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Bpt > Oncology > Flashcards

Oncology Flashcards

1
Q

ECOG 0

A

Fully active, able to carry on all pre disease performance without restriction

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2
Q

ECOG 1

A

Restricted physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature (light house work, office work)

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3
Q

ECOG 2

A

Ambulatory and capable of all selfcare but unable to carry out any work activities. Yp and about more than 50% of waking hours

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4
Q

ECOG 3

A

Capable of only limited self care, confined to bed or chair more than 50% of waking hours

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5
Q

ECOG 4

A

Completely disabled. Cannot carry on any selfcare. totally confined to bed or chair

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6
Q

ECOG 4

A

Dead

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7
Q

Best imaging for staging of NSCLC

A

PET-CT if possible
(finds occult LN/distant mets - and higher sensitivity for mediastinal LN)
-Need to get tissue sample of suspicious LN to confirm mets

CT/MRIB for patients who are for curative intent as well

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8
Q

Incidence of of different NSCLC histo

A

Adenocarcinoma (approx. 50%),
squamous cell (~20%), adenosquamous
large cell

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9
Q

NSCLC - Immunohistochemistry for adeno and SCC

A

Adenocarcinoma: TTF-1, mucin, Napsin-A

Squamous: p63, CK 5/6 (CK 7 neg)

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10
Q

NSCLC - Adenocarcinoma molecular characteristics/driver mutations

A

EGFR mutation,
ALK
ROS1 gene rearrangement

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11
Q

Tx for Stage 1 NSCLC

A

Essentially. Resect and monitor.

Surgical resection and LN resection for intraoperative staging
VATS preferred

Stereotactic ablative body RTx is alternative for elderly patients or in COPD

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12
Q

Tx of Stage 2 NSCLC

A

Resect + Adjuvant chemo

  • 2 platinum based drugs:
  • Cisplatin/Vinorelbine
  • or Carboplatin if cisplatin not tolerated
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13
Q

Tx of Stage 3 NSCLC

A

Resect and adjuvant chemo if N0/N1 (hilar LN)

Chemoradiotherapy if N2+ disease, not resectable, or not a surgical candidate

  • 6 weeks RTx and concurrent 2 weeks double platinum chemo
  • -Cisplatin/Etoposide (superior)
  • -Carboplatin-Paclitaxel (less toxic)

Post chemo maintanence:
-PDL1 antibody: Durvalumab (improved survival) - irrespective of PDL1 expression

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14
Q

Tx Stage 4 NSCLC

A

Chemo in all stage 4 with EGFR and ALK negative disease and ECOG 0-2
-Improved survival 1.5m and QOL

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15
Q

Leading cause of cancer death in australia

A
  1. Lung cancer
  2. Prostate
  3. Breast
  4. Colorectal
  5. Pancreas
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16
Q

Definition of Stage 1 Lung cancer

A

Parenchymal lesion < 4 cm with no node invovlement

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17
Q

Definition of Stage 2 Lung cancer

A

Parenchymal lesion > 4 cm OR smaller lesion with hilar LN

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18
Q

Definition of Stage 3 Lung cancer

A

Essentially more than hilar nodes and definitely if any contralateral LN involvement

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19
Q

Definition of Stage 4 Lung cancer

A

Any form of mets

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20
Q

Cisplatin

A

Platinum based chemo

SE: ototoxicity, Peripheral neuropathy, mephrotoxicity, electrolyte disturbance, myelosuppression, mucositis, partial alopecia

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21
Q

Vinorelbine

A

Platinum based chemo

SE: peripheral neuropathy, arthralgia, myalgia, myelosuppression, mucositis, partial alopecia

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22
Q

Pancoast tumor and Stage 3 Lung Ca

A

Chemoradiotherapy prior to resection if it is resectable (below N2)

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23
Q

Durvalumab

A

Pacific Trial
anti PD-L1
Improved mortality post chemo for NSCLC

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24
Q

Anti PD 1 Ab

A

Pembrolizumab
Nivolumab

Bind to PD-1 on T cell

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25
Q

Anti PD-L1 Ab

A

Durvalumab
Atezolizumab

Bind to PD-L1 on Tumor cells

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26
Q

Stage 4 SCC lung cancer

A

Need to know PDL1 status
-If >50% on staining, then treat with Pembrolizumab (tripling survival to 30m)

-If <50% on staining, then Bevacizumab and chemo (mOS 16m)

Chemo choice:
-Cisplatin or Carboplatin plus paclitaxel

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27
Q

Approach to Stage 4 Adenocarcinoma Lung cancer

A

First: Mutation status

  • EGFR mutation (10-15%)
  • ALK translocation
  • ROS1 translocation

Then: if negative to all mutations - PDL1 status and treat with Pembro if >50% staining

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28
Q

Clinical phenotype of EGFR mutatnt adenocarcinoma

A

Asian, light or never smoked, female

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29
Q

Stage 4 adenocarinoma EGFR mutation treatment

A

First and second gen EGFR TKIs
-Erlotinib, gefitinib, afatinib

SE: Rash, diarrhea, nail changes, hair changes, pulmonary toxicity, LFT derrangement

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30
Q

Mutation in EGFR mutant adenocarinoma that leads to treatment failure

A

T790M mutation

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31
Q

Tx of EGFR mutant adenocarinoma with T790M mutation

A

Osimertinib

  • 3rd gen TKI resistant to T790M mutation
  • Increased mOS and better brain activity

If no T790M mutation
-Chemo/Bev/IT/Clincial trial

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32
Q

NSCLC ALK mutation phenotype

A

Light/never smoked
younger age
Adenocarinoma with acinar or signet ring histo

Need FISH testing for confirming

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33
Q

Stage 4 adenocarinoma ALK Translocation treatment

A

1st Line: Alectinib
SE: myalgia, constipation, oedema, photosensitivity, bradycardia

2nd line: Crizotinib
SE: vision disorders, N+D, oedema

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34
Q

Stage 4 adenocarinoma ROS1 Translocation treatment

A

Crizotinib

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35
Q

KRAS mutatons in NSCLC

A

20-25%
Commonly detected
Not targetable yet
Treat as per wild type tumors

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36
Q

Tx of Stage 4 Adenocarcinoma without driver mutation

A

PDL1 >50%
-Pembro

PDL1 <50%
Bevacizumab +chemo (cisplatin/carboplatin +pemetrexed or paclitaxel)

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37
Q

Definition Limited Stage SCLC

A

Ipsilateral hemithorax and regional nodes

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38
Q

Definition Extensive Stage SCLC

A

Disease on contralateral nodes/distant mets

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39
Q

Tx limited stage SCLC

A

Chemoradiotherapy (platinum/etopiside)

+Prophylactic cranial irradiation (improves survival)

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40
Q

Tx Extensive stage SCLC

A

Chemoradiotherapy (platinum/etopiside)

+Atezolizumab (improves 2 month survival)

+Thoracic radiation if residual disease (improves survival)

+Prophylactic cranial irradiation in select patient (contraversial)

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41
Q

Paraneoplastic Syndromes associated with which cancer: Hypercalcemia

A

Squamous cell cancer

-PTHrP release by tumor

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42
Q

Paraneoplastic Syndromes associated with which cancer: SIADH and Neurologic syndromes

A

Small Cell Lung cancer

Neuro: Lambert eaton syn, cerenellar ataxia, sensory neuroapathies

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43
Q

Risk factors for breast cancer

A
  • Early menarche/late menopause
  • Nulliparity/increased age first pregnancy
  • Proliferative type benign breast disease
  • Family/PHx
  • Genetic mutations
  • HRT
  • Weight (increased postM, low preM
  • Ionising radiation

Breast feeding and physical activity is protective

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44
Q

Most common type of breast cancer

A

Invasive carcinoma NST (80%)

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45
Q

Invasive lobular carcinoma (Breast cancer) features

A

More likely to be bilateral or multicentric
Lower grade and ER+
Unusual mets (GI, peritoneum, meninges)

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46
Q

Bad subtype of Breast cancer

A

Micropapillary

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47
Q

Breast Cancer: Stage 1

A

Small and node negative

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48
Q

Breast Cancer: Stage 2

A

Large and/or <4LN

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49
Q

Breast Cancer: Stage 3

A

Infamm or chest wall and/or >4LN

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50
Q

Breast Cancer: Stage 4

A

Metastatic

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51
Q

Inflammatory breast cancer features

A

Diffuse erythema/oedema (peau d’orange) of >1/3 of breast skin, lymphoedema caused by tumor emboli in dermal lymphatics

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52
Q

Surgery for early breast cancer (Stage 1-3)

A

Primary Cancer

  • Wide local excision
  • Mastectomy if multicentric, high tumor:breast ratio, risk reduction, or CI to RTx

Nodes

  • Clinically node negative - sentinal LN Bx
  • Clinically node positive then Axillary clearance
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53
Q

Radiation for early breast cancer (Stage 1-3)

A

Reduction in local recurrence and breast cancer deaths

Would do after mastectomy if node positive, large tumor >5 cm, or multiple high risk features

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54
Q

Strongest prognostic factor in Breast cancer

A

LN involvement

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55
Q

Definition of Neoadjuvant chemotherapy and role in breast cancer

A

Chemo before surgery

  • Can decrease size and make cancer resectable
  • Can aid in assessing if patient gets complete pathological response, if not can change treatment used in adjuvant setting
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56
Q

Role for Bisphosphonates in Breast Cancer Mx

A

Zolindronic and pomindronate adn denosumab

-Improve survival in post menopausal or OFS population if given for 3 years

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57
Q

Mx ER positive EARLY Breast Ca and prognosis

A

Low Risk: Endocrine therapy

  • PreM: Tamoxifen OR OFS+AI if high risk
  • PostM: AI, but can trial tamoxifen (inferior)

High Risk: Chemo (taxane and anthracycline) then Endocrine therapy

Good prognosis, but late recurrence > 5 yrs can occur

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58
Q

Mx HER positive EARLY Breast Ca and prognosis

A

Trastuzumab 52 weeks + Chemo (anthracycline +Taxane)

-If High risk: Consider adding other HER2 agents (pertuzumab, neratinib)

Good prognosis due to treatment

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59
Q

Mx Triple negative EARLY Breast Ca and prognosis

A

Chemotherapy
-Anthracycline +Taxane

Poorest prognosis, but late recurrences >5 years are uncommon

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60
Q

Endocrine Therapy in Breast Cancer (Premenopausal)

A

Ovarian function suppression + aromatase inhibitor is best for 5 years

Can use tamoxifen alone for 10 years, but inferior

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61
Q

Endocrine Therapy in Breast Cancer

Post menopausal

A

Aromatase inhibitors are best

Tamoxifen is an option if CI or intolerant

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62
Q

Tamoxifen MOA

A

Selective estrogen receptor modulator

  • Anti-estrogenic: Breast
  • Pro-estrogenic: Bones (partial), uterus
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63
Q

Tamoxifen SE

A 
Hot flushes
VTE (2-3x)
Uterine cancer
Cataracts
NAFLD
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64
Q

Mx of hot flushes on Tamoxifen

A

stay cool, avoid cheese, wine, and chocolate
Gabapentin
Venlafaxine

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65
Q

MOA Aromatase inhibitors and Names

A

Inhibit peripheral conversion of androgen to estrogen
-Not suitable in PreM unless OFS

Anastrozole, letrozole

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66
Q

Aromatase inhibitor side effects

A

Hot flushes
Accelerated BMD loss
AIMSS: joint pain and stiffness (hands mainly)
Vaginal dryness

More CVD, high chol, DM compared to
Tamoxifen

If used in premenopausal women without OFS can cause increase in estrogen levels

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67
Q

Chemotherapy classes used in breast cancer

A

Anthracyclines (epirubicin/doxorubicin)

Taxanes (Paclitaxel/docetaxel)

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68
Q

Anthracyclines SE

A 
Cardiotoxicity - irreversible
ORange urine
Alopecia
myelosuppression
mucositis
N+V
Fatigue
Amenorrhea (risk increases with age)
Risk of secondary leukemia
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69
Q

Taxanes SE:

A 
Peripheral neuropathy
Fluid retention
Infusion reaction
nail changes 
Alopecia
myelosuppression
mucositis
N+V +D
Fatigue
Amenorrhea (risk related to age)
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70
Q

Trastuzumab MOA

A

Monoclonal Ab that binds to Her2

Inhibits proliferation and survival

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71
Q

Trastuzumab SE

A 
Cardiac Dysfunction (10% drop LVEF)
-Reversible myocyte stunning

RF: Age >60, Chest RTx, Anthracycline use, high dose cyclophosphamide, HTN, known CAD

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72
Q

Tx of ER positive metastatic breast ca

A

Endocrine therapy is FIRST line
-unless highly symptomatic and high volume visceral disease

PreM:

  • OFS w/ GnRH analogue +AI +CDK 4/6 inhibitor
  • OR Tamoxifen alone

PostM: AI + CDK 4/6

+Chemo - single agent first

PI3-kinase inhibitor (causes proliferation -oncogenes)

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73
Q

CDK 4/6 inhibitor

A

Ribociclib, palbociclib, abemaciclib

Inhibit progress of of cell from G to S phase

Improve overall survival in Breast Ca

SE: reversible neutropenia, LFT derrangement, QT prolongation

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74
Q

Tx of HER2 postive metastatic Breast Cancer

A

Trastuzumab/pertuzumab/taxane chemo

Second line:

  • T-DM1 (drug antibody conjugate -trastuzumab and emtansine)
  • SE: thrombocytopenia, liver toxicity
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75
Q

Tx of triple negative metastatic breast cancer

A

Atezolizumab + Taxane

  • PARP inhibitors after chemo if BRCA mutant
  • Carboplatin if BRCA mutant
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76
Q

Role for Bone modifying agents in metastatic Breast cancer

A

First line: Denosumab

  • Decrease time to first/prevalence of skeletal related events
  • -Fracture, need for surgery/RTx, spinal cord compression, hypercalcemia

-Improve bone pain

DO NOT IMPROVE SURVIVAL

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77
Q

BRCA1/2 phenotype

A

younger age of cancer

Triple negative subtype with BRCA 1

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78
Q

Who to do BRCA testing in

A
  • Relative who is positive
  • High grade ovarian cancer
  • Triple neg Breast Ca and age <50
  • Male with breast ca
  • 2 primary Breast ca and one <50yo
  • Breast Ca and age <40
  • 2 first/second degree relatives +breast ca <50, jewish, male breast ca
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79
Q

BRCA gene positive: Ovarian screening

A

Nil screening program

BSO by age 45 to exclude occult malignancy

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80
Q

BRCA gene positive:

Breast Screening

A

Prophylactic bilateral mastectomy by 40

30-40 yo: annual MRI +/- US
40-50 yo: annual MRI +/- MMG +/- US
>50 yo annual MMG+/- US

81
Q

WHO Criteria for screening test

A
  • Important health problem
  • Recognisable latent or early symptomatic stage
  • Natural Hx understood
  • Tx available for disease
  • Test/examination has high accuracy
  • Cost effective
82
Q

Lead time bias

A

LEngth of time by which diagnosis advanced by screening

-Will length time between diagnosis and death independent of intervention

83
Q

Length time bias

A

More indolent tumors have a longer latent period

  • More likely to be screen detected
  • Artificial advantage to screen detected cases
84
Q

Breast Cancer Screening Program

Low risk

A

Women 50-74 yo have MMG every 2 years

85
Q

Breast Cancer Screening Program

Mod risk

A

One 1st degree relative diagnosed <50 yo OR two 2nd degree <50 yo
-Start at age 40, consider annual MMG

Two 2nd degree relatives >50 yo
-Annual MMG

86
Q

Breast Cancer Screening Program

High risk

A

Two first degree or second degree relatives with breast or ovarian cancer plus

  • other relatives
  • Breast Ca <50yo
  • Relative with >1 BC or ovarian cancer
  • Jewish
  • Male breast ca

Refer to familial cancer clinic

87
Q

Cervical Cancer Screening

A

Age 25-74
Every 5 years

  1. No HPV - Repeat in 5 years
  2. HPV non 16/18 detected, no abnormal cells - Repeat in one year
  3. HP non 16/18 and abnormal cells OR HPB 16/18 detected - Refer for colposcopy
  4. Unsatisfactory sample: retest 6-12 weeks
88
Q 
Bowel Cancer screening
General population (5-10% risk)
A

iFOBT every 2 years from 50-74 yo

Generally:
-Start at 50yo or 10 yr prior to FDR diagnosis

89
Q

Bowel Cancer Screening

(Mod Risk) 15-30% risk

A
  • One FDR <55 yo
  • Two FDR at any age
  • One FDR and >one SDR at any age

iFOBT every 2 years from 40-49 AND Colonoscopy every 5 years from 50-75 yo

90
Q

Bowel Cancer Screening

(High Risk) 30-40% risk

A
  • Three FDR at any age
  • Three FDR or SDR, one diagnosed <55 yo

iFOBT every 2 years from 35-44yo AND Colonscopy every 5 years 45-74 yo

91
Q

Types of ovarian cancer

A
  • High grade serous (most common - from distal fallopian tube)
  • mucinous invasive (GI source)
  • Endometroid (endometrial source)
  • Clear cell ( endometrial source)
92
Q

Reccomendation for testing for women <70 with high grade non-mucinous epithelial ovarian, fallopian tube, or primary peritoneal cancer

A

REferral for BRCA1/2 testing

93
Q

Which BRCA gene is associated with better ovarian outcomes

A

BRCA2

94
Q

What stage does ovarian cancer present at

A

Stage 3 and 4

-Due to non specific symptoms of early stages

95
Q

Tx of Ovarian cancer

A

Debulking surgery + Adjuvant chemo

+Bevacizumab (stage 3 and 4)

+PARPi if BRCA +ve (maintainence)

(Neoadjuvant can be done if +++Symptoms)

-Carboplatin + Paclitaxel
(15-16 mo PFS)

96
Q

Recurrence rate post initial Tx for ovarian cancer and outcome

A

80%

  • Platinum sensitive (present >6 mo post chemo) Have 2nd remission post chemo before possible recurrence and progression
  • Platinum resistant (present <6 mo post chemo) - Progress :(
97
Q

Role for intraperitoneal chemo in Ovarian Ca

A

Contraversial, but first line option

-MAny patients cease early due to toxicity and worse QOL

98
Q

Synthetic lethality

A

Refers to the ability of PARP inhibitors to selectively kill tumor cells that have BRCA mutations because they are unable to repair DNA damage

99
Q

PARP inhibitors

A

Olaparib
Niraparib
Rucaparib

Used in BRCA positive metastatic breast cancer

100
Q

Role for CA-125 in monitoring for recurrence of ovarian Ca

A

not recommended

101
Q

Most common gynecological malignancy

A

Endometrial cancer

  • Due to increasing rates of obesity and metabolic syndrome
  • Median age of diagnosis 63
102
Q

Risk factors for endometrial cancer

A
  • Unopposed estrogen
  • Obesity
  • PCOS
  • Tamoxifen use
  • Nulliparity
  • Age
  • Lynch Syndrome

OCP is protective

103
Q

Type 1 endometrial cancer

A

Most common (80%)

  • Adenocarcinomas
  • estrogen dependent
  • Good prognosis
104
Q

Type 2 endometrial cancer

A
  • High grade endometriod, serous, or clear cell
  • Estrogen independent
  • Poor prognosis
105
Q

Tx of endometrial cancer

A

Surgery is main stay
-Total hysterectomy and BSO +/- LN sampling

Low risk: Monitor post
Intermediate: +RTx
High: RTx +/- chemo Carboplatin+Paclitaxel)

Consider Hormone therapy if ER/PR Positive

Evidence for PDL1 inhibitors if mismatch repair genes present (MSI high)

106
Q

Early Cervical Cancer Treatment

A

Surgical for small lesions

+/- adjuvant chemoradiation if high risk features (Cisplatin)

107
Q

Advanced Cervical Cancer tx

A

Incurable, survival year

  • Bevacizumab + Carboplatin +Paclitaxel
  • Consider palliative RTx
108
Q

Method of inheritance of cancer predisposition genes

A

AD with incomplete penetrance

109
Q

BRCA Gene function

A

part of a complex that repairs double strand breaks in DNA via the homologous recombination pathway and maintains genomic stability (Tumor suppressor genes)

110
Q

BRCA 1 Breast cancer pathology

A
  • Medullary carcinoma more common
  • Grade: High mitotic count, pleomorphic, high tubule
  • Triple negative usually
  • Ovarian: High grade serous adenocarcinomas
111
Q

BRCA2 Breast cancer pathology

A
  • Grade: lack tubules and lower mitotic counts

- ER/PR not significantly different in proportion to general population

112
Q

RANK L in BRCA breast cancer

A

May be a role for denosumab in the future to inhibit RANKL

113
Q

Spontaneous CRC vs Lynch - most common gene affected

A

MLH1 methylation

114
Q

BRAF V600E mutation

A

Seen in Sporadic CRC not Lynch

115
Q

Pembrolizumab in MMR deficient CRC

A

Shown to improve outcomes in CRC that is MMR deficient - not on PBS

116
Q

Lynch Syndrome Genetic inheritance

A

AD, heterozygous germline mutation in MMR genes

-MLH1, MSH2, MSH6, PMS2, EPCAM (silences MSH2)

117
Q

Loss of what genes more so associated with Lynch

A

MSH2 and MSH6

118
Q

Loss of what genes more so associated with sporadic CRC

A

Loss of MLH1 and BRAF positive

If MSI not high and BRAF positive - very very aggressive cancer

119
Q

Cell cycle: Transition between stages is regulated by what?

A

CDK - Cell Dependent Kinases

120
Q

Alkylating Agents: Subclasses and names

A

Mustards:
-Cyclosporin, cyclophosphamide, chlorambucil, Dacarbazine, Temozolomide, Lomustine, Streptozotocin

Platinums:
-Cisplatin, Carboplatin, Oxaliplatin

121
Q

Alkylating Agents MOA

A

Cell cycle non specific
“Alkylates” guanine, distorts DNA structure, repair enzymes fail
Prevents helicase from seperating dsDNA and prevents replication

122
Q

Antimetabolites: Subclasses and names

A

Purine antagonists (A,G)

  • Fludarabine, 6-mercaptopurine, 6-thioguanine
  • MTX

Pyramidine antagonist (T,C)

  • Fluoropyrimidines (5-FU, capecitabine, S-1, TAS-102)
  • Gemcitabine
123
Q

Antimetabolites MOA

A

Work by interfering with T G C A

Interfere with DNA and RNA production

124
Q

Role for DPD in 5-FU metabolism

A

it breaks down 5-FU, so if deficienct will get toxicity

Capecitabine is a prodrug of 5-FU (longer half life)

125
Q

Ankaloids: Vinca - Names and MOA

A

-Vincristine, vinblastine, vinorelbine

Bind to tubulin, stop microtubulin formation

126
Q

Ankaloids: Taxanes - Names and MOA

A

Paclitaxel, Docetaxel

  • Binds to tubulins
  • Stops microtubule disassembly
127
Q

Ankaloids: Camptothecins - Names and MOA

A

Irinotecan, topotecan, etoposide

-Topoisomerase inhibiters - Cause DNA tensioning during S phase, so cannot replicate (S phase specific)

128
Q

Anthracyclins - Names and MOA

A

Doxorubicin, Daunoribicin, Epirubicin, Mitoxantrone

  • From strepmyces bacteria (antibiotic)
  • Non cell cycle specific, interfere with Topoisomerase 2, metabolite is a free radical causing widespread damage
  • Induces histone eviction from chromatin
129
Q

LHRH analogues

A

Lucrin, Zoladex (Goserelin)

130
Q

-omab

A

mouse

131
Q

-uximab

A

chimeric

132
Q

-uzumab

A

humanised

133
Q

-umumab

A

fully human

134
Q

CRC CIMP Phenotype

A

Right sided CRC
Older patients
Arise in “Serrated” adenoma

135
Q

FAP inheritance and phenotype

A

AD, 90% penetrance
Virtually all develop CRC by 40

APC gene as germ line mutation (tumor suppressor)

-25% have on FHx

  • Associated Ca
  • -papillary thyroid, ileal carcinoid, gastric cancer
136
Q

Amsterdam criteria

A

For HNPCC

  • 3 cases
  • 2 generations
  • 1 <50 yo - either CRC or related cancer
137
Q

CRC number of adequate LN needed during resection

A

> 12

138
Q

Lynch Syndrome associated cancers

A 
Endometrial ca
Ovarian
Gastric/SB/ hepatic
Brain
Renal
139
Q

Lynch Syndrome screening

A

At risk family members:

Annual or 2 yearly Cscope from age 25 or 5 years prior to earliest age of cancer Dx in family

140
Q

FAP screening

A

Start yearly flexi sig/Cscope age 10-12

Likely will need colectomy in teens or early 20s

141
Q

MUTYH associated polyposis

A

AR
Biallelic mutation in MUTYH gene
Polyposis by age 50-60
CRC risk 70-75%

142
Q

Aspirin and CRC

A

Shown to have reduced the incidence of CRC

  • Delayed benefit after 5 years
  • Thought to be via COX 2 inhibition which is expressed in CRC
143
Q

Tx of Stage 1 CRC

T1/T2 N0

A

Surgery alone

144
Q

Tx of Stage 2 CRC

T3/T4 N0

A 
Surgery
\+Adjuvant chemo if high risk features: (5-FU or Capecitabine)
-T4 tumor
Perforation/obstruction
-Lymphovascular invasion
-Poorly differentiated
-Inadequate LN samples
-High pre op CEA?
-MSI normal (stable)
145
Q

Tx of Stage 3 CRC

any T and N1/N2

A

Surgery + Adjuvant chemo

  • 6 months FOLFOX (Folic acid, 5-FU, Oxaliplatin)
  • IF low risk (N1) can do 3 months CAPOX (Capecitabine, Oxaliplatin)
146
Q

Tx of locally advanced rectal cancer

A

MRI for staging
Neoadjuvant chemoradiation
(5FU or Capcitabine)

Post op adjuvant chemotherapy dependent on histo and response to neoadjuvant and if node positive

147
Q

Tx of low rectal cancer <6 cm from anal verge

A

Not able to be resected

Neoadjuvant chemoradiation

148
Q

Surveillance after early stage colon cancer

A

First 2 years:
-3 monthly CEA + 6 monthly CT CAP

Year 3-5:
-6 monthly CEA and annual CT

Colonoscopy at anniversary and then second yearly

149
Q

Tx of metastatic CRC

-Group 1: Resectable mets

A

Aim to cure.

  • Surgery and adjuvant chemo
  • Can do neoadjuvant chemo if borderline resectable
150
Q

Tx of metastatic CRC

-Group 2: Unresectable and high tumor burden

A

Not curable

Chemo +/- targeted therapy

  • FOLFOX or FOLFIRI (Folinic acid, 5-FU, Irinotecan)
  • Trifluridine/Tipiracil (Lonsurf) - new alt to 5-FU - last line therapy (refractory CRC)

-Targeted:
–Bevacizumab (VEGF) (right side)
If KRAS wild type:
–Cetuximab (left sided CRC) or Panitumumab
(EGFR)

-If MSI High - Role for PDL1 inhibitor, but not on PBS

151
Q

Sister Mary Joseph Nodule

A

Gastric mets to umbilical area

152
Q

Virchow’s node

A

Gastric met to left supraclavicular LN

153
Q

Mx of Gastric CAncer Stage 1-3

A

Stage 1 - resect
Stage 2/3 Neoadjuvant chemo, resection, and follow up chemo

Consdier radical gastrectomy up to stage 3

FLOT4
(Docetaxel, 5-FU, Leucovorin, oxaliplatin)

154
Q

Mx of stage 4 gastric cancer

A

Platinum based chemo
(Docetaxel/cisplatin/5FU)
+Irinotecan

PD1 therapy in dMMR/MSI high (Pembro)

If HER2 positive, can also add trastuzumab

155
Q

GIST Diagnosis

A

“mesenchymal” tumor
-connective tissue/smooth muccle tissue

C-kit positive
CD117
Spindle shaped cells

Rx: Imatinib

156
Q

Role for pre-operative portal vein embolisation in Cholangiocarcinoma

A

to increase the limits of safe hepatic resection (induces lobar hypertrophy)

157
Q

Tx of Cholangiocarcinoma

A

Surgery is only cure.

Adjuvant chemo:
-Capecitabine

Palliative Chemo:
-Gemcitabine/Cisplatin

158
Q

Tx of Pancreatic cancer

A

Surgery +Adjuvant chemo

mFOLFIRINOX
5FU, oxaliplatin, leucovorin, irinotecan

159
Q

Definition of castration resistant prostate cancer

A

Prostate cancer growth despite castrate levels of testosterone (<1.7 nmol/L)

160
Q

Mx of metastatic castration sensitive prostate cancer

A

ADT (androgen deprivation therapy) +Docetaxel if high volume cancer

  • GnRH agonists (goserelin, leuprolide)
  • GNRH antagonist (degarelix) - avoids flare response
161
Q

What is the flare response associated with ADT in prostate cancer

A

Initial surg of testosterone when GnRH agonist is given that may worsen cancer and symptoms

162
Q

Mx of castration resistant prostate cancer

A

Chemo
-Docetaxel or Cabazitaxel

Androgen receptor targeted therapy

  • Abiratone (inhibts 17 alpha hydroxylase and given with pred 10 mg daily)
  • Enzalutamide (CI in seizures)

Role for PARP inhibitors too if DNA repair abnormalities

163
Q

Docetaxel SE

A

sensory/motor PN, cytopenias (neutropenic sepsis), hypersensitivity reactions

164
Q

Cabazitaxel SE

A

diarrhoea, cytopenias, sensory/motor PN (less common than D), less alopecia

165
Q

Fleischner Criteria

A

Single:
<6mm: low risk - no f/u
<6 mm high risk- CT 1yr

6-8mm: low or high risk - CT 6-12 mo

> 8 mm: low or high risk - CT/PET/tissue in 3 mo

Multiple:
<6mm - low: no f/u
<6mm - high: CT 1 yr

6-8mm or >8 mm and low or high risk: CT 306 mo

166
Q

Ki-67

A

marker of cell proliferation

167
Q

Which tumor marker goes up with smoking

A

CEA

168
Q

Which cancer is obesity a greatest risk factor in

A

endometrial

169
Q

Abitaterone MOA and SE

A

17 alpha hydroxylase inhibitor

SE:
-HTN, Hypokalemia, peripheral oedema, tranaminitis

Give with pred to reduce SE

170
Q

PSMA (prostate specific mebrane antigen)

A

Overexpressed in prostate cancer.

Possible use in future targeted disease treatment

171
Q

Most common renal cell cancer

A

Clear cell

172
Q

Role of VHL protein in Renal cell cancer

A

VHL keeps HIF in check
HIF promotes angiogenesis, cell proliferation
VHL mutation leads to excessive HIF with promites carcinogenesis

173
Q

Poor prognostic signs in Renal cell cancer

A

High ECOG
Hypercalcemia
Low Hb
High LDH and Plt

174
Q

Mx of renal cell cancer

A

1st: TKI
- Sunitinib or Pazopanib

2nd: Nivolumab, Sorafenib, atixinib
3rd: Everolimus

175
Q

Most common bladder cancer in developed countries

A

Transitional cell carcinoma (urothelial)

176
Q

Treatment of muscle invasive bladder cancer

A

Neoadjuvant chemo improved survival
(Cisplatin+gemcitabine)

Radical cystectomy preferred, but alternative is chemoradiation

2nd line: PD1/PDL1 - not PBS approved

177
Q

Differentiating seminoma vs non seminoma testicular cancer

A

AFP NOT produced by pure seminoma

BHCG and LDH can be produced by both

178
Q

Mx of seminoma testicular cancer

A

Carboplatin only

Risk of recurrence if tumor >4 cm or rete testis invasion

179
Q

Mx of non-seminoma testicular cancer

A

BEP

Bleomycin, etopiside, cisplatin

180
Q

Prognostication factors of melanoma

A
  1. Tumor thickness
  2. Mitotic rate
    Ulceration, older age, male, LN involvement, location
    LDH
181
Q

Mx of stage 1 melanoma

A

resect and consider sentinal LN Bx if >1mm or high risk features

182
Q

Mx of stage 2 melanoma

A

Resect + Sentinal LNBx +Adjuvant RTx +/- systemic Tx

183
Q

Mx of stage 3 melanoma

LN involvement

A

Resect + Nodal dissection + Adjuvant RTx +/- systemic Tx

184
Q

Mx of stage 4 melanoma

A

BRAF mutation:

  • 1st line: BRAF +MEK inhibitor
  • 2nd line: Ipilimumab +Nivolumab

No BRAF mutation:
-1st Line: Ipilimumab +Nivolumab

185
Q

BRAF Mutations in Melanoma

A

More common in little chronic skin exposure, younger patients

80% BRAF V600E
5-30% BRAF V600K

186
Q

BRAF inhibitors names, MOA, and SE

A

Vemurafenib, Dabrafenib

Attach to mutant BRAF V600. BRAF results in downstream activation of MEK and ERK with leads to uncontrolled cell proliferation. This is ceased.

SE: fevers, tachycardia, diarrhea, rash and pruritis, SCCs

187
Q

Complication with only BRAF inhibitor use in melanoma

A

Cx: 80% pts develop resistance via the MAPK reactivation through MEK (prevented by combo MEK and BRAF inhibitor)

188
Q

MEK inhibitors

A

Cobimetinib, Trametinib

MOA: Inhibition of downstream MAPK pathway

Decreases side effects from BRAF inhibitors alone

SE: photosenitivity

189
Q

Which drug is most associated with pseudoprogression

A

CTLA 4 inhibitor

Ipilimumab

190
Q

When is the peak time of immunotoxicity with immunotherapy and which drugs are most likely the cculprit

A

first 3 months, but can occur anytime

Ipi/Nivo>Ipi>Nivo

191
Q

Mx of Brain mets in Breast cancer

A

Resection if possible or stereotactic RTx

-Stereotactic done if <5 mets, otherwise have to do whole brain RTx

192
Q

At what size of mass are PET scans not helpful

A

<1 cm

If cold on PET scan, then still cannot rule out cancer

193
Q

Common immune related AEs

A 
AI colitis
AI dermatitis
AI hepatitis
AI hypophysitis
-p/w fatigue, headache, nausea
-Adrenal insufficiency, hypo/hyperthyroidism, or hypogonadism
Pneumonitis
-Non productive cough and dyspnea

Generally:
-Rash first, then diarrhea, then liver and hypohysitis later

194
Q

Mx of IRAEs

A

Grade 1: Mild
-Symptomatic (loperimide for colitis, topical steroid for rash)

Grade 2: Mod
-PO steroid

Grade 3: Hospital
-IV Steroids

Grade 4: Severe
-IV steroid + other immunosuppressant

195
Q

Breast cancer Brain met - receptor status?

A

HER2 +ve

196
Q

Breast cancer Bone and LN mets - receptor status?

A

ER/PR positive

197
Q

PSMA scan

A

PET scan with prostate specific membrane antigen enabling better detection of mets
Highly sensitive and specific

198
Q

Prostate cancer: Role for denosumab and zolendronic acid

A

REduce skeletal related events in castrate resistant bony mets

Bpt (15 decks)

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