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RB Y2 Renal > Prostate Cancer > Flashcards

Prostate Cancer Flashcards

1
Q

epidemiology

A
  • the most common male malignancy
  • incidence highest in the western world
  • black men at greater risk
  • 2nd highest cancer mortality
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2
Q

typical course

A
  • long history and indolent course, often not the actual cause of death
  • can often exist as a latent carcinoma and only some progress to clinically significant disease
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3
Q

at what age does it tend to occur

A

rare before 50

80% in males over 80

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4
Q

effect of family history

A

increase risk by 2-3 times

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5
Q

which gene is associated

A

BRCA2 gene

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6
Q

where is the apex of the prostate

A

inferior portion, continuous with the striated sphincter

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7
Q

where is the base of the prostate

A

superior portion, continuous with the bladder neck

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8
Q

describe the epithelial lining of the urethra

A
  • The prostatic urethra is lined by transitional epithelium.
  • Changes to stratified columnar epithelium at the membranous urethra
  • Finally stratified squamous epithelium at the tip of the penis
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9
Q

what is the verumontanum

A

a landmark near the netrance of the ejaculatory duct into the prosate

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10
Q

what are teh ejaculatory ducts formed from

A

union of the seminal vesicles and each vas deferens

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11
Q

which zone of the prostate do cancers arise in

A
  • peripheral zone
  • peri urethral zone may be affected at a later stage
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12
Q

which zone of the prostate is palpated during DRE

A

peripheral

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13
Q

spread

A
  • Local (seminal vesicles, bladder, rectum, urethral obstruction)
  • Haematogenously – bone (lumbosacral area) osteosclerotic metastases, lungs, liver
  • Lymphatic – sacral, iliac, para-aortic nodes
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14
Q

clinical presentation

A
  • the majority are asymptomatic and picked up by PSA testing and abnormal DRE findings
  • most have locally advanced or metastatic disease at presentation
  • LUT symptoms
  • haematuria/haematospermia
  • signs of metastases: bone pain, anorexia, weight loss
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15
Q

how specific is a DRE exam in detecting cancer

A

50% of those with abnormal DREs have cancer

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16
Q

how may cancer present on a DRE

A

hard, irregular prostate with nodules, and a fixed craggy mass

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17
Q

where is PSA produced from

A
  • it is a glyocprotein enzyme produced by the secretory epithelial cells of the prostate gland
  • involved in the liquefaction of semen
  • in health, semen levels are high and serum levels low
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18
Q

what is the sensitivity and specificity of PSA

A
  • sensitivity 90%
  • specificity 40%
  • 1 in 3 with a high PSA have cancer
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19
Q

role of PSA as an asympomatic blood test

A
  • not very accurate
  • even if they have prostate cancer, most will be fine and die from an unrelated cause
  • may cause needless worry
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20
Q

what also can elevate PSA

A
  • manual eg DRE, prostatitis/UTI, retention, catheter
  • long distance cycling may elevate
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21
Q

what is PSA actually useful for

A

monitoring disease progression

22
Q

imaging of prostate cancer

A

US, skeletal X ray bone scan

23
Q

indications for PSA testing

A

symptomatic patients, counselling is required before testing asymptomatic

24
Q

indications for a TRUS biopsy

A
  • abnormal DRE, elevated PSA
  • previous biopsy showing PIN or ASAP (changes in cells in prostate)
  • previous normal biopsy but rising PSA trends
  • note, it is an uncomfortable procedure
25
Q

describe the TRUS process

A
  • USS probe passed through rectum and the prostate is visualized in the transverse and sagittal sections
  • 10 biopsies taken - 5 in each lobe
26
Q

complications of TRUS biopsy

A
  • 1% risk of sepsis
  • bleeding
  • vaso vagal fainting
27
Q

what pathology are the majority of prostate cancers

A

multifocal adenocarcinomas

28
Q

where are the most common sites for metastases (and what is a characteristic feature of prostate metastases)

A
  • pelvic lymph nodes
  • skeleton - characteristic sclerotic lesions (most metastatic tumoura in the skeleton are lytic, but prostatic ones can induce bone formation)
29
Q

Gleasons scoring

A
  • a scoring system based on architectural appearance rather than cytological features
  • Gleason grade assess differentiation: 1-5 (5 is the worst and has the poorest prognosis)
  • Gleason score: the 2 most abundant cell patterns are assessed and added together to give a score out of 10
  • very good predictor of prognosis and is therefore widely used
30
Q

what are the assoicated risk levels with Gleasons scores

A
  • Low risk = <6
  • Intermediate risk = 7
  • High risk = 8-10
31
Q

TNM staging of prostate cancer

A

T-Primary Tumour

  • T1 Clinically inapparent, tumour not palpable or visible by imaging
  • T2 Tumour confined within the prostate
  • T3 Tumour extends through the prostatic capsule
  • T4 Tumour fixed or invades adjacent structures other than seminal vesicles: bladder neck, external sphincter, rectum, levator muscles or pelvic wall

N – Regional Lymph Nodes

  • N0 No regional lymph nodes metastasis
  • N1 Regional lymph nodes metastasis

M – Distant Metastasis

  • M0 N0 Distant Metastasis
  • M1 Distant Metastasis
32
Q

imaging for staging

A
  • bone scan
  • MRI
  • CT
33
Q

mangement considerations

A
  • influencing factors are category of tumour, age, co-morbiditites, life expectancy, patient preference, QOL
  • MDT approach is key
34
Q

what prognostic factors are there to be considered before management

A

PSA level, tumour grafe (Gleason), stage (TNM)

35
Q

4 options for mangement of organ confined disease

A
  • Watchful waiting/deferred treatment/symptom-guided treatment
  • Active surveillance/active monitoring
  • radical surgery
  • radical radiotherapy
36
Q

Watchful waiting/deferred treatment/symptom-guided treatment

A
  • conservative management until the development of local/systemic progression
  • palliative treatment - aims to relieve symptoms and improve QOL
  • may be used in patients who dont accept treatment related complications or those with life expectancy <10 years
37
Q

describe active surveillance/monitoring

A
  • active decision not to treat patient immediately but instead to follow with close surveillance and treat at pre-defined thresholds that classify progression (eg short PSA doubling time and deteriorating histopathological features on repeat biopsy)
  • in these cases, the treatment option would then be curative
38
Q

surgery available and complications

A
  • radical prostatectomy (whole prostate)
  • ED, incontinence, bladder neck stenosis
39
Q

how can radiotherapy be delivered to the prostate

A
  • EBRT
  • brachytherapy (insert directly into area)
40
Q

complications of radiotherapy

A
  • irritative LUTS
  • haematuria
  • GI symptoms
  • ED
  • incontinence
41
Q

role of hormonal therapy

A
  • can be given with radiotherapy
  • alone just delays tumour progression, refractory disease will eventually develop
  • can be used for those who need palliation of symptoms
42
Q

management of metastatic disease

A
  • androgen deprivation therapy
    • hormonal - LHRH analogues, anti androgens
    • bilateral orchidectomy
    • maximal androgen blockage
  • Diethylstilbestrol and steroids
  • cytotoxic chemotherapy
43
Q

what can be used for bone metastases

A

radiotherapy

44
Q

normal hormonal control of the prostate

A
  • growth of prostate cells is under the influence of testosterone and DHT
  • 90% of testosterone comes from the Leydig cells in the testis and some from the adrenal gland. secretion is regulated by the HPG axis
45
Q

mechanism behind hormonal control of prostate cancer

A

if prostate cells are deprived of androgenic stimulation they undergo apoptosis

46
Q

LHRH agonists

A
  • eg goserelin
  • chronic exposure causes a downregulation in GnRH receptors and a subsequent decrease in LH and FSH secretion and testosterone production
  • initially there is a rise in LH and FSH release called a surge/flare-up
  • this is covered by anti-androgens for one week before and 2 weeks after
47
Q

how is a LHRH agonist caused testosterone surge sometimes manifested

A

catastrophic spinal cord compression

48
Q

side effects of LHRH agonists

A
  • loss of libido
  • ED
  • hot flushes and sweats
  • weight gain
  • gynaecomastia
  • anaemia
  • osteoporosis
49
Q

anti-adrogens

A
  • compete with testosterone and DHT for binding sites on their receptors in the prostate nucleus
  • thus promoting apoptosis and inhibiting CaP growth
50
Q

steroidal anti-androgens

A
  • eg crypoterone acetate
  • Side effects - loss of libido and erectile dysfunction, gynaecomastia (rare), cardiovascular toxicity and hepatotoxicity
51
Q

non steroidal anti androgens

A
  • (nilutamide, flutamide and bicalutamide)
  • Sexual interest and libido maintained
  • Side effects - gynaecomastia, breast pain and hot flashes, hepatotoxicity

RB Y2 Renal (26 decks)

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