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
describe the TRUS process
* USS probe passed through rectum and the prostate is visualized in the transverse and sagittal sections * 10 biopsies taken - 5 in each lobe
26
complications of TRUS biopsy
* 1% risk of sepsis * bleeding * vaso vagal fainting
27
what pathology are the majority of prostate cancers
multifocal adenocarcinomas
28
where are the most common sites for metastases (and what is a characteristic feature of prostate metastases)
* pelvic lymph nodes * skeleton - characteristic sclerotic lesions (most metastatic tumoura in the skeleton are lytic, but prostatic ones can induce bone formation)
29
Gleasons scoring
* 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
what are the assoicated risk levels with Gleasons scores
* Low risk = \<6 * Intermediate risk = 7 * High risk = 8-10
31
TNM staging of prostate cancer
**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
imaging for staging
* bone scan * MRI * CT
33
mangement considerations
* influencing factors are category of tumour, age, co-morbiditites, life expectancy, patient preference, QOL * MDT approach is key
34
what prognostic factors are there to be considered before management
PSA level, tumour grafe (Gleason), stage (TNM)
35
4 options for mangement of organ confined disease
* Watchful waiting/deferred treatment/symptom-guided treatment * Active surveillance/active monitoring * radical surgery * radical radiotherapy
36
Watchful waiting/deferred treatment/symptom-guided treatment
* 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
describe active surveillance/monitoring
* 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
surgery available and complications
* radical prostatectomy (whole prostate) * ED, incontinence, bladder neck stenosis
39
how can radiotherapy be delivered to the prostate
* EBRT * brachytherapy (insert directly into area)
40
complications of radiotherapy
* irritative LUTS * haematuria * GI symptoms * ED * incontinence
41
role of hormonal therapy
* 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
management of metastatic disease
* androgen deprivation therapy * hormonal - LHRH analogues, anti androgens * bilateral orchidectomy * maximal androgen blockage * Diethylstilbestrol and steroids * cytotoxic chemotherapy
43
what can be used for bone metastases
radiotherapy
44
normal hormonal control of the prostate
* 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
mechanism behind hormonal control of prostate cancer
if prostate cells are deprived of androgenic stimulation they undergo apoptosis
46
LHRH agonists
* 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
how is a LHRH agonist caused testosterone surge sometimes manifested
catastrophic spinal cord compression
48
side effects of LHRH agonists
* loss of libido * ED * hot flushes and sweats * weight gain * gynaecomastia * anaemia * osteoporosis
49
anti-adrogens
* compete with testosterone and DHT for binding sites on their receptors in the prostate nucleus * thus promoting apoptosis and inhibiting CaP growth
50
steroidal anti-androgens
* eg crypoterone acetate * *Side effects -* loss of libido and erectile dysfunction, gynaecomastia (rare), cardiovascular toxicity and hepatotoxicity
51
non steroidal anti androgens
* (nilutamide, flutamide and bicalutamide) * Sexual interest and libido maintained * *Side effects -* gynaecomastia, breast pain and hot flashes, hepatotoxicity