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RDS Test 3 > B8.048 Prework 2: Evaluation and Treatment of Prostate Cancer > Flashcards

B8.048 Prework 2: Evaluation and Treatment of Prostate Cancer Flashcards

1
Q

incidence of prostate cancer

A

1 in 9 men will be diagnosed

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2
Q

prostate cancer mortality

A

1 in 41 men will die of prostate cancer

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3
Q

risk factors for prostate cancer

A

age
race
family history
familial cancer syndromes

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4
Q

impact of race on prostate cancer risk

A

AA men

  • 1.6x incidence
  • 2.4x mortality
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5
Q

impact of family history on prostate cancer risk

A

father or brother: 2-3x incidence

2 first degree males: 5x increased incidence

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6
Q

impact of familial cancer syndrome on prostate cancer risk

A

BRCA 1/2: 4.5-8.6x incidence

Lynch: 10x incidence

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7
Q

signs of prostate cancer

A

most often: NONE

sometimes:
- prostate nodule

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8
Q

symptoms of prostate cancer

A 
most often: NONE
sometimes:
-obstructive urinary symptoms
-hematuria
-pain
-weight loss
-fatigue
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9
Q

biology of prostate cancer

A

hormonal cancer

LHRH from hypothalamus > LH from pituitary > T from Leydig cells + T from adrenal gland

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10
Q

impact of T on prostate cells

A

converted to DHT
DHT binds to androgen receptor (AR) > AR dimerizes and translocates into nucleus> AR binds to DNA > increased PSA, increased growth, increased survival of the cell

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11
Q

grade groups of prostate cancer

A

1: gleason 3+3
2: gleason 3+4
3: gleason 4+3
4: gleason 8
5: gleason 9-10
* *correlates to risk of recurrence after treatment

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12
Q

clinical staging of prostate cancer

A

all based on DRE
if you can feel it: it is a higher stage (T2-T4)
T1 = not palpable
T2 = palpable within prostate
T3 = extraprostatic tmor that is not fixed or does not invase adjacent structures
T4= tumor is fixed or invades adjacent structures other than the seminal vesicles (external sphincter, rectum, bladder, levator, pelvic wall)

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13
Q

what is risk stratification based on

A

clinical stage
PSA
grade group

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14
Q

clinically insignificant prostate cancer

A 
very low and some low risk
-grade group 1
AND
-PSA < 10
AND
-non palpable disease
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15
Q

clinically significant prostate cancer

A

grade group 2-5
OR
PSA > 10
OR palpable

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16
Q

3 ways of spreading of prostate cancer

A
  1. locally
  2. lymph
  3. hematogenous
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17
Q

staging studies for prostate cancer

A
  1. CT/MRI: used in intermediate risk prostate cancer and above to look for nodal involvement
  2. bone scan
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18
Q

when is a bone scan indicated

A 
PSA > 20
grade 4-5
cT3b
N1 on scans
symptoms (bone pain, obstruction)
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19
Q

treatment options for prostate cancer based on staging and risk groups

A

active surveillance
radical prostatectomy
radiation therapy
systemic therapy

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20
Q

what is active surveillance

A

monitoring of low/very low risk prostate cancer (clinically insignificant) with deferred intervention on identification of progression

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21
Q

rationale for active surveillance

A

grade group 1 prostate cancer is unlikely to metastasize or cause harm
avoid treatment harm
active monitoring reduces risk of mis classified higher grade disease

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22
Q

what % of patients will undergo treatment within 5-10 years of starting active surveillance

A

25-50%

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23
Q

what are curative intent options

A

radiation and surgery

24
Q

when is curative intent indicated

A

localized: cT1-2N0M0

locally advanced: cT3N0-1M0

25
what is a radical prostatectomy
removal of prostate and seminal vesicles - can be open or robotic (95%) - +/- removal of the pelvic lymph nodes, indicated if predicted risk of nodal disease is >2%
26
pros of prostatectomy
ultimate biopsy -40% of the time a biopsy is inconsistent with the final pathology can improve urinary symptoms if present ability to give radiation as an adjuvant treatment in the setting of aggressive disease or recurrence
27
cons of prostatectomy
incontinence: 2-5% at 1 year post op -management: pelvic floor physical therapy erectile dysfunction: 20-25% at 1 year post op -related to impact of surgery on parasympathetic nerves adjacent to the prostate -management: PDE5 therapy, penile injection therapy, vacuum erection devices
28
what is radiation
delivery of energy to tissue to exact DNA strand breaks for cellular death
29
types of radiation
external beam radiotherapy stereotactic body radiotherapy brachytherapy
30
pros of radiation
``` non-invasive no recovery time negligible risk of urinary incontinence no immediate impact on erectile function -expedites normal age related decline in erectile health tho (eventually evens out w surgery) ```
31
cons of radiation
paired with androgen deprivation therapy if intermediate or high risk irritative urinary/bowel side effects -can make existing symptoms worse hard to salvage with additional local therapy in the setting of failure
32
ADT courses with radiation
grade group 3: 6 months of ADT | grade group 4/5: 3 years of ADT
33
follow up after curative intent treatment
PSA checks at a decreasing frequency over 5-10 years -q3mo for 1 year, q6mo for 1 year, then yearly management of treatment related side effects
34
definition of biochemical recurrence
post surgery: PSA > 0.2 | post-radiation: PSA > 2.0 + nadir
35
treatment of biochemical recurrence
radiation if prior surgery | otherwise: simple ADT if after radiation
36
mechanism of ADT
impairment of the testosterone-androgen receptor interaction | -results in arrest of cell growth
37
side effects of ADT
``` hot flashes fatigue decreased bone mineralization decreased muscle mass impotence/decreased libido weight gain/metabolic syndrome CVD risk ```
38
different ADT options
``` all work on H-P-T/A axis hypothalamus -LHRH antagonist -LHRH agonist -estrogen testis -orchiectomy adrenal -CYP 17:20 lyase inhibitors target tissue -anti-androgens (block binding to receptor) ```
39
LHRH antagonist
degarelix
40
degarelix mechanism
prevents activation of gonadotropin releasing hormone receptors > no LH > no T
41
leuprolide mechanism
binds to and over stimulated the gonadotorpin releasing hormone receptor - results in and initial stimulation of the receptor > T surge - within 2 weeks, receptor down-regulates > no more LH > no T
42
LHRH agonist
leuprolide
43
antiandrogens
ketoconazole 5a reductase inhibitors bicalutamide enzalutamide
44
bicalutamide mechanism
competitive inhibitor of the androgen receptor | -can be used at the initiation of LHRH agonist therapy to block the effects of the T surge
45
interesting side effect w biclutamide
breast pain/tenderness does not reduce T levels > increased peripheral conversion to E more bioavailable T bc less is working in tissues
46
how long does first line hormonal therapy typically work after failed local therapy
8-10 years
47
what is the pathophysiology of castration resistant prostate cancer
prostate cancer is hormonally driven with prolonged hormonal suppression, the prostate cancer cells will develop the ability to grow despite castrate levels of T
48
treatment for CRPC
``` advanced ADT (abiraterone, enzalutamide) chemotherapy (docetaxel) ```
49
enzalutamide mechanism
1. prevents T binding to AR 2. prevents translocation of the AR to the nucleus 3. prevents binding of the AR to the DNA * *give in conjunction with typical ADT
50
mechanism of abiraterone acetate
inhibition of CYP17:20 lyase | -results in a reduction in the production of steroid hormones, including DHEA
51
special side effects of abiraterone acetate
hypokalemia hypertension fluid overload due to hyperaldosteronism: since pathway is shunted away from cortisol and DHEA, more aldosterone is made from the pathway
52
docetaxel mechanism
microtubule inhibitor
53
side effects of docetaxel
vomiting, diarrhea, constipation, and fatigue
54
how long after failure of first line therapy does a typical pt survive
10-20 yrs
55
progressive prostate cancer
bed bound >50% of the time pain from osseous mets neuro symptoms from spinal cord compression renal failure from local growth causing ureteral obstruction

RDS Test 3 (15 decks)

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