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FRACP Shuyu > RPA MONC > Flashcards

RPA MONC Flashcards

1
Q

Adjuvant chemotherapy in stage 2 colon cancer

A

very small benefits (1-5%) w adjuvant chemotherapy
but previous studies showed superior response in FOLFOX (vs 5FU) which resulted in significant peripheral neuropathy

(MOSAIC study 2007)

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2
Q

what agent causes peripheral neuropathy in FOLFOX

A

Oxaliplatin

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3
Q

Duration of adjuvant therapy in stage 3 colon cancer

A

6 months for high risk (T4 N2)

and 3 months in low risk

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4
Q

capecitadine SE

A

(prodrug of 5FU)

palmer planter erythema

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5
Q

what is the most useful clinical situation to test CEA

A

recurrence of bowel cancer

or monitoring of metastatic disease who produces this protein

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6
Q

AE of bevacizumab

A

HTN, proteinuria, thromboembolism, bleeding, leukopenia

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7
Q

EGFR in colon cancer vs lung cancer

A

in lung cancer, small molecule TK EGFR-1 inhibitors are used in patients with EGFR mutations

where as in colon cancer, EGFR mabs are used if they are RAS (KRAS/NRAS) wildtype

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8
Q

Cetuximab rash

A

rash means response

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9
Q

which colorectal patients benefit from immunotherapy

A 
MMR deficient
(pembrolizumab)
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10
Q

where do bowel cancers metastasis first cf rectal cancer

A

bowel cancer drain through the portal system to the liver first where as rectal cancer go to lungs

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11
Q

surveillance program after colon cancer

A

first 2 years: 3 monthly CEAs + physical exam + 1-2 CT scans/year + colonoscopy at anniversary then 3-5 years after diagnosis then every 3-5 years after that

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12
Q

breast tissue density

A

dense tissue makes it more difficult for mammography and US to see cancer; more likely to present at a later stage
high risk from increased glandular tissue to fatty tissue

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13
Q

high scoring criteria for manchester scoring for genetic testing for breast cancer

A

the scoring is the sum of all first degree relatives on 1 side:

breast cancer age <30 +11
ovarian cancer <59 13
ovarian cancer >59 10
bilateral breast cancer

HER2 -4
LCIS -4

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14
Q

BRCA1 mutation breast cancers hormone markers

A

majority triple negative (69% vs 15% in general population)

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15
Q

BRCA2 mutation breast cancers hormone markers

A

more similar to general population

77% ER positive 16% triple negative

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16
Q

bilateral risk reducing mastectomys in BRCA1/2

A

reduction by 90%

due to mets prior to mastectomy or microremnants

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17
Q

bilateral risk reducing salpingooperectomy (BRRSO)

A

important to remove fallopian tubes as most “ovarian cancers” actually arise from cells in the fimbriae of the fallopian tube
80% risk reduction of ovarian cancer

guidelines recommend BRRSO 35-40 in BRCA 1 and to 45 in BRCA 2

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18
Q

breast cancer risk modification w genetic predisposition

A

SERMS - 33% relative reduction
but assos risk of increased endometrial ca

aromatase inhibitors - works in post menopausal people. Reduces RR by ~ half

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19
Q

who might benefit from US with mammography

A

younger women, smaller and denser breasts

but generally not much evidence for US

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20
Q

MRI screening for breast cancer

A

familial breast cancer (identified gene mutation or not) or radiotherapy for hodgkin lymphoma

reduces risk of stage 2 or high er Br Ca in this group by 70% risk reduction

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21
Q

what must be done in conjunction w WLE in breast cancer

A

radiotherapy to get the same benefits w mastectomy

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22
Q

when is postmastectomy radiotherapy considered

A

<40yr, >4cm primary, >4 lymph nodes, positive surgical margins

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23
Q

early stage breast ca treatment

A 
surgery - WLE vs mastectomy
radio therapy - always w WLE, w high risk mastectomy
chemotherapy ?herceptin
endocrine therapy
monoclonal antibodies
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24
Q

prognostic markers in ealry stage breast cancer

A 
tumour grade
nodal status
HER2 status
tumour size
ER/PR status
age at diagnosis
gene assay (oncotype DX) - how well you are likely to response to chemotherapy
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25
Q

most aggressive early breast cancer syndrome

A

basal like
“triple negative”

most benefit from adjuvant therapies

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26
Q

histology subtypes of breast cancer

A

ductal vs lobular (lower grade, ER+)

other types: endocrine responsive, high risk endocrine responsive, low risk endocrine non responsive)

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27
Q

chemotherapy regimens for early stage breast cancer

A

AC-T Doxorubicin and Cyclophosphamide, Followed by Paclitaxel or Docetaxel.

TC docetaxel and cyclophosphamide
dose dense regimens are more toxic but more effective at reducing cancer recurrence

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28
Q

which endocrine therapy block steroidogenesis

A

aromatase inhibitors

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29
Q

which endocrine therapy block receptors in breast tissue

A

SERMS - tamoxifen

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30
Q

first choice estrogen receptor positive breast cancer endocrine therapy post menopausal

A

aromatase inhibitors

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31
Q

AE of aromatase inhibitors

A

vasomotor symptoms, myalgias, mood change, osteoporosis

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32
Q

5 yr to 10 yr aromatas inhibitor

A

10 years HR 0.66 of recurrent disease or contralateral de novo breast cancer
however no change in overall survival
increased risk of osteoporosis

MA17R trial

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33
Q

AE of SERMs

A

vasomotor symptoms
DVT
endometrial cancer

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34
Q

which endocrine therapy is better for bone

A

SERM as ER agonist in bone thus osteoprotective

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35
Q

Adjuvant therapy of in situ disease

A

women who did not have invasive disease (in situ) were resected and given adjuvant therapy
recent data that low dose SERM for 3 years reduces 5 year development of invasive breast cancer from 11% to 6.4%

the thought is that people who develop insitu cancers are at higher risk of developing more breast cancers
moreover, there is a small effect on stopping any remnant disease to metastasise

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36
Q

endocrine therapy in premenopausal women

A

ovarian suppression w GnRH agonist in conjunciton w aromatase inhibitor

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37
Q

duration of trastuzumab

A

1 year

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38
Q

transtzuzumab emtansine

A

used in histological setting if there is residual disease if neoadjuvant therapy did not work

it’s chemotherapy attached to monoclonal

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39
Q

difference of MOA of neratinib vs trastuzumab

A

trastuzumab stops dimerization of HER2 receptors on the surface
HER2 only causes effect if it dimerizes

however there is escape mechanisms - e.g. if HER2 dimerizes with other HER molecules

neratinib is a pan-HER TKI

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40
Q

molecule risk analysis in breast cancer

A

oncotype dx
patented 21 gene expression assay
predictive value to response to chemotherapy

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41
Q

denosumab as adjuvant in breast cancer

A

osteoporosis dose
improved disease free survival
used in high risk group

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42
Q

fulvestrant

A

selective estrogen receptor downregulator

use w aromatase inhibitor better than aromatase inhibitor alone (but high risk disease is now used w aromatase inhibitor w GnRH)

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43
Q

palbociclib and ribociclib

A

CDK4/6

metastatic breast cancer ER/PR+
used w fulvestrant
metabolised by CYP3A4

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44
Q

pertuzumab

A

see slides

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45
Q

which BRCA carries higher chance of breast cancer in men

A

brca2 7% (BRCA1 1%)

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46
Q

triple negative liver metastatic breast ca treatmnet

A

chemotherapy
not CDK4

visceral mets is like threatening and more aggressive and should use agents w anti mitotic effects (E.g. Paclitaxel) rather than antimetabolite effects (e.g. capecitabine)

47
Q

MAP kinase pathway

A

RAs-> raf -> mek -> erk

which stimulates MF

48
Q

BRAF mutated melanoma cells - MAP kinase pathway effects

A

upregulation of RAF

49
Q

B-raf mutation prevalence melanoma

A

50% melanoma

50
Q

B-raf inhibitor toxicity

A 
rash
fatigue
photosensitivity
arthralgias
SCCs
51
Q

what toxicity is not present when you use BRAF/MEK inhibitor dual combination

A

no SCCs

52
Q

why does PD-1 have action on the tumour environment compared with CTLA-4

A

normally when t cells are upregulated, the cancer cells will produce more PDL1, which was a way to get around the CTLA4

however, the PD-1 inhibitor was still able to act on it

53
Q

markers for doing poorly metastatic melanoma (3)

A

elevated LDH
high tumour burden
intracranial mets

54
Q

sonic hedgehog

A

implicated in BCC
The hedgehog gene in the HH pathway codes for an extracellular protein, the sonic hedgehog (SHH) protein. SSH binds to the cell membrane receptor complex to start a cascade of cellular events leading to cell proliferation.

55
Q

vismodigid

A

treat metastatic basal cell carcinoma via inhibition of sonic hedgehog

56
Q

prostate cancer confined to the prostate management

A

risk stratify

  • tumour grade, size, extension, volume, PSA
  • predicted survival

low risk -> active surveillance or observation
intermediate/higher risk -> stage w CT CAP and WBBS and if truly local disease than radical prostatectomy or prostate radiotherapy (<74yr)

then survey w 6 monthly PSAs

57
Q

Prostate cancer recurrence

A

biochemical recurrence is common
can contemplate salvage radiotherapy
can consider imaging including PSMA PET if PSA >0.2 as if there is spread salvage radiotherapy wil be futile

adjuvant antiandrogen therapy for 24mo

(see slides)

58
Q

metastatic prostate therapy management

A

GnRH agonists
can have a pulse sudden increase in FSH, LH, testosterone with GnRH agonism, can flare metastatic prostate disease
cover w GnRH antagonist

59
Q

role of antiandrogens in metastatic prostate cancer

A

bicalutamid, nilutamide

adjunct to GnRH agonists/antagonists as second line therapy for non metastatic castrate sensitive prostate cancer and historically for castrate resistant prostate cancer

60
Q

MOA of abiraterone

A

inhibitors CYP17 irreversibly

can get upstream accumulation of steroid precursors causing hypokalaemia

give 10mg prednisolone indefinitely

see slides

61
Q

MOA of enzalutamide

A

antiandrogen

broader mechanism of action than older antiandrogenics

62
Q

metastatic prostate disease - chemotherapy

A

upfront chemotherapy docetaxel w GnRH agonist

used in high risk (>3 bone mets)

63
Q

sequencing of therapy for metastatic prostate disease

A

abiraterone before enzalutamide

64
Q

what type of renal cell carcinomas are the most common

A

clear cell

65
Q

what are VHL mutations

A

in clear cell variants in RCC

small arm of chromosome 3
mutation/complete loss of 3p causes hypoxia inducible factors which causes transcription of the hypoxia inducible genes (inc VGEF).

66
Q

poor prognostic factors for metastatic risk in RCC

A

less than 1 yr from diagnosis to systemic therapy
karnofsky less than 80
high calcium
anaemia
neutrophil higher than the upper limit of normal (high immunogenecity)
plt higher than the upper limit of normal

67
Q

first line therapy for favourable prognosis in metastatic RCC

A

sunitinib and pazopanib
chose based on toxicity profile

pazopanib more likely LFT derangement and all hair turns white
sunitinib more likely diarrhoea, rash, hypertension

68
Q

pazopanib AE

A

pazopanib more likely LFT derangement and all hair turns white

69
Q

Sunitinib AE

A

sunitinib more likely diarrhoea, rash, hypertension

70
Q

first line therapy for poor prognosis in metastatic RCC

A

immunotherapy

71
Q

RCC and radiotherapy

A

generally radioresistant but may be fairly effective for symptom palliation

72
Q

bladder cancer cell

A

transitional cell epithelium

so renal tract cancers get same treatment

73
Q

Bladder cancer staging

A

muscle invasive vs non muscle invasive

whether or not it invades through muscularis propriate

74
Q

non muscle invasive bladder cancer treatment

A

single dose intravesical chemotherapy

if high grade, can give adjuvant immunotherapy
BCG - raises IL-12, IFN-gamma stimualte Th1 activation and CD8+ cytolytic T cells
increases intracellular NO levels, inhibiting tumour growth

75
Q

muscle invasive bladder cancer treatment

A

neoadjuvant or adjuvant chemo

cystectomy or radical radiotherapy

76
Q

testicular cancer histology classification

A

seminoma -aFP always normal

non seminoma - AFP elevated

77
Q

which testicular cancer have elevated AFP

A

non seminoma

78
Q

staging of testicular germ cell cancer

A

stage 1 - testicles
stage 2 - nodal spread
stage 3 - metastasis

79
Q

management of stage 1 testicular germ cell tumours

A

orchidectomy

seminoma - radiotherapy or chemo or surveillance
non-seminoma - chemo or surveillance - RADIO DOES NOT WORK

80
Q

bleomycin AE

A

pneumonitis

81
Q

Which testicular ca does not respond to radio

A

non seminoma

82
Q

stage 1 testicular ca with beta HCG >5000 or AFP >10000

A

brain MRI

83
Q

li-fraumeni syndrome

A

p53 mutation

38 fold increase in lung ca

84
Q

what lung ca is familial retinoblastoma assoc w

A

small cell lung cancer

85
Q

high yield to reduce tobacco use

A

increase tobacco tax

86
Q

screening for lung cancer

A

low dose CT showed mortality benefit 20% reduction in RR
however only 0.5% reduction in absolute risk
?cost effective

currently not recommended in Australia

87
Q

size of lung nodule that is significant of causing mortality

A

> 6mm

some smaller ones could still be cancer in their infancy though

88
Q

what PET scan to use in lung cancer

A

PDG pet scan

glucose w radioactive isotope

89
Q

what lung cancer is more assoc w smokers

A

squamous cell carcinoma

90
Q

which lung cancer is more PD1/PDL1 positive

A

squamous cell carcinoma

91
Q

what is the location of squamous cell carcinomas

A

central

92
Q

commonest lung cancer in on smokers

A

adenocarcinoma (but smokes are still more common)

93
Q

small cell lung cancer histology/characteristics

A

almost always assoc w smoking
neuroendocrine staining
central
aggressive

94
Q

small cell limited treatment

A

1 half of lung and sometimes the mediastinum (whether you can get a radiotherapy field around it w curative extent)

concurrent chemoradiotherapy
consider prophylactic crabial irradiation

95
Q

small cell extensive treatment

A

chemotherapy 4-6 cycles platinum based drug

96
Q

stage IIIb NSCLC

A

mediastinum involved but probably not curable w surgery
limited to thorax

tx:
chemoradiotherapy
chemotherapy followed by chemoradiotherapy
practice changing last 18 months is addition of immunotherapy

97
Q

what size of lung cancer would you not consider adjuvant therapy

A

<5mm

98
Q

stage IV NSCLC no driver mutation treatment

A

chemo/immunotherapy

99
Q

which type of lung cancer have driver mutations

A

not squamous cell carcinona

100
Q

EGFR TKI availbale

A

erlotinib
gefitinib
afatinib
osimertinib (t790M and at relapse)

101
Q

EGFR TKI AE

A

rash - predictor of response
GI symptoms
rarely pneumonitis

102
Q

treatment of TKI rash

A

grade 1 - topic emollients/steroids
grade 2 - topical steroid cream + smollients
grade 3 - doxycycline + topical steroid

if rash is not improving or progressing, then TKI is stopped until this improves to a grade 1 and consideration of dose reduction

103
Q

what TKI EGFRs have with less rash

A

osimertinib and newer generation TKIs as they are selective for mutant EGFRs

104
Q

what TKI EGFRs is associated with prolonged QT interval

A

osimertinib

crizotininib

105
Q

what is the most common mutation to acquire in 1st line TKI resistance

A

T790M

106
Q

crizotinib AE

A

alk inhibitor + ros1
Visual disturbance
QT prolongation
pneumonitis

107
Q

what can be used in combo with aromatase inhibitors for metastatic breast cancer

A

ribociclib and palbociclib

108
Q

what is the proportion of metastatic castrate resistance prostate cancer whose disease will harbour a homologous recombination DNA repair?

A

30%

HRD is homologous with a BRCA mutation

109
Q

oral hydromorph to parentral hydromorphone

A

3:1

110
Q

metastatic seminoma germ cell tumour prognosis

A

very good prognosis (>80% at 5 yr even in very advanced metastatic disease)

111
Q

what thyroid cells are affected in medullary thyroid cancer

A

C cells - calcitonin producing

112
Q

what is the most common type of thyroid cancer

A

papillary

113
Q

what type of thyroid cancer doesn’t respond to to radioiodine

A

medullary cancers

114
Q

when to perform lobectomy in papillary thyroid cancer

A

stage I only

larger tumours need iodione and radioablation

FRACP Shuyu (65 decks)

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