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BPT Flashcards > Oncology > Flashcards

Oncology Flashcards

1
Q

PSA screening recommendations

A

Age - offer PSA testing every 2 yrs from 50-69
FHx
- one first degree relative 2.5-3x risk - from >45yrs
- 3x first degree relatives - from > 40 yrs

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2
Q

Prostate cancer investigations

A

Indicated if elevated PSA +/- abnormal DRE

MRI prostate
Multifocal core biopsy

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3
Q

Features suspicious of metastatic prostate cancer

A

PSA > 100ng/dl
Distribution of metastatic disease - sclerotic bone metastases

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4
Q

Prostate management options

A

Localised
- prostatectomy
- radiotherapy

Advanced disease
- hormonal therapy/bilateral orchiectomy
- chemotherapy
- supportive therapy –> RTx, bisphosphonates, palliative care

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5
Q

MOA of androgen deprivation therapy

A

ADT –> reduce GnRH –> reduce LH –> reduce testicular testosterone production

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6
Q

Side effects of ADT

A

Vasomotor symptoms
Reduced libido
Bone density loss
Muscle mass loss
Cardiovascular risk factors
Estrogen deficiency - gynaeocomastia, hot flushes
Testosterone deficiency - erectile dysfunction, diabetes, muscle weakness

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7
Q

Relationship between testosterone and estradiol

A

Testosterone converts to estrogen via CYP19/aromatase

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8
Q

Chemotherapy for prostate cancer

A

Taxanes - docetaxel, cabazitaxel

Used in combination with ADT for “high volume” disease, visceral metastases, multiple bone metastases

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9
Q

MOA of taxane chemotherapy

A

Interferes with microtubule growth, causing cell arrest in G2/M phase
Inactivates bcl-2 –> apoptosis

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10
Q

Side effects of taxane chemotherapy

A

Hair loss
N+V
Pancytopenia
Mucositis/diarrhoea
Lethargy
Fluid retention
Hypersensitivity reactions
Myalgias and arthralgias
Peripheral neuropathy
Nail changes

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11
Q

Examples of direct androgen receptor antagonist

A

Enzalutamide
Apalutamide
Darolutamide

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12
Q

Examples of androgen biosynthesis inhibitor (17a-hydroxylase)

A

Abiraterone
Blocks synthesis of testosterone in adrenal gland via inhibition of 17a-hydroxylase and C17,20-lyase activity

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13
Q

Mechanism of cortisol inhibition of abiraterone

A

Abiraterone (androgen biosynthesis inhibitor via 17a hydroxylase)

ACTH rises in response to increase in deoxycortisterone (due to decrease in 17OH-progesterone) –> leads to decrease in cortisol (thus should have mandatory concurrent steroids)

Also results in increased shunting, causing excess mineralocorticoid (hyperaldosteronism)

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14
Q

Side effects of direct androgen receptor antagonists

A

Fatigue
Cognitive impairment
Falls
Seizures
Rash

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15
Q

Side effects of androgen biosynthesis inhibitor

A

Cardiac toxicity
Hypertension
Concurrent steroids

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16
Q

Bone protection methods for prostate cancer

A

Calcium and vitamin D supplementation
Weight bearing exercise
DEXA scan monitoring
High risk - denosumab, ZA

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17
Q

Common complications of prostate cancer

A

Acute urinary retention
Bilateral ureteric obstruction
Spinal cord compression
Pancytopenia from BM infiltration
Bilateral lower limb lymphoedema secondary to pelvic obstruction

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18
Q

Genetic defects in prostate cancer

A

Aberrations in ~1/3rd of pts
BRCA2 most common alteration seen

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19
Q

Testicular cancer classification

A

Pure seminoma - AFP not elevated
Non seminoma/mixed germ cell tumour - often elevated

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20
Q

Testicular cancer epidemiology

A

Most commonly seen in 25-40 yrs
Median age at diagnosis is 33 yrs
Increased risk with cryptorchidism
5 yr relative survival ~98%

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21
Q

Tumour markers for prostate cancer

A

AFP, beta HCG, LDH

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22
Q

Role of AFP and beta HCG

A

Useful for surveillance/follow up
Associated with prognosis and used to guide treatment in advanced disease

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23
Q

Treatment of testicular cancer

A

Localised disease
- Orchiectomy
- Surveillance

Metastatic/advanced disease
- Chemotherapy (Bleomycin, etoposide, platinum)
- Resection of residual masses

Relapsed/refractory disease
- Second line chemotherapy
- High dose chemo and mini-autografts

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24
Q

Toxicities associated with chemotherapy for testicular cancer

A

Pancytopenia, alopecia, lethargy

Cisplatin
- Hearing impairment
- Tinnitus
- Peripheral neuropathy
- Renal impairment

Bleomycin
- Hypersensitivity
- Pneumonitis/lung toxicity

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25
Q

Risk factors for CRC

A

Excess body weight
Low levels of physical activity
High consumption of processed meat and EtOH
Low fibre consumption
Cigarette smoking
IBD
- Pancolitis > left sided colitis
- CD
FHx
Familial cancer syndromes

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26
Q

Common heritable syndromes for CRC

A

HNPCC/Lynch syndrome
FAP

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27
Q

Genetic factors for CRC

A

High penetrance genes - APC, biallelic MUTYH, BRCA1/2, PALB2, CDKN2A, TP53
Moderate penetrance genes - monoallelic MUTYH, APC allele, p.I1307K, CHEK 2

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28
Q

Characteristics of HNPCC/Lynch syndrome

A

Autosomal dominant, high penetrance
Mean age - 48 yrs
Defect in DNA mismatch repair (MMR) genes

Phenotype
- 60-70%: R sided/proximal colonic tumours
- 10% synchronous or metachronous tumours
- Polyps may be present, can overlap with AFAP
- Extracolonic tumours - endometrial, ovarian, stomach, SB, hepatobiliary, brain, renal, pelvis/ureter

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29
Q

Pts at risk of HNPCC

A

Amsterdam criteria
- >/ 3 relatives with Lunch associated Ca (of which one is a 1st degree relative)
- Lynch associated Ca involving at least 2 generations
- >/ 1 diagnosed before 50 yrs

Bethesda criteria
- CRC Dx < 50 yrs
- Synchronous, metachronous or other Lynch associated Ca, regardless of age
- CRC with MSI-like histology (TILs, mucinous/signet ring, poorly differentiated)
- >/ 1st degree relatives with Lynch associated Ca with 1 diagnosed < 50y/o
- CRC diagnosed in >/ 2 1st degree relatives with Lynch associated Ca

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30
Q

BRAFV600E mutation and Lynch syndrome

A

If BRAFV600E ABSENT - would rule out Lynch syndrome

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31
Q

MMR genes

A

MLH1, MSH2, MSH6, PMS2

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32
Q

MAPK pathway

A

EGFR > RAS > BRAF > MEK > ERK > cell growth and differentiation

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33
Q

BRAF mutation positive CRC

A

Poor prognosis
Poor response to standard chemo

Requires BRAF inhibitor with EGFR inhibitor (due to upregulation of EGFR in pathway)

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34
Q

FAP features

A

Germline mutation of APC gene on chromosome 5

FAP - Average age of polyposis 16 yrs (100-1000s), CRC by 45 yrs if untreated
–> screening from 10-15 yrs

AFAP - < 100 polyps, CRC 54 yrs
–> screening at 25 yrs

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35
Q

Colonoscopy timing for Lynch syndrome

A

1-2 yrly colonoscopies from age 25 yrs or 5 years younger than youngest affected case

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36
Q

Colonoscopy timing for APC mutation

A

Classic FAP
Surveillance from 10-15 yrs
Once adenoma detected, annual colonoscopy until total colectomy and ileorectal anastomosis

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37
Q

Examples and side effects of fluoropyrimidines

A

5-FU
Capecitabine

S/E:
Hand foot syndrome
Diarrhoea/mucositis
Haematological/myelosuppression
Coronary artery spasm
Acute coronary events

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38
Q

SEs of oxaliplatin

A

N+V, diarrhoea
Lethargy
Haematological/myelosuppression
Peripheral neuropathy - cumulative
Cold sensitivity/dysaesthesias
Laryngopharyngeal dysaesthesia
Hypersensitivity reaction

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39
Q

Factors to consider for treatment of CRC

A

L vs R sided primary
RAS/RAF status
MMR status
If metachronous/relapsed

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40
Q

Chemotherapy for metastatic CRC

A

Single agent:
- Fluoropyrimidines (5FU or capecitabine)
- Irinotecan
- TAS102

Doublet:
- Fluoropyrimidines with addition of oxaliplatin (FOLFOX/CAPOX) or irinotecan (FOLFIRI/CAPIRI)

Triplet: 5FU, oxiliplatin and irinotecan (FOLFOXIRI)

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41
Q

MOA and SE of irinotecan

A

Topoisomerase inhibitor
Metabolised by UGT1A1*28 genetic polymorphisms

S/E: Diarrhoea, anticholinergic effects, myelosuppression, alopecia

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42
Q

Targeted therapies for mCRC

A

VEGF inhibitors - bevacizumab (used regardless of RAS/RAF status, location)

EGFR inhibitor - cetuximab/panitumumab (only in RAS WT tumours, left sided primary)

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43
Q

Side effects of VEGF inhibitors

A

HTN
Delayed wound healing
Intestinal perforation/fistula formation
Proteinuria/nephrotic syndrome
Increased risk of bleeding/haemorrhage
Increased risk of arterial thrombotic events

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44
Q

Mechanisms of resistance for EGFR inhibitors

A

Downstream mutations of MAPK pathway
- KRAS/NRAS mutations
- BRAF mutations

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45
Q

S/E of EGFR inhibitors

A
  • Cutaneous
  • Skin - xerosis (dry skin), paronychia/fissures
  • Diarrhoea
  • Hypomagnesaemia
  • Infusion reactions
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46
Q

Use of pembrolizumab in mCRC

A

Used in MSI high (or dMMR) mCRC
MSI –> increases presence of neoantigens with increase TILs –> over expression of PD-1 and PDL-1

47
Q

Oesophageal cancer classification and prognosis

A

Classified - adenocarcinoma or SCC

Poor prognosis due to aggressive course and metastatic disease

48
Q

Treatment for oesophageal cancer

A

Neoadjuvant chemoradiation

Chemotherapy
- 5FU or capecitabine
- Platinum drugs - cisplatin, carboplatin, oxaplatin
- Irinotecan
- Taxanes - paclitaxel
- TAS102

Targeted egents
- HER2 positive - trastuzumab
- Ramicirumab

Immunotherapy
- Nivolumab (for PDL1 positive)

49
Q

Management of pancreatic cancer

A

Resection for early stage pancreatic cancer - Whipple’s procedure

Neoadjuvant/Adjuvant therapy with chemotherapy (FOLFIRINOX or gemcitabine based therapy)

+/- chemoradiation or stereotactic therapy

50
Q

MOA of gemcitabine + adverse effects

A

Pyrimidine analog chemotherapy

Pneumonitis
- potent radiosensitiser
- synergistically worsens gemcitabine-induced lung toxicity

51
Q

Clinical features of carcinoid syndrome

A

Cutaneous flushing
Venous telangiectasia
Secretory diarrhoea
Bronchospasm
Cardiac valvular lesions in right side of heart (inactivation of humoral substances by lungs protects left heart)

52
Q

Risk factor for breast cancer

A

Female gender
Increasing age
Older age at first birth
Oestrogen
EtOH
Family history

53
Q

Genetic factors involved in breast cancer

A

BRCA 1/2
STK11 (Peutz-Jeghers)
PTEN (PTEN hamartoma tumour syndrome/Cowden)
CDH1 (Hereditary diffuse gastric Ca)
MSH1/ML1/MSH6/PMS2/EPCAM (Lynch)
PALB2
CHEK2
ATM

54
Q

High risk factors of breast Ca

A

Multiples relatives with breast or ovarian Ca
> 1 primary Ca
Vertical transmission
FHx of rare malignancies
Epithelial ovarian Ca

55
Q

Screening of breast Ca

A

6 monthly breast examination
Annual mammogram from 40 (or 5 yrs younger than relative)
MRI breast (particularly if pre-menopausal)

56
Q

Investigations of breast cancer

A

Mammogram +/- US
FNA/Core biopsy
Referral to breast surgeon

57
Q

Poor prognostic features of breast Ca

A

Positive axillary lymph nodes
Increasing size
Higher grade
Negative hormone receptors
HER 2+ve
Younger age
Lymphovascular invasion

58
Q

Treatment of early stage breast Ca

A

Surgery
- Wide local excision
- Total mastectomy
(Neo)adjuvant chemo
Adjuvant RTx
Adjuvant hormone therapy
Adjuvant trastuzumab

59
Q

Indications of hormonal therapy for breast cancer

A

All ER+/PR+ breast cancer

Pre-menopausal: SERM (tamoxifen, toremifene), GnRH agonist
Post-menopausal: Aromatase inhibitors (anastrozole, letrozole, exemestane)

60
Q

MOA and adverse events of SERMs

A

Antagonist on oestrogen receptor in breast tissue or cancer
(However agonist effects on some receptors i.e. bones, uterus, liver)

Increases BMD in post-menopausal women
Risk of VTE, uterine Ca

61
Q

MOA and adverse events of aromatase inhibitors

A

Blocks DHEA –> reduces oestrogen

Reduces BMD
Arthralgias
No increased risk of VTE, uterine Ca

62
Q

Indications for and MOA of trastuzumab

A

HER2+ve tumour
Given with chemotherapy

Mechanism of action: Targets HER2/neu (c-erbB2) tyrosine kinase receptor → ↓ of HER2 initiated cellular signaling and ↑ antibody-dependent cytotoxicity → ↓ tumor growth

63
Q

Adverse effects of trastuzumab

A

Cardiomyopathy (usually reversible, however should have TTE prior)
GI side effects

64
Q

Indications of chemotherapy for breast cancer

A
  • Tumor size > 2 cm
  • Triple-negative breast cancer and tumor size ≥ 0.5 cm
  • HER-2 positive breast cancer and tumor size > 1 cm
  • Positive lymph nodes
  • Aggressive tumor histology
65
Q

Treatment for ER+/HER2- breast Ca

A

First line - CDK4/6 inhibitor + hormonal therapy
(chemo if rapid response required)

CDK4/6 inhibitor - ribociclib, abemaciclib, palbociclib

66
Q

Treatment for HER2+ breast Ca

A

1st line - trastuzumab/pertuzumab/taxane

2nd line -
Trastuzumab emtansine (T-DM1/Kadcyla) - conjugate with antimicrotubule agent
Trastuzumab deruxtecan (T-DXed) - conjugate with topoisomerase inhibitor

3rd line - Lapatinib

67
Q

MOA of Pertuzumab

A

Monoclonal Ab, used in combo with trastuzumab
Binds to dimerisation domain of HER2 receptor but also prevents binding with itself or other EGFR

68
Q

Treatment for BRCA+ve cancer

A

PARP inhibitor
Repairs DNA damage

69
Q

Clinical presentation of Pancoast tumour

A

Superior sulcus tumour
Usually NSCLC
Pain in shoulder/neuropathic arm pain
Horner’s syndrome (though rare)
Wasting hand muscles

70
Q

Clinical features of lung cancer

A

Cough
Haemoptysis
Chest pain
Dyspnoea - bronchial obstruction, pleural effusion
Hoarse voice
SVC obstruction
Extrathoracic mets
Hypercalcaemia
SIADH (especially SCLC)
Hypertrophic pulmonary arthropathy

71
Q

Features of SCLC

A

Early to metastasise, high mitotic rate
Classically bulky lymphadenopathy
Very chemo and radiosensitive
Almost all cases are smokers
Doesn’t cause clubbing
Paraneoplastic syndromes

72
Q

Treatment of SCLC

A

Chemoimmunotherapy

1st line - Atezolizumab (PD-L1) + carboplatin + etoposide

2nd line
- Topotecan/irinotecan
- Lurbinectedin
- Cyclophosphamide/doxorubicin/vincristine

73
Q

Features of mesothelioma

A

Asbestos + tobacco related
Long latency (30-40 yrs)

74
Q

Treatment for mesothelioma

A

Generally incurable
- Radical treatment - extrapleural pneumonectomy
- Platinum + pemetrexed (folate antimetabolite)
- Dual immunotherapy: nivolumab and ipilimumab

75
Q

Staging principles

A

Stage 1: small tumour
Stage 2: large tumour or small tumour with nodal involvement
Stage 3: very large tumour, invasion into mediastinum, ipsilateral lung nodules (3a) or contralateral hilar nodes (3b)
Stage 4: pleural effusion, contralateral lung nodules, distant mets

76
Q

Driver mutations in lung adenocarcinoma

A

EGFR
ALK rearrangement
ROS1 fusion
BRAF
ERBB2
MET
RET
NTRK
KRAS

77
Q

EGFR inhibitor examples

A

1st gen: Gefitinib, erlotinib
2nd gen: Afatinib
3rd gen: Osimertinib

78
Q

Adverse effects of EGFR inhibitors

A

Acne like rash
Diarrhoea
Nausea
Pulmonary fibrosis

79
Q

Mechanism of action of EGFR inhibitor resistance

A

Due to T790M resistance mutation
Use of osimertinib highly active against T790M

80
Q

Targeted therapy for ALK gene rearrangement

A

ALK phosphorylation inhibitors
1st gen: crizotinib
2nd gen: ceritinib
3rd gen: alectinib (better CNS penetration), lorlatinib, brigitinib

81
Q

Targeted therapy for ROS-1 fusion

A

Responsive to ALK inhibitors
- Crizotinib, lorlatinib, entrectinib

82
Q

Treatment for KRAS +ve lung adenocarcinomas

A

More common in smokers
Chemo as first line
Sotorasib (KRAS G12C inhibitor) as 2nd line therapyT

83
Q

Treatment for NSCLC with no driver mutations

A

PD-L1 score
If < 50% - chemoimmunotherapy
–> platinum doublet + PD-L1 inhibitor

If > 50% –> single agent PD-L1 inhibitor

84
Q

Tumour markers

A

CEA - colon cancer
CA125 - ovarian cancer
CA15.3 - breast cancer
CA19.9 - breast cancer
AFP - germ cell tumours/hepatocellular cancer
PSA - prostate cancer

85
Q

Predictive marker of melanoma

A

Breslow depth of lesion and presence or absence of ulceration

86
Q

Clinical signs of melanoma

A

Asymmetry
Borders (uneven vs even)
Colour
Diameter
Enlargement or evolution

87
Q

Melanoma subtypes

A

Radial growth phase
- Superficial spreading
- Lentigo maligna
- Acral lentiginous

Vertical growth phase
- Nodular

88
Q

Clinical features looked at in early nodular melanoma

A

Symmetry
Raised
Colour
Firmness
Progressive growth

89
Q

Major determinants of outcome for stage III melanoma

A

Number of metastatic lymph nodes
Tumour burden
Presence of absence of ulceration of primary melanoma
Presence or absence of satellite or in-transit metastasis

90
Q

Pathway activated in melanoma

A
  • MAPK cascade activated in almost all types of melanoma – 80% due to mutations in NRAS or BRAF genes
  • BRAF mutations present in 40-60% of metastatic melanomas
  • More common in cutaneous melanomas without chronic sun damage (mutations in c-kit more common in CSD)
  • With treatments, disease related to BRAF mutations has significantly improved
91
Q

Management of stage III melanoma

A

Stage 3A - observation

Stage 3B/3C/3D/resected stage 4 - adjuvant therapies
- BRAF mutant: Dabrafenib and trametinib (BRAF and MEK inhibitor)
- Anti-PD1 for all patients: Nivolumab/Pembolizumab

92
Q

Treatment of stage IV melanoma

A

Targeted therapy with immunotherapy (PDL1 inhibitor, BRAF mutant targeted therapy)
Surgical resection of metastasis

93
Q

BRAF targeted therapy

A

Dabrafenib
Trametinib

94
Q

Molecular biology profile of melanoma

A

Intermittent sun exposure:
- BRAF
- NRAS
- PTEN
- AKT
- p16

Chronic sun exposure:
- KIT
- CDK4
- Cyclin D1

Acral exposure:
- NRAS
- KIT
- CDK4
- Cyclin 4

Mucosal exposure
- CDK4
- KIT

95
Q

BRAF inhibitors

A

Vemurafenib (selective V600E mutations)
Dabrafenib (inhibits all V600 mutations)
Encorafenib (inhibits all V600 mutations)

96
Q

MEK inhibitors

A

Cobimetinib
Trametinib
Binimetinib

97
Q

cKIT inhibitors

A

Imatinib

98
Q

Management of activating BRAF mutations

A

BRAF kinase inhibitor (e.g., vemurafenib) is used in metastatic or unresectable melanomas that have the BRAF V600E mutation (substitution of glutamic acid in place of valine at amino acid position 600 caused by activating mutations in the BRAF gene)

99
Q

BRAF inhibitor adverse events

A

Cutaneous SCC and keratoacanthoma
Hyperkeratosis
Skin papilloma
Hand foot syndrome
Alopecia
Photosensitivity and sunburn

100
Q

MOA of CTLA-4

A

Receptor expressed on activated helper T cells and CTLs
Inhibits T cell activation and proliferation
- Binds to B7 molecule on APCs surface with higher affinity than CD28
- Puts break on T cell proliferation

CTLA4 ligands (CD80 and CD86)

101
Q

Immune related adverse events with CTLA-4 inhibitors

A

Rash
Colitis
Arthritis
Hepatitis
Hypo/hyperthyroidism
Pneumonitis

102
Q

Management of IRAEs

A

Grade III/IV –> generally reversible and can be treated with standard anti-inflammatory therapies i.e. corticosteroids

Grade IV –> prolonged steroid taper and TNF blockade with infliximab or prolonged bowel rest with TPN

103
Q

Anti-PD1 MOA

A

Restores anti-tumour T cell function
Enhances pre-existing T cell response
Increases cytokine production

104
Q

Anti-CTLA4 MOA

A

Induces de novo anti-tumour T cell responses
Enables adaptation to evolving tumour
Promotes emergence of memory T cells
Causes compensatory increase in tumour PD-L1

105
Q

PD-1 protein

A

T cell coinhibitory receptor structurally similar to CTLA-4 but with distinct biologic function and ligand specificity
Two known ligands, PD-L1 and PD-L2

Selectively expressed on many tumours and on cells within tumour microenvironment in response to inflammatory stimuli

106
Q

VEGF inhibitor side effects

A

HTN - predictive marker
Reversible posterior leukoencephalopathy
Proteinuria/renal dysfunction
Haemorrhage

107
Q

mTOR inhibitors toxicity

A

Oral ulceration - mouth ulcers, stomatitis
Rash
Fatigue
HTN
Hand and foot syndrome
Diarrhoea
Infections
Pneumonitis

108
Q

TKIs rash predictive marker

A

Higher grade rash, higher probability of response

109
Q

VEGF receptor TKIs

A

Pazopanib
Sunitinib
Sorafenib
Cabozantinib
Tivozanib
Axitinib
Lenvatinib

110
Q

mTOR inhibitors

A

Everolimus
Temsirolimus

111
Q

Anti-VEGF antibodies

A

Bevacizumab

112
Q

RCC paraneoplastic syndrome

A
  • Secondary hypercortisolism: due to ectopic ACTH release
  • Secondary polycythemia: due to ectopic erythropoietin (EPO) secretion
  • Hypertension: due to the release of renin
  • Hypercalcemia: due to the release of PTHrP (parathyroid hormone-related protein)
  • Leukemoid reaction: due to bone marrow stimulation
  • Limbic encephalitis: Memory loss, Psychosis, Depression
113
Q
A
114
Q

Features of Li Fraumeni syndrome

A

Mutation of p53 tumour suppression gene
BLAST 53
- Breast cancer/brain tumour
- leukaemia/lymphoma
- adrenocortical carcinoma
- sarcoma
- Tp53

BPT Flashcards (32 decks)

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