Renal & Urology Cancer Flashcards

(84 cards)

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
How are results of Multiparametric MRI reported? Outline what this means
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.
26
Complications of TRUS biopsy:
sepsis: 1% of cases pain: lasting >= 2 weeks in 15% and severe in 7% fever: 5% haematuria and rectal bleeding
27
What is PSA?
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.
28
When should men be referred in prostate cancer
men aged 50-69 years should be referred if the PSA is >= 3.0 ng/ml OR there is an abnormal DRE
29
After prostatitis and urinary tract infection NICE recommend to postpone the PSA test for at least?
1 month after treatment
30
Describe sensitivity & specificity of PSA?
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)
31
*whether digital rectal examination actually causes a rise in PSA levels is a matter of debate
true
32
Describe histopathology of PC?
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.
33
How is PC graded? Describe
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.
34
In PC lymphatic spread occurs where?
first to the obturator nodes spread to the seminal vesicles is associated with distant disease.
35
In PC when would you watch and wait'?
Elderly, multiple co-morbidities, low Gleason score
36
What stage is localised PC? How would you treat this?
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
What stage is localised ADVANCED PC? How would you treat this?
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
What hormonal therapy could you use in PC?
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
Why is hormonal therapy used in PC?
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
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
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
Candidates for active surveillance should (PC)
have had at least 10 biopsy cores taken | have at least one re-biopsy.
42
If men on active surveillance show evidence of disease progression, offer ? (PC)
offer radical treatment. Treatment decisions should be made with the man, taking into account co-morbidities and life expectancy.
43
Testicular cancer is the most common malignancy in men aged 20-30 years
true
44
How do you categorise testicular cancer?
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
The peak incidence for teratomas is
25yrs
46
The peak incidence for seminomas is
35yrs
47
risk factors for testicular cancer
``` infertility (increases risk by a factor of 3) cryptorchidism family history Klinefelter's syndrome mumps orchitis ```
48
Testicular cancer usually is a painless lump
yes a painless lump is the most common presenting symptom pain may also be present in a minority of men
49
Other than painless lump, how else might testicular cancer present
hydrocele | gynaecomastia
50
Why do you get gynaecomastia in testicular cancer?
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
Describe bloods in germ cell tumours
AFP is elevated in around 60% of germ cell tumours | LDH is elevated in around 40% of germ cell tumours
52
Describe bloods in seminomas
hCG may be elevated in around 20%
53
Diagnosis testicular cancer?
US
54
Management testicular cancer?
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
Prognosis testicular cancer?
5 year survival for seminomas is around 95% if Stage I | 5 year survival for teratomas is around 85% if Stage I
56
Risk factors for transitional cell carcinoma of the bladder include:
Smoking Exposure to aniline dyes in the printing and textile industry: examples are 2-naphthylamine and benzidine Rubber manufacture Cyclophosphamide
57
Risk factors for squamous cell carcinoma of the bladder include:
Schistosomiasis | Smoking
58
Bladder cancer is the second most common urological cancer. It most commonly affects males aged between
50 and 80 years of age.
59
Those who are current, or previous (within 20 years), smokers have a 2-5 fold increased risk of bladder cancer
true
60
Exposure to hydrocarbons such as 2-Naphthylamine increases the risk of bladder cancer
true
61
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.
true
62
Which lymph nodes are in the true pelvis
hypogastric, obturator, external iliac, or presacral lymph node
63
What are the types of bladder cancer?
Transitional cell carcinoma (>90% of cases) Squamous cell carcinoma ( 1-7% -except in regions affected by schistosomiasis) Adenocarcinoma (2%)
64
Describe the typical growth of TCC
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
Bladder cancer - describe T part of TNM
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
Bladder cancer - describe N part of TNM
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
Bladder cancer - describe M part of TNM
M0 No distant metastasis | M1 Distant disease
68
bladder cancer - Those with T3 disease or worse have a 30% (or higher) risk of regional or distant lymph node metastasis.
true
69
Describe typical presentation of bladder cancer?
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
Describe how bladder cancer is investigated?
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
Describe treatment of bladder cancer?
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
Describe prognosis of bladder cancer
``` T1 90% T2 60% T3 35% T4a 10-25% Any T, N1-N2 30% ```
73
Nephroblastoma (Wilm's tumours) | Usually present in
first 4 years of life
74
Nephroblastoma presents
May often present as a mass associated with haematuria (pyrexia may occur in 50%) Often metastasise early (usually to lung)
75
mx nephroblastoma
nephrectomy
76
Prognosis nephroblastoma
Younger children have better prognosis (<1 year of age =80% overall 5 year survival)
77
Tumour markes in seminoma
AFP usually normal HCG elevated in 10% seminomas Lactate dehydrogenase; elevated in 10-20% seminomas (but also in many other conditions)
78
Pathology seminoma
Sheet like lobular patterns of cells with substantial fibrous component. Fibrous septa contain lymphocytic inclusions and granulomas may be seen.
79
Non seminomatous germ cell tumours markers?
AFP elevated in up to 70% of cases HCG elevated in up to 40% of cases Other markers rarely helpful
80
Pathology non eminomatous germ cell tumours?
Heterogenous texture with occasional ectopic tissue such as hair
81
Tyoes of Non seminomatous germ cell tumours
``` Non seminomatous germ cell tumours (42%) Teratoma Yolk sac tumour Choriocarcinoma Mixed germ cell tumours (10%) ```
82
seminoma is a type of germ cell tumour
true
83
Key features of seminoma
``` Commonest subtype (50%) Average age at diagnosis = 40 Even advanced disease associated with 5 year survival of 73% ```
84
Key features of Non seminomatous germ cell tumours
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