists
    • LHRH analogues eventually downregulates androgen receptors by negative feedback
    • Tumour flare in first week of therapy, LHRH antagonists do not cause tumour flair
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25
Q

How does oestrogen hormonal therapy for prostate cancer work?

A
  • Inhibits LHRH and testosterone secretion inactivates androgens and has direct cytotoxic effects on prostatic epithelial cells
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26
Q

What are some metastatic prostate cancer complications?

A
  • Bone
    • Pain, pathological fractures, anaemic, spinal cord compression
  • Rectal
    • Constipation, bowel obstruction
  • Ureteric
    • Obstruction from renal failure
  • Pelvic lymphatic obstruction
    • Lymphoedema, DVT
  • Lower urinary tract dysfunction

Haematuria, acute retention

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27
Q

What is the treatment for metastatic prostate cancer?

A
  • Hormonal therapy
  • Supportive treatment
    • Palliative radiotherapy
    • Colostomy
    • Nephrostomy
    • Palliative supportive care
28
Q

How does the prognosis of prostate cancer change with stage?

29
Q

What is the presentation of testicular cancer?

A
  • Usually
    • Painless lump
  • Less often
    • Tender inflamed swelling
    • History of trauma (although trauma is not a risk factor)
    • Symptoms/signs from nodal or distant metastases
      • Para-aortic lymph nodes
      • Chest
      • Bone
30
Q

What is one of the commonest cancers in young men?

A

Testicular cancer

31
Q

What are risk factors for testicular cancer?

A
  • Higher risk if Caucasians
    • Risk also higher in testicular maldescent, infertility, atrophic testis, previous cancer in contralateral testis
32
Q

In what decade of life is the peak incidence of testicular cancer?

A
  • Peak incidence in 3rd decade
33
Q

What is the aetiology of testicular cancer?

A
  • Aetiology is unknown but testicular germ cell neoplasia in situ is a precursor lesion
34
Q

What are different types of tumour markers for testicular cancer?

A
  • AFP (alpha-fetoprotein)
    • Teratoma
  • BHCG (human chorionic gonadotrophin)
    • Seminoma
  • LDH (lactate dehydrogenase)
    • Non-specific marker of tumour breakdown
35
Q

What does AFP stand for?

A

Alpha-fetoprotein

36
Q

Alpha-fetoprotein is a biomarker for what?

37
Q

BHCG stands for what?

A

Human chorionic gonadotrophin

38
Q

Human chorionic gonadotrophin (BHCG) is a biomarker for what?

39
Q

LDH stands for?

A

Lactase dehydrogenase

40
Q

Lactate dehydrogenase is a tumour biomarker for what?

A
  • Non-specific marker of tumour breakdown
41
Q

What investigations are done to diagnose testicular cancer?

A
  • Lump in testicle is treated as tumour until proven otherwise
  • Differential diagnosis
    • Infection
    • Epididymal cyst
    • Missed testicular torsion
  • MSSU
  • Testicular ultrasound scan and chest x-ray
  • Tumour markers
42
Q

What is the differential diagnosis of testicular cancer?

A
  • Infection
  • Epididymal cyst
  • Missed testicular torsion
43
Q

What are the different pathological types of testicular cancer?

A
  • Germ cell tumour (95%) vs non-germ cell tumour (5%)
  • Germ cell tumour (GCT)
    • Seminomatous GCT (classical, spermatocytic or anaplastic)
      • Affects mainly 30-40 years olds
    • Non-seminomatous GCT (teratoma, yolk sac, choriocarcinoma, mixed GCT)
      • Affects mainly 20-30 year olds
  • Non GCT (sex cord/stromal)
    • Leydig
    • Sertoli
    • Lymphoma rare
44
Q

Are germ cell tumours or non-germ cell tumours more common?

A
  • Germ cell tumour (95%) vs non-germ cell tumour (5%)
45
Q

What does GCT stand for?

A

Germ cell tumour

46
Q

What are the different kinds of germ cell tumours?

A
  • Seminomatous GCT (classical, spermatocytic or anaplastic)
    • Affects mainly 30-40 years olds
  • Non-seminomatous GCT (teratoma, yolk sac, choriocarcinoma, mixed GCT)
    • Affects mainly 20-30 year olds
47
Q

What are the different kinds of non-GCTs?

A
  • Leydig
  • Sertoli
  • Lymphoma rare
48
Q

Which age group does seminomatous GCT and non-seminomatous GCT normally affect?

A

Seminomatous - 30 to 40 years

Non-seminomatous - 20 to 30 years

49
Q

What is grading of testicular cancer an assessment of?

A

Aggressiveness

50
Q

What is grading of testicular cancer based on?

A
  • Based on histological assessment of differentiation
    • Low grade is well differentiated
    • High grade is poorly differentiated
51
Q

What is staging an assessment of?

A

Assessment of spread

52
Q

What are the 3 ways that testicular cancer can spread?

A
  • Local spread
    • Such as local invasion to adjacent structures
  • Regional spread
    • Lymphatic invasion
  • Distant spread
    • Lungs, bone, liver
53
Q

Where does testicular cancer commonly metastasis to?

A

Lungs

Bone

Liver

54
Q

What system is used to stage testicular cancer?

A

TNM system

55
Q

What investigations are done to stage testicular cancer?

A
  • Local staging via pathological assessment or orchidectomy specimen
  • Nodal staging via CT scan
  • Distant staging via chest, abdomen and pelvis CT scan
  • Tumour markers also provide staging and prognostic information
56
Q

What are the different stages of testicular cancer?

A
  • Stage 1 – disease is confined to the testis
  • Stage 2 – infradiaphragmatic nodes involved
  • Stage 3 – supradiaphragmatic nodes involved
  • Stage 4 – extralymphatic disease
57
Q

What is stage 1 testicular cancer?

A
  • Stage 1 – disease is confined to the testis
58
Q

What is stage 2 testicular cancer?

A
  • Stage 2 – infradiaphragmatic nodes involved
59
Q

What is stage 3 testicular cancer?

A
  • Stage 3 – supradiaphragmatic nodes involved
60
Q

What is stage 4 testicular cancer?

A
  • Stage 4 – extralymphatic disease
61
Q

What is the prognosis of testicular cancer?

A

Good if treated

62
Q

What is the treatment of testicular cancer?

A
  • Radical orchidectomy is essential
  • Occasionally may need biopsy of normal contralateral testis if high risk for tumour
  • Further treatment depends on tumour type, stage (TNM) and grade
    • Low stage, negative markers
      • Orchidectomy followed by
        • Surveillance or
        • Adjuvant radiotherapy (SGCT only) or
        • Prophylactic chemotherapy
    • Nodal disease, persistent tumour markers or relapse on surveillance
      • Combination chemotherapy (BEP) or
      • Lymph node dissection (NSGCT only)
    • Metastases
      • First line chemotherapy
      • Second line chemotherapy
63
Q

What is the further treatment of low grade testicular cancer?

A
  • Orchidectomy followed by
    • Surveillance or
    • Adjuvant radiotherapy (SGCT only) or
    • Prophylactic chemotherapy
64
Q

What is the further treatment of nodal disease, persistent tumour markers or relapse on surveillance testicular cancer?

A
  • Combination chemotherapy (BEP) or
  • Lymph node dissection (NSGCT only)
65
Q

What is the treatment for testicular cancer with metastasis?

A
  • First line chemotherapy
  • Second line chemotherapy

2A - Urinary System (30 decks)

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