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Hematology, oncology > Prostate Cancer > Flashcards

Prostate Cancer Flashcards

1
Q

Medications with survival benefit in metastatic CR prostate cancer

A

Four
1) Taxanes
2) second generation antiandrogens
3) immunotherapy (sipuleucel-T)
4) radium-223

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2
Q

What are the aggressive variant prostate cancers?

A

1) *Pure small cell
2) neuroendocrine carcinomas

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3
Q

abiraterone mechanism

A
  • androgen synthase inhibiotr
  • irreversibly inhibits the products of the cytochrome P450, family 17 (CYP17) gene (including both 17,20-lyase and 17-alpha-hydroxylase). In doing so, abiraterone blocks the synthesis of androgens in the tumor as well as in the testes and adrenal glands.
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4
Q

only cytotoxic chemotherapy that has been shown to prolong survival in prostate cancer

A

taxanes

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5
Q

cabizataxel contraindications and SE profile

A

myelosuppression and may require premedication to minimize the risk of infusion reactions. Contraindications include underlying hepatic dysfunction or compromised bone marrow function.

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6
Q

Indication for radium 223 in prostate cancer

A

Isolated and symptomatic bone metastases without (no other clinically significant sites of disease (including visceral metastases))

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7
Q

Hereditary cancer syndromes associated with PC

A

BRCA 1 and 2, HOXB13

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8
Q

Evidence for prophylaxis against prostate cancer?

A

Some evidence that finasteride decreases risk of developing low-grade prostate cancer

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9
Q

% of adenocarcinoma in PC

A

95%

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10
Q

Primary vs. secondary Gleason grade

A

primary = dominant histologic pattern
secondary = next most common histologic pattern

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11
Q

Cutoffs to know for Gleason grade

A

Less than 6 = not considered to be PC
8-10 = high-risk disease

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12
Q

Term for premalignant lesions for prostate cancer

A

High-grade prostatic intraepithelial neoplasia (PIN)

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13
Q

Signs/symptoms of advanced prostate cancer

A
  • weight loss, fatigue, DIC, bone pain
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14
Q

Indications for prostate biopsy

A

1) Rapidly rising PSA
2) Palpable hard nodule on DRE

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15
Q

What to adjust for for PSA

A

Always age adjusted

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16
Q

Management of palpable hard nodule on DRE

A

Always biopsy, even if low PSA

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17
Q

How is prostate cancer biopsied — # of cores + scoring

A

12 cores are generally obtained to ensure adequate sampling, with highest score found in gland used (prostate cancer is multifocal)

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18
Q

Staging of intermediate/high risk PC

A

Bone scan + CT abdomen/pelvis

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19
Q

Prostate cancers that can be observed

A

1) Very low-risk
2) low-risk PC w/ life expectancies under 10 years

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20
Q

what active surveillance entails

A

1) Monitor PSA
2) DRE
3) periodically rebiopsying prostate gland

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21
Q

why is doubling time important to measure

A

Correlates to mortality

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22
Q

When lymph node dissection is indicated during radical prostatectomy

A

Patients with regional lymph node involvement and no evidence of distant metastatic disease (confirm)

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23
Q

Complications of radical prostatectomy

A
  • urinary incontinence and leakage
  • urinary stricture
  • impotence
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24
Q

management of ED after radical prostatectomy

A

Trial ED meds (may still be helpful)

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25
Q

Complications of radiation

A

Acute = inflammation of surrounding structures (cystitis, proctitis, enteritis)
Fatigue
Mild cytopenias
Impotence, urethral stricture, cystitis, hematuria
Diarrhea and proctitis

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26
Q

Neoadjuvant treatment prior to RP or radiation?

A

Not indicated

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27
Q

adjuvant chemo following RP?

A

Not indicated, adjuvant ADT plays a role in certain circumstances

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28
Q

Role for adjuvant radiation after RP

A

1) extracapsular extension
2) positive surgical margins

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29
Q

Definition of biochemical recurrence

A

2 separate serum PSA’s >0.2 ng/mL

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30
Q

Treatment options for castrate sensitive metastatic prostate cancer

A

ADT +
1) novel second generation antiandrogen (abiraterone/prednisone OR apalatumide or enzalutamide
2) docetaxal
3) ADT alone

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31
Q

Treatment options for castrate resistant metastatic prostate cancer

A

Continue ADT +
1) Same options as castrate sensitive. Next step depends on what patient has received before.

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32
Q

GnRH agonists + typical formulation

A
  • leuprolide
  • buserelin
  • goserelin
  • triptorelin
    *depot formulation to permit less frequent administration
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33
Q

next step when patient has a rising PSA on total androgen blockade

A

check serum testosterone to ensure patient is truly castrate

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34
Q

Prevalence of castration-resistant prostate cancer

A

With time, all patients with metastatic PC eventually progress to develop castration-resistant disease

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35
Q

Explain how castration-resistant PC develops

A

1) Upregulation of androgen receptors
2) Activation of androgen receptor by other steroid hormones
3) Splice variants of the androgen receptors
4) Prostate cancer cells synthesize their own androgens, so the local tumor androgen environment is higher

36
Q

Treatment options for patients with CRPC

A

1) secondary hormonal therapy
2) chemo with taxanes
3) vaccines (sipuleucel-T)
4) Radiopharmaceuticals (Radium-223)
5) Clinical trials

37
Q

What is secondary hormonal therapy?

A

Blocking other sources of testosterone production in the body (testosterone produced from adrenal glands and the tumor itself) or inhibiting androgen receptor signaling

38
Q

What are the bone-targeting agents

A

Denosumab
Bisphosphonates

39
Q

when radiation is indicated for bone mets

A

1) painful (most patients get significant palliation of pain when radiation is used)
2) at risk for pathologic fracture
3) lesions concerning for or causing spinal cord compression

40
Q

how is radiographic progression defined?

A

2 or more new lesions on a bone scan OR interval growth of visceral OR lymph node disease

41
Q

Adverse effects of ADT?

A

1) hot flashes
2) fatigue
3) loss of libido, decline in sexual function
4) increased risk for DM (ADT reduces insulin sensitivity)
5) increased cardiovascular disease risk (ADT can augment LDL, HDL, and triglyceride
6) osteoporosis
7) small but increased risk of alzheimer’s disease

42
Q

Management of painful gynecomastia

A

Refer to plastics for breast reduction

43
Q

How to optimize bone health in men on chronic ADT

A

1) Baseline bone density test prior to starting ADT
2) Repeat bone density test every 2 years while on ADT
3) calcium + vitamin D daily
4) lift weights + stop smoking

44
Q

management options for localized, intermediate risk PC

A

RT + ADT
OR
Radical prostatectomy

45
Q

term for genetic syndrome associated with BRCA

A

hereditary breast and ovarian cancer syndrome

46
Q

what risk stratification is based on

A

T stage
Gleason Grade
PSA

47
Q

management options for localized, high risk PC

A

IF limited life expectancy → external beam RT with or without brachytherapy + long term ADT OR ADT alone
IF longer life expectancy → radical prostatectomy

48
Q

ADT options + gist of ADT

A
  • GnRH agonists are most commonly used (eligard) except when concern for flare phenomenon OR immediate rapid decrease in testosterone level is required
49
Q

Eligard typical formulation

A

long acting 6 month

50
Q

Use of bisphosphonates in management of bone mets in castration sensitive PC

A

Not used. only indicated in CRPC.

51
Q

class of medications used to treat bone mets in CRPC

A

osteoclast inhibitors

52
Q

When to stage prostate cancer

A

Intermediate or higher risk (assuming 10 year life expectancy)
*NOT low risk or favorable intermediate risk if less than 10 year life expectancy

53
Q

Gleason score range + connotation of higher number

A

2 (well differentiated) - 10 (poorly differentiated)

54
Q

Categories defining low risk PC

A

1) Stage T1c, T2a
2) PSA less than 10
3) Low gleason score (less than 6

55
Q

why prostate cancer with low PSA is often more aggressive

A
  • these are often the aggressive variant prostate cancers (neuroendocrine)
56
Q

Eligard generic name

A

Leuprorelin

57
Q

Eligard mechanism

A
  • GnRH analogue
  • GnRH agonism initially results in stimulation of LH and FSH but HPG axis is depedent on pulsatile hypothalamic GnRH secretion so continuous agonism leads to desensitization of GnRH receptors and downregulation
58
Q

Indication for germline testing in prostate cancer

A

1) Positive family history of prostate cancer
2) High or very high risk prostate cancer
3) Metastatic disease

59
Q

What is a castrate serum level of testosterone?

A

less than 50 ng/dL

60
Q

when you never want to give GnRH agonists

A
  • metastatic disease at diagnosis (GnRH agonism initially causes a flare of LH and FSH, which is termed “flare phenomenon”, this can be of particular concern with impending epidural cord compression or urinary tract outflow obstruction)
61
Q

what are the GnRH antagonists?

A

Degarelix
Relugolix

62
Q

Utility of axium scan

A

No longer used in PSMA era

63
Q

Indication for sipuleucel

A

slowly progressive PC

64
Q

Novel androgen therapy typically referred to as

A

hormonal therapy

65
Q

Sipuleucel-T indication

A

asymptomatic or mild slowly progressive disease AND no visceral mets

66
Q

visceral mets refers to what?

A
  • liver, lung, adrenal, peritoneal, and brain mets (soft tissue or nodal mets not considered visceral)
67
Q

definition of biochemical failure after RT

A
  • rise in PSA of 2 above nadir
68
Q

Indications for observation in PC

A
  • very low risk disease with less than 10 years of survival
  • low risk disease with less than 10 years of survival
  • favorable or unfavorable intermediate disease with less than 10 year survial
69
Q

basic process for sipuleucel

A

WBCs are extracted during leukapheresis, blood product is sent to a production facility and incubated with a fusion protein, activated blood product is returned and reinfused

70
Q

response assessment with sipuleucel

A

NOT PSA. You don’t normally see a PSA drop with sipuleucel.

71
Q

what is xofigo

A

Ra-223

72
Q

Relative contraindications to enzalutamide and apalutamide

A

Seizure history

73
Q

Mitoxantrone SE’s

A
  • cardiomyopathy
  • blue discoloration of fingernails, sclera, and urine
74
Q

significance of N1 disease in prostate cancer

A
  • metastatic (stage IVA disease)
75
Q

Clinical features of small cell cancer of the prostate

A
  • extensive local disease, visceral crises,
  • low PSA
76
Q

Unique management of small cell cancer of the prostate

A
  • normally don’t benefit much from ADT
77
Q

Management of small cell cancer of the prostate + regimens you can use

A

(platinum based chemo)
cisplatin-etoposide
carbo-etoposide
carbo-docetaxel

78
Q

abiraterone SE’s

A

HTN + hypokalemia + AF + CHF + liver dysfunction

79
Q

what to tell patients about abiraterone

A
  • must be taken on an empty stomach (food will increase absorption). Can’t eat 2 hours before or 1 hour after.
80
Q

denosumab mechanism

A

RANKL inhibitor

81
Q

denosumab vs zometa in terms of SRE’s

A
  • there is phase III data that densoumab prevents SREs about 20% better than zometa
82
Q

pred dosing with abi in castrate sensitive and resistant

A

5 mg daily for castrate sensitive
5 mg po BID for castrate resistant

83
Q

why steroids are given with abiraterone

A
  • decrease risk of mineralocorticoid excess, which can lead to fluid retention, HTN, and hypokalemia
  • also cortisol rescue
84
Q

OS benefit of ADT in early-stage prostate cancer

A
  • no effect on OS
85
Q

Indications for RT after RP and caveat

A
  • positive margins
  • seminal vesicle invasion
  • extracapsular extension
  • detectable PSA
    *but many argue RT should be reserved for salvage setting
86
Q

Evidence for RT after RP when high risk features are present

A

PFS benefit but OS benefit hasn’t been shown

87
Q

FDA indications for Ga 68 PSMA

A

1) patients with suspected mets who are potentially curable by surgery or RT
2) BCR

Hematology, oncology (218 decks)

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