Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Bpt > Oncology > Flashcards

Oncology Flashcards

1
Q

ECOG 0

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ECOG 3

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ECOG 4

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ECOG 4

A

Dead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Incidence of of different NSCLC histo

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

NSCLC - Immunohistochemistry for adeno and SCC

A

Adenocarcinoma: TTF-1, mucin, Napsin-A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

NSCLC - Adenocarcinoma molecular characteristics/driver mutations

A

EGFR mutation,
ALK
ROS1 gene rearrangement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Tx of Stage 2 NSCLC

A

Resect + Adjuvant chemo

  • 2 platinum based drugs:
  • Cisplatin/Vinorelbine
  • or Carboplatin if cisplatin not tolerated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Leading cause of cancer death in australia

A
  1. Lung cancer
  2. Prostate
  3. Breast
  4. Colorectal
  5. Pancreas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Definition of Stage 1 Lung cancer

A

Parenchymal lesion < 4 cm with no node invovlement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Definition of Stage 2 Lung cancer

A

Parenchymal lesion > 4 cm OR smaller lesion with hilar LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Definition of Stage 3 Lung cancer

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Definition of Stage 4 Lung cancer

A

Any form of mets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Cisplatin

A

Platinum based chemo

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Vinorelbine

A

Platinum based chemo

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Pancoast tumor and Stage 3 Lung Ca

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Durvalumab

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Anti PD 1 Ab

A

Pembrolizumab
Nivolumab

Bind to PD-1 on T cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Anti PD-L1 Ab

A

Durvalumab
Atezolizumab

Bind to PD-L1 on Tumor cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Clinical phenotype of EGFR mutatnt adenocarcinoma

A

Asian, light or never smoked, female

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Mutation in EGFR mutant adenocarinoma that leads to treatment failure

A

T790M mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

NSCLC ALK mutation phenotype

A

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

Need FISH testing for confirming

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Stage 4 adenocarinoma ROS1 Translocation treatment

A

Crizotinib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

KRAS mutatons in NSCLC

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Tx of Stage 4 Adenocarcinoma without driver mutation

A

PDL1 >50%
-Pembro

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Definition Limited Stage SCLC

A

Ipsilateral hemithorax and regional nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Definition Extensive Stage SCLC

A

Disease on contralateral nodes/distant mets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Tx limited stage SCLC

A

Chemoradiotherapy (platinum/etopiside)

+Prophylactic cranial irradiation (improves survival)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Paraneoplastic Syndromes associated with which cancer: Hypercalcemia

A

Squamous cell cancer

-PTHrP release by tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Most common type of breast cancer

A

Invasive carcinoma NST (80%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Bad subtype of Breast cancer

A

Micropapillary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Breast Cancer: Stage 1

A

Small and node negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Breast Cancer: Stage 2

A

Large and/or <4LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Breast Cancer: Stage 3

A

Infamm or chest wall and/or >4LN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Breast Cancer: Stage 4

A

Metastatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Strongest prognostic factor in Breast cancer

A

LN involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Mx Triple negative EARLY Breast Ca and prognosis

A

Chemotherapy
-Anthracycline +Taxane

Poorest prognosis, but late recurrences >5 years are uncommon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Endocrine Therapy in Breast Cancer

Post menopausal

A

Aromatase inhibitors are best

Tamoxifen is an option if CI or intolerant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Tamoxifen MOA

A

Selective estrogen receptor modulator

  • Anti-estrogenic: Breast
  • Pro-estrogenic: Bones (partial), uterus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Tamoxifen SE

A 
Hot flushes
VTE (2-3x)
Uterine cancer
Cataracts
NAFLD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Mx of hot flushes on Tamoxifen

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

MOA Aromatase inhibitors and Names

A

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

Anastrozole, letrozole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Chemotherapy classes used in breast cancer

A

Anthracyclines (epirubicin/doxorubicin)

Taxanes (Paclitaxel/docetaxel)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Anthracyclines SE

A 
Cardiotoxicity - irreversible
ORange urine
Alopecia
myelosuppression
mucositis
N+V
Fatigue
Amenorrhea (risk increases with age)
Risk of secondary leukemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Trastuzumab MOA

A

Monoclonal Ab that binds to Her2

Inhibits proliferation and survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Tx of triple negative metastatic breast cancer

A

Atezolizumab + Taxane

  • PARP inhibitors after chemo if BRCA mutant
  • Carboplatin if BRCA mutant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

BRCA1/2 phenotype

A

younger age of cancer

Triple negative subtype with BRCA 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

BRCA gene positive: Ovarian screening

A

Nil screening program

BSO by age 45 to exclude occult malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

131
Q

-uximab

132
Q

-uzumab

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

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

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?

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions