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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
Q

what is a radical prostatectomy

A

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
Q

pros of prostatectomy

A

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
Q

cons of prostatectomy

A

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
Q

what is radiation

A

delivery of energy to tissue to exact DNA strand breaks for cellular death

29
Q

types of radiation

A

external beam radiotherapy
stereotactic body radiotherapy
brachytherapy

30
Q

pros of radiation

A 
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
Q

cons of radiation

A

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
Q

ADT courses with radiation

A

grade group 3: 6 months of ADT

grade group 4/5: 3 years of ADT

33
Q

follow up after curative intent treatment

A

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
Q

definition of biochemical recurrence

A

post surgery: PSA > 0.2

post-radiation: PSA > 2.0 + nadir

35
Q

treatment of biochemical recurrence

A

radiation if prior surgery

otherwise: simple ADT if after radiation

36
Q

mechanism of ADT

A

impairment of the testosterone-androgen receptor interaction

-results in arrest of cell growth

37
Q

side effects of ADT

A 
hot flashes
fatigue
decreased bone mineralization
decreased muscle mass
impotence/decreased libido
weight gain/metabolic syndrome
CVD risk
38
Q

different ADT options

A 
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
Q

LHRH antagonist

A

degarelix

40
Q

degarelix mechanism

A

prevents activation of gonadotropin releasing hormone receptors > no LH > no T

41
Q

leuprolide mechanism

A

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
Q

LHRH agonist

A

leuprolide

43
Q

antiandrogens

A

ketoconazole
5a reductase inhibitors
bicalutamide
enzalutamide

44
Q

bicalutamide mechanism

A

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
Q

interesting side effect w biclutamide

A

breast pain/tenderness
does not reduce T levels > increased peripheral conversion to E
more bioavailable T bc less is working in tissues

46
Q

how long does first line hormonal therapy typically work after failed local therapy

A

8-10 years

47
Q

what is the pathophysiology of castration resistant prostate cancer

A

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
Q

treatment for CRPC

A 
advanced ADT (abiraterone, enzalutamide)
chemotherapy (docetaxel)
49
Q

enzalutamide mechanism

A
  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
Q

mechanism of abiraterone acetate

A

inhibition of CYP17:20 lyase

-results in a reduction in the production of steroid hormones, including DHEA

51
Q

special side effects of abiraterone acetate

A

hypokalemia
hypertension
fluid overload
due to hyperaldosteronism: since pathway is shunted away from cortisol and DHEA, more aldosterone is made from the pathway

52
Q

docetaxel mechanism

A

microtubule inhibitor

53
Q

side effects of docetaxel

A

vomiting, diarrhea, constipation, and fatigue

54
Q

how long after failure of first line therapy does a typical pt survive

A

10-20 yrs

55
Q

progressive prostate cancer

A

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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