Renal & Urology Cancer Flashcards

1
Q

Renal cell cancer is also known as

A

hypernephroma

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2
Q

Renal cell cancer accounts for 85% of primary renal neoplasms.

A

true

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3
Q

Renal cell cancer arises from?

A

proximal renal tubular epithelium.

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4
Q

Most common subtype of renal cell cancer?

A

clear cell (75 to 85 percent of tumours).

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5
Q

Associations for renal cell cancer?

A

more common in middle-aged men
smoking
von Hippel-Lindau syndrome
tuberous sclerosis

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6
Q

Classical triad of renal cell cancer?

A

haematuria, loin pain, abdominal mass

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7
Q

Why might RCC present with left varicocele?

A

due to occlusion of left testicular vein

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8
Q

RCC never presents with pyrexia

A

false

pyrexia of unknown origin

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9
Q

endocrine effects of rcc?

A

may secrete erythropoietin (polycythaemia), parathyroid hormone (hypercalcaemia), renin, ACTH

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10
Q

in rcc ?% have metastases at presentation

A

25%

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11
Q

What is paraneoplastic hepatic dysfunction syndrome? why does it arise?

A

Typically presents as cholestasis/hepatosplenomegaly. It is thought to be secondary to increased levels of IL-6

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12
Q

rcc is associated with Stauffer syndrome

A

true

another name for paraneoplastic hepatic dysfunction syndrome

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13
Q

Outline management for rcc

A

for confined disease a partial or total nephrectomy depending on the tumour size

tyrosine kinase inhibitors (e.g. sorafenib, sunitinib) and interleukin-2 have been used to reduce tumour size and also treat patients with metatases

receptor tyrosine kinase inhibitors (e.g. sorafenib, sunitinib) have been shown to have superior efficacy compared to interferon-alpha

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14
Q

Prostate cancer a common condition and up to 30,000 men are diagnosed with the condition each year.

A

true

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15
Q

Up to 9,000 will die in the UK from prostate cancer per year.

A

true

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16
Q

Early prostate cancers have few symptoms.

A

true

Locally advanced disease may present as pelvic pain or with urinary symptoms.

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17
Q

prostate cancer mets may present as bone pain

A

true

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18
Q

What tests would you do prostate cancer?

A

Prostate specific antigen measurement
Digital rectal examination
Trans rectal USS (+/- biopsy)
MRI/ CT and bone scan for staging.

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19
Q

The normal upper limit for PSA is

A

4ng/ml

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20
Q

Why might PSA be raised? What is an alternative?

A

False positives may be due to prostatitis, UTI, BPH, vigorous DRE.

The percentage of free: total PSA may help to distinguish benign disease from cancer.

Values of <20% are suggestive of cancer and biopsy is advised.

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21
Q

risk factors for prostate canceR?

A

increasing age
obesity
Afro-Caribbean ethnicity
family history: around 5-10% of cases have a strong family history

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22
Q

wHY is prostate cancer (localised) often asymptomatic?

A

partly because cancers tend to develop in the periphery of the prostate and hence don’t cause obstructive symptoms early on.

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23
Q

Features of PC & DRE?

A

bladder outlet obstruction: hesitancy, urinary retention
haematuria, haematospermia
pain: back, perineal or testicular
digital rectal examination: asymmetrical, hard, nodular enlargement with loss of median sulcus

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24
Q

Prostate cancer investigations - NICE have now advocated the increasing use of what first line?

A

multiparametric MRI as a first-line investigation.

replaced trus biopsy

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25
Q

How are results of Multiparametric MRI reported? Outline what this means

A

5‑point Likert scale

If the Likert scale is >=3 a multiparametric MRI-influenced prostate biopsy is offered

If the Likert scale is 1-2 then NICE recommend discussing with the patient the pros and cons of having a biopsy.

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26
Q

Complications of TRUS biopsy:

A

sepsis: 1% of cases
pain: lasting >= 2 weeks in 15% and severe in 7%
fever: 5%
haematuria and rectal bleeding

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27
Q

What is PSA?

A

serine protease enzyme produced by normal and malignant prostate epithelial cells. It has become an important tumour marker but much controversy still exists regarding its usefulness as a screening tool.

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28
Q

When should men be referred in prostate cancer

A

men aged 50-69 years should be referred if the PSA is >= 3.0 ng/ml OR there is an abnormal DRE

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29
Q

After prostatitis and urinary tract infection NICE recommend to postpone the PSA test for at least?

A

1 month after treatment

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30
Q

Describe sensitivity & specificity of PSA?

A

PSA of 4-10 ng/ml 33% will be found to have prostate cancer.
PSA of 10-20 ng/ml this rises to 60%

around 20% with prostate cancer have a normal PSA

various methods are used to try and add greater meaning to a PSA level including age-adjusted upper limits and monitoring change in PSA level with time (PSA velocity or PSA doubling time)

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31
Q

*whether digital rectal examination actually causes a rise in PSA levels is a matter of debate

A

true

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32
Q

Describe histopathology of PC?

A

95% adenocarcinoma. Often multifocal- 70% lie in the peripheral zone.

In situ malignancy is sometimes found in areas adjacent to cancer. Multiple biopsies needed to call true in situ disease.

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33
Q

How is PC graded? Describe

A

Graded using the Gleason grading system

2 is best prognosis and 10 the worst.

Grades awarded for most dominant grade (on scale of 1-5)
and also for second most dominant grade (scale 1-5).

The two added together give the Gleason score.

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34
Q

In PC lymphatic spread occurs where?

A

first to the obturator nodes

spread to the seminal vesicles is associated with distant disease.

35
Q

In PC when would you watch and wait’?

A

Elderly, multiple co-morbidities, low Gleason score

36
Q

What stage is localised PC? How would you treat this?

A

t1/t2
Treatment depends on life expectancy and patient choice. Options include:
conservative: active monitoring & watchful waiting
radical prostatectomy
radiotherapy: external beam and brachytherapy

37
Q

What stage is localised ADVANCED PC? How would you treat this?

A

T3/T4)
hormonal therapy
radical prostatectomy: erectile dysfunction is a common complication
radiotherapy: external beam and brachytherapy. Patients are at increased risk of bladder, colon, and rectal cancer following radiotherapy for prostate cancer

38
Q

What hormonal therapy could you use in PC?

A

Synthetic GnRH agonist e.g. Goserelin (Zoladex) - cover initially with anti-androgen to prevent rise in testosterone

Anti-androgen: Cyproterone Acetate prevents DHT binding from intracytoplasmic protein complexes

Orchidectomy

39
Q

Why is hormonal therapy used in PC?

A

Testosterone stimulates prostate tissue and prostatic cancers usually show some degree of testosterone dependence.

95% of testosterone is derived from the testis and bilateral orchidectomy may be used for this reason.

Pharmacological alternatives include LHRH analogues and anti androgens (which may be given in combination).

40
Q

In the UK the National Institute for Clinical Excellence (NICE) suggests that active surveillance is the preferred option for low risk men in PC. when is this suitable

A

clinical stage T1c
Gleason score 3+3
PSA density < 0.15 ng/ml/ml
Those who have cancer in less than 50% of their biopsy cores, with < 10 mm of any core involved.

41
Q

Candidates for active surveillance should (PC)

A

have had at least 10 biopsy cores taken

have at least one re-biopsy.

42
Q

If men on active surveillance show evidence of disease progression, offer ? (PC)

A

offer radical treatment. Treatment decisions should be made with the man, taking into account co-morbidities and life expectancy.

43
Q

Testicular cancer is the most common malignancy in men aged 20-30 years

A

true

44
Q

How do you categorise testicular cancer?

A

95% of cases of testicular cancer are germ-cell tumours. Germ cell tumours may essentially be divided into:

  1. seminomas
  2. non-seminomas: including embryonal, yolk sac, teratoma and choriocarcinoma

Non-germ cell tumours include Leydig cell tumours and sarcomas.

45
Q

The peak incidence for teratomas is

A

25yrs

46
Q

The peak incidence for seminomas is

A

35yrs

47
Q

risk factors for testicular cancer

A
infertility (increases risk by a factor of 3)
cryptorchidism
family history
Klinefelter's syndrome
mumps orchitis
48
Q

Testicular cancer usually is a painless lump

A

yes
a painless lump is the most common presenting symptom
pain may also be present in a minority of men

49
Q

Other than painless lump, how else might testicular cancer present

A

hydrocele

gynaecomastia

50
Q

Why do you get gynaecomastia in testicular cancer?

A

this occurs due to an increased oestrogen:androgen ratio

germ-cell tumours → hCG → Leydig cell dysfunction → increases in both oestradiol and testosterone production, but rise in oestradiol is relatively greater than testosterone

leydig cell tumours → directly secrete more oestradiol and convert additional androgen precursors to oestrogens

51
Q

Describe bloods in germ cell tumours

A

AFP is elevated in around 60% of germ cell tumours

LDH is elevated in around 40% of germ cell tumours

52
Q

Describe bloods in seminomas

A

hCG may be elevated in around 20%

53
Q

Diagnosis testicular cancer?

A

US

54
Q

Management testicular cancer?

A

treatment depends on whether the tumour is a seminoma or a non-seminoma
orchidectomy
chemotherapy and radiotherapy may be given depending on staging and tumour type

55
Q

Prognosis testicular cancer?

A

5 year survival for seminomas is around 95% if Stage I

5 year survival for teratomas is around 85% if Stage I

56
Q

Risk factors for transitional cell carcinoma of the bladder include:

A

Smoking
Exposure to aniline dyes in the printing and textile industry: examples are 2-naphthylamine and benzidine
Rubber manufacture
Cyclophosphamide

57
Q

Risk factors for squamous cell carcinoma of the bladder include:

A

Schistosomiasis

Smoking

58
Q

Bladder cancer is the second most common urological cancer. It most commonly affects males aged between

A

50 and 80 years of age.

59
Q

Those who are current, or previous (within 20 years), smokers have a 2-5 fold increased risk of bladder cancer

A

true

60
Q

Exposure to hydrocarbons such as 2-Naphthylamine increases the risk of bladder cancer

A

true

61
Q

Although rare in the UK, chronic bladder inflammation arising from Schistosomiasis infection remains a common cause of squamous cell carcinomas, in those countries where the disease is endemic.

A

true

62
Q

Which lymph nodes are in the true pelvis

A

hypogastric, obturator, external iliac, or presacral lymph node

63
Q

What are the types of bladder cancer?

A

Transitional cell carcinoma (>90% of cases)
Squamous cell carcinoma ( 1-7% -except in regions affected by schistosomiasis)
Adenocarcinoma (2%)

64
Q

Describe the typical growth of TCC

A

may arise as solitary lesions, or may be multifocal, owing to the effect of ‘field change’ within the urothelium.

Up to 70% of TCC’s will have a papillary growth pattern.
These tumours are usually superficial in location and accordingly have a better prognosis.

The remaining tumours show either mixed papillary and solid growth or pure solid growths. These tumours are typically more prone to local invasion and may be of higher grade, the prognosis is therefore worse.

65
Q

Bladder cancer - describe T part of TNM

A

T0 No evidence of tumour
Ta Non invasive papillary carcinoma
T1 Tumour invades sub epithelial connective tissue
T2a Tumor invades superficial muscularis propria (inner half)
T2b Tumor invades deep muscularis propria (outer half)
T3 Tumour extends to perivesical fat
T4 Tumor invades any of the following: prostatic stroma, seminal vesicles, uterus, vagina
T4a Invasion of uterus, prostate or bowel
T4b Invasion of pelvic sidewall or abdominal wall

66
Q

Bladder cancer - describe N part of TNM

A

N0 No nodal disease
N1 Single regional lymph node metastasis in the true pelvis
N2 Multiple regional lymph node metastasis in the true pelvis N3 Lymph node metastasis to the common iliac lymph nodes

Lymph nodes in true pelvis: hypogastric, obturator, external iliac, or presacral lymph node metastasis

67
Q

Bladder cancer - describe M part of TNM

A

M0 No distant metastasis

M1 Distant disease

68
Q

bladder cancer - Those with T3 disease or worse have a 30% (or higher) risk of regional or distant lymph node metastasis.

A

true

69
Q

Describe typical presentation of bladder cancer?

A

Most patients (85%) will present with painless, macroscopic haematuria.

In those patients with incidental microscopic haematuria, up to 10% of females aged over 50 will be found to have a malignancy (once infection excluded).

70
Q

Describe how bladder cancer is investigated?

A

Most will undergo a cystoscopy and biopsies or TURBT, this provides histological diagnosis and information relating to depth of invasion.

Locoregional spread is best determined using pelvic MRI and distant disease CT scanning. Nodes of uncertain significance may be investigated using PET CT.

71
Q

Describe treatment of bladder cancer?

A

Those with superficial lesions may be managed using TURBT in isolation.

Those with recurrences or higher grade/ risk on histology may be offered intravesical chemotherapy.

Those with T2 disease are usually offered either surgery (radical cystectomy and ileal conduit) or radical radiotherapy.

72
Q

Describe prognosis of bladder cancer

A
T1	90%
T2	60%
T3	35%
T4a	10-25%
Any T, N1-N2	30%
73
Q

Nephroblastoma (Wilm’s tumours)

Usually present in

A

first 4 years of life

74
Q

Nephroblastoma presents

A

May often present as a mass associated with haematuria (pyrexia may occur in 50%)
Often metastasise early (usually to lung)

75
Q

mx nephroblastoma

A

nephrectomy

76
Q

Prognosis nephroblastoma

A

Younger children have better prognosis (<1 year of age =80% overall 5 year survival)

77
Q

Tumour markes in seminoma

A

AFP usually normal
HCG elevated in 10% seminomas
Lactate dehydrogenase; elevated in 10-20% seminomas (but also in many other conditions)

78
Q

Pathology seminoma

A

Sheet like lobular patterns of cells with substantial fibrous component. Fibrous septa contain lymphocytic inclusions and granulomas may be seen.

79
Q

Non seminomatous germ cell tumours markers?

A

AFP elevated in up to 70% of cases
HCG elevated in up to 40% of cases
Other markers rarely helpful

80
Q

Pathology non eminomatous germ cell tumours?

A

Heterogenous texture with occasional ectopic tissue such as hair

81
Q

Tyoes of Non seminomatous germ cell tumours

A
Non seminomatous germ cell tumours (42%)
Teratoma
Yolk sac tumour
Choriocarcinoma
Mixed germ cell tumours (10%)
82
Q

seminoma is a type of germ cell tumour

A

true

83
Q

Key features of seminoma

A
Commonest subtype (50%)
Average age at diagnosis = 40
Even advanced disease associated with 5 year survival of 73%
84
Q

Key features of Non seminomatous germ cell tumours

A

Younger age at presentation =20-30 years
Advanced disease carries worse prognosis (48% at 5 years)
Retroperitoneal lymph node dissection may be needed for residual disease after chemotherap