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Urinary System > Lecture 16: Tumours of the Urinary System > Flashcards

Lecture 16: Tumours of the Urinary System Flashcards

1
Q

what is the most common cancer diagnosed in men?

A

prostate cancer
- 14% of cancer deaths in men, 2nd commonest

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2
Q

prostate cancer non-modifiable and modifiable risk factors

A

Non modifiable risk factors:
- african ethnicity
- BRCA gene mutations
- Lynch sybdrine (HNPCC)
- family history of prostate cancer
- age (risk increases with advancing age)

Modifiable risk factors:
- obesity
- smoking
- diet rich in animal fats and dairy products (low evidence)

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3
Q

which of McNeal’s prostatic zones are usually affected by prostate cancer?

A

peripheral zone

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4
Q

what % of newly diagnosed prostate cancers are localised?

A

80%
- mostly asymptomatic
- diagnosed through opportunistic ad hoc PSA testing

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5
Q

signs and symptoms of prostate cancer

A

In its early stages, prostate cancer often produces no symptoms as it affects the peripheral prostate. However, as the disease progresses with local advancement (which can cause compression of the urethra), symptoms may include:

  • Urinary symptoms, including difficulty initiating or stopping urination
  • Poor urine stream
  • Haematospermia (blood in semen)
  • Pelvic discomfort
  • Bone pain, potentially indicating metastatic disease
  • Erectile dysfunction
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6
Q
A

b

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7
Q

what are the upper limits of normal for PSA dependant on age?

A

Age-specific range; levels increase 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
>70 years: 6.5 is upper limit

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8
Q

what factors can cause elevations in PSA?

A
  • UTI
  • chronic prostatitis
  • instrumentation (e.g. catheterisation)
  • physiological (e.g. recent ejaculation)
  • recent urological procedure
  • BPH
  • prostate cancer
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9
Q

how can we differentiate between a transient vs persistent rise in PSA?

A

recheck PSA in at least 3 weeks (i.e. 8 half-lives)

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10
Q

what are the % probabilities of cancer based on PSA levels?

A

0-1: 5%
1-2.5: 15%
2.5-4: 25%
4-10: 40%
greater than 10: 70%

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11
Q

prostate cancer investigations

A
  • digital rectal examination and a urine dip test.
  • PSA blood test
  • multi-parametric MRI: shows specific areas which can be targetted for biopsy.
  • if metastatic disease is suspected: CT scans and bone isotope scans may be required.
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12
Q

what score is the grading for prostate cancer based upon?

describe it

A

Gleason sum score
- involves analysing the morphological features of prostatic tissue and assigning a score from 1 (normal tissue) to 5 (very poorly differentiated cells)
- the sum of the two most common scores represents the Gleason score, which has prognostic value: 3 + 4 = 7

Grading is the assessment of the aggressiveness, based on histology

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13
Q

what is the risk of death within 15 years from prostate cancer with a Gleason score of 6?

A

4-30%

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14
Q

what is the risk of death within 15 years from prostate cancer with a Gleason score of 7?

A

42-70%

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15
Q

what is the risk of death within 15 years from prostate cancer with a Gleason score of 8-10?

A

60-87%

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16
Q

describe the staging of localised prostate cancer by DRE

A
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17
Q

for the purposed of treatment and prognosis, it is useful to divide prostate cancer into which 4 clinical stages?

A
  • localised stage
  • locally advanced stage
  • metastatic stage
  • castrate-resistant/hormone-refractory stage
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18
Q

what risk classification is used for the localised disease stage of prostate cancer?

A

D’Amico risk classification

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19
Q

what is the treatment for localised prostate cancer (T1-T2c)?

A

T1:
- active surveillance (for low-risk cases)
- watchful waiting
- radical prostatectomy (for selected cases)

T2:
- radical prostatectomy (standard treatment)
- external beam radiation therapy
- brachytherapy (seed implantation)
- active surveillance (for low-risk cases)

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20
Q

what is the treatment for locally advanced prostate cancer (T3-4N0M0)?

A
  • watchful waiting
  • hormone therapy (to slow progression) followed by radical prostatectomy
  • hormone therapy followed by radiation
  • hormone therapy alone (palliative, delays progression)
  • intermitted hormone therapy (clinical research)
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21
Q

describe the types of hormonal therapy used for prostate cancer

A
  • chemical castration (i.e. LHRH analogue - goserelin, leuprorelin; or LHRH antagonists e.g. Degarelix). LHRH analogues cause a tumour flare in 1st week of therapy (need to use anti-androgen during this period).
  • anti-androgens (e.g. bicalutamide, flutamide, cyproterone acetate) > not effective on its own; must be used with LHRH analogue.
  • Oestrogens (i.e. diethylstilboestrol)
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22
Q

what are the complications of metastatic and hormone refractory prostate cancer?

bone, rectal, ureteric, lymphatic, lower urinary tract

A
  • bone: pain, pathological fractures, anaemia, spinal cord compression
  • rectal: constipation, bowel obstruction
  • ureteric: obstruction resulting in renal failure
  • pelvic lymphatic obstruction: lymphoedema, DVT
  • lower urinary tract dysfunction: haematuria, acute urinary retention
23
Q

what is the treatment for metastatic and hormone refractory prostate cancer?

A
  • immediate hormonal therapy is standard of treatment for metastatic prostate cancer, + docetaxel chemotherapy in fit patients or targeted theraoues like abiraterone, enzalutamide.
  • supportive treatment e.g. palliative radiotherapy to bony metastases, nephrostomy, zoledronic acid, palliative care support etc.
  • hormone refractory: continuing HT combined with docetaxel, abiraterone or enzalutamide if not already given; or other alternative chemo drugs, diethylstilboestrol can be tried
24
Q
A

e

25
Q
A

b

26
Q

testicular cancer signs and symptoms

A
  • primary clinical manifestation is a painless lump in the scrotum.
  • germ cell tumours may be hormone-producing and can increase the oestrogen;androgen ratio, resulting in gynaecomastia.
  • symptoms/signs from nodal or distant metastasis: para-aortic lymph nodes, chest, bone
27
Q

testicular cancer risk factors

A
  • age under 45 years
  • caucasian
  • previous history of testicular cancer
  • cryptorchidism (undescended testicles)
  • HIV infection
  • previous mumps orchitis infection
  • Klinefelter’s syndrome
28
Q

testicular cancer differential diagnoses

A
  • infection i.e. epididymo-orchitis
  • epididymal cyst
  • missed testicular torsion
29
Q

testicular cancer investigations

A
  • if they have a non-painful enlargement or change in shape or texture of the testis then 2 week wait referral
  • MSSU
  • scrotal US first-line
  • serum tumour markers: alpha-fetoprotein (AFP, teratoma), hCG (seminoma), and lactate dehydrogenase (LDH)
  • further imaging if there are concerns about metastatic spread: CT TAP (thorax, abdomen, pelvis)
30
Q

outline the management of testicular cancer

A

multi-modality approach:
- radical orchidectomy: removal of affected testicle, usually initial step.
- radiotherapy
- chemotherapy: used as adjuvant therapy for advanced disease, with cisplatin-based regimens being the most effective.

31
Q

for testicular cancer, the main lymphatic spread to regional lymph nodes occurs in which group of lymph nodes?

A

para-aortic lymph nodes

32
Q

when performing radical inguinal orchidectomy for testicular cancer, where is the incision made and why?

A
  • using an inguinal incision centred over the inguinal canal is essential, as a diagnostic procedure (i.e. to obtain tissue for histology) and therapeutic procedure (may potentially be cured by surgery alone)0.
33
Q

describe the types of germ cell tumour (GCT) accounting for 95% of testicular cancer pathology

A
  • seminomatous GCT (classical, spermatocytic, or anaplastic) mainly affect 30-40y/o
  • non-seminomatous GCT (teratome, yolk sac, choriocarcinoma, mixed GCT) mainly affect 20-30 y/o
34
Q

describe types of non-GCT accounting for 5% of testicular cancer pathology

A

sex cord/ stromal cells
- Leydig
- Sertoli
- Lymphoma rare (usually in older men)

35
Q

describe the classification criteria of testicular cancer from stage 1-4

A
  • stage 1: disease confined to testis
  • stage 2: infra-diaphragmatic para-aortic lymph nodes involved
  • stage 3: supra-diaphragmatic para-aortic lymph nodes involved
  • stage 4: extra-lymphatic disease i.e. involving solid organs e.g. lungs, liver, bone etc.
36
Q

bladder cancer pathology

A
  • the tumour type is most often transitional cell carcinoma (i.e. 90% in UK)
  • where schistosomiasis is endemic, squamous cell carcinoma of the bladder is the most common type
37
Q

bladder cancer risk factors based on histological subtype

A

transitional cell carcinoma:
- smoking
- exposure to aromatic amines (employed in rubber, dyes and chemical industry)
- use of cyclophosphamide

squamous cell carcinoma:
- schistosomiasis infection
- chronic cystitis (e.g. recurrent UTI, long term catheterisation 10+ years, bladder stone
- cyclophosphamide therapy
- pelvic radiotherapy

38
Q

bladder cancer clinical presentation

A
  • painless visible haematuira (most common), can be frank or microscopic
  • occasionally symptoms due to invasive or metastatic disease
  • recurrent UTI
  • storage bladder symptoms: dysuria, frequency, nocturia, urgency +/- urge incontinence, bladder pain
39
Q

what investigations are performed in a patient presenting with haematuria?

potential bladder cancer

A
  • urine dipstick test
  • urine culture
  • CT urogram: identifies filling defects indicating a tumour
  • US
  • flexible cytoscopy: allows for visualisation of any defects in the bladder and the morphology of any suspicious lesion. If a lesion is identified a biopsy can be taken.
40
Q

risk of malignancy in > 50y/o with frank haematuria?

A

25-35%

41
Q

risk of malignancy in > 50y/o with dipstix or microscopic haematuria?

A

5-10%

42
Q

non-muscle invasive bladder cancer treatment (CIS, Ta, T1)

A
  • surgery: transurethral resection of the bladder tumour (TURBT) is gold-standard
  • chemotherapy: e.g. mitomycin C
  • immunotherapy: BCG immunotherapy for high-risk non-muscle invasice cancers of carcinoma in situ (CIS)
  • radical cystectomy may be considered for CIS
43
Q

muscle invasive bladder cancer treatment (T2 and above)

A
  • radical cystectomy with urinary diversion is gold-standard: options include an ileal conduit, neo-bladder, or Mitrofanoff procedure
  • radiotherapy and chemotherapy: can be curative and palliative
44
Q

upper tract TCC or upper tract urothelial cancer UTUC presenting features

A
  • frank haematuria
  • unilateral ureteric obstruction
  • flank or loin pain
  • symptoms of nodal or metastatic disease: e.g. bone pain, hypercalcaemia, lung, brain
45
Q

upper tract urothelial cancer (UTUC) diagnostic investigations

A

CT-IVU or IVU
urine cytology
ureteroscopy and biopsy

46
Q

what area of the upper urinary tract is most commonly affected in TCC?

A

renal pelvis

47
Q

upper tract TCCs treatment

A
  • nephro-ureterectomy
  • if unfit for above, or bilateral disease: nephron-sparing endoscopic treatment (i.e. ureteroscopic laser ablation); needs regular surveillance ureteroscopy
  • all cases need surveillance cytoscopy dueto dive risk of reocurrence
48
Q

give examples of benign renal tumours

A

onocytoma
angiomyolipoma

49
Q

most common renal cancer?

A

renal adenocarcinoma
- most arise from proximal tubules

50
Q

what are the histological subtypes of renal adenocarcinoma

A
  • clear cell (85%)
  • papillary (10%)
  • chromophobe (4%)
  • bellini type ductal carcinoma (1%)
51
Q

renal adenocarcinoma risk factors

A
  • family history: autosomal dominany e.g. vHL, familial clear cell RCC, hereditary papillary RCC; can be bilateral and/or multifocal
  • smoking
  • anti-hypertensive medication
  • obesity
  • end-stage renal failure
  • acquired renal cystic disease
52
Q

renal adenocarcinoma presentation

A
  • asymptomatic 50%
  • ‘classic triad’ of flank pain, mass and haematuria: 10%
  • paraneoplastic syndrome: 30% - anorexia, cachexia, purexia, hypertension, hypercalcaemia, abnormal LFTs, anaemia, polycythaemia and raised ESR
  • metastatic disease: 30% - bone, brain, lungs, liver
53
Q

renal adenocarcinoma investigations

A
  • CT scan (triple phase) of abdomen and chest is mandatory: provides radiological diagnosis and complete TNM staging, assesses contralateral kidney
  • bloods: U&Es, FBC
  • optional tests: US differentiates tumour from cyst, DMSA or MAG-3 renogram to assess split renal function if doubts about contralateral kidney
54
Q

renal adenocarcinoma treatment

A

Surgical i.e. radical nephrectomy:
- laparoscopic radical nephrectomy is standard of care for T1 tumours
- worthwhile even with majour venous invasion
- curative is </- T2

metastases - little effective treatment since RCC is radioresistant and chemoresistant
- multitargeted receptor tyrosine kinase inhibitors e.g. sunitinib, sorafenib, panzopanib, temsirolimus
- immunotherapy: interferon alpha, interleukin-1

Urinary System (21 decks)

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