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FRACP Written Exam 2023 > Oncology > Flashcards

Oncology Flashcards

1
Q

Most common causes of positive FOBT result

A

Haemorrhoids (1), diverticular disease (2)
Only 1/29 positive FOBT diagnosed with cancer

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2
Q

Risk factors for CRC (6)

A
  • IBD (UC, PSC, Crohn’s disease)
  • Previous abdominopelvic radiation
  • Obesity
  • Diabetes & insulin resistance
  • Meat consumption esp. processed meats
  • Hereditary syndromes
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3
Q

Familial adenomatous polyposis (FAP)
- % of CRC
- Risk of developing CRC
- What gene involved?

A

<1% of CRC
Characterised by >100 polyps with >90% risk of CRC by age 45
Due to loss of APC gene on Chr 5
100% penetrance

Clinical syndromes:
Gardner’s Syndrome - osteomas, epidermoid cysts, desmoid tumours
Turcot’s Syndrome - CNS malignancies
Attenuated FAP - 100% penetrance, later in life, less polyps

(MAP - MUTYH associated polyposis - loss of MUTYH gene, AR inheritance)

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4
Q

Lynch Syndrome (HNPCC)
- % of CRC
- Risk of developing CRC
- What gene involved?

A

Approx. 3% of CRC
Greatest risk with MLH1 def - lifetime risk is 50%
Due to loss of MLH1, MSH2, PMS2 or MSH6 - leads to presence of large repeat sequences (microsatellite instability)
AD inheritance
80% penetrance

3-2-1 rule
3 (or more) relatives with HNPCC-related cancer, one of whom is a FDR of the other 2
At least 2 successive affected generrations
1 (or more) diagnosed under age of 50
FAP excluded

MLH1 can also be sporadic mutation - due to promoter methylation (thus if MLH1 methylated - not Lynch)

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5
Q

Cetuximab, panitumumab

A

Anti-EGFR
Role in RAS/RAF wt CRC

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6
Q

RAS/RAF wt association with anti-EGFR agents?

A

Crystal study showed that addition of cetuximab to FOLFIRI improved OS in RAS/RAF wt but not in RAS/BRAF mt

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7
Q

Where does rectal cancer more commonly metastasise to c.f. right/left sided bowel?

A

Pulmonary mets due to direct drainage into IVC

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8
Q

Management of T3-4 rectal Ca

A

Either short course RTx or long course chemoRTx with radiosensitising 5FU/capecitabine

Long course superior for local tumour response/control

Approx 15-30% will haev complete pathological response

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9
Q

Relevance of ctDNA in CRC

A

Presence of ctDNA is marker of those who will likely relapse

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10
Q

Surveillance guidelines post curative therapy for CRC

A

No Australian guidelines but:
C’scope at 3 years post then 5 yearly
CEA every 3 months for 3 years then 6 monthly
CT CAP annually for 3 years

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11
Q

Prognosis of BRAF mt CRC

A

Poor prognosis - poor response, rapid development of resistance and often nodal spread

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12
Q

Metastatic CRC management

A

Palliative intent CTx + targeted therapy

FOLFOX or FOLRIRI or capecitabine
+
Anti-EGFR/VEGF etc.

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13
Q

Differences between right and left sided CRC & prognosis

A

Right sided CRC has poor prognosis
Right colon originates from midgut
Left colon originates from hindgut
BRAF mutations more common in right sided CRC
RAS/RAF wt more common in left sided CRC

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14
Q

How do fluoropyrimidines (e.g. 5FU/capecitabine) work?

A

Through thymidine synthesis inhibition
Metabolites incorporated into DNA leading to apoptosis

Capecitabine is oral 5FU

Can be single agent or in combination (e.g. FOLFIRI/FOLFOX)

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15
Q

FOLFIRI

A

5FU + leucovorin + irinotecan

Irinotecan = topoisomeraise-1 inhibitor
Leucovorin = folic acid

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16
Q

FOLFOX

A

5FU + leucovorin + oxaliplatin

Leucovorin = folic acid

Oxaliplatin = only platinum agent that does not have single agent efficacy, binds directly to DNA impairing replication

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17
Q

Toxicities of fluoropyrimidines (4)

A

Mucositis, diarrhoea/vomiting, coronary artery spasm and myelosuppression

5FUs metabolised by dihydropyrimidine dehydrogenase (DPD) - deficiency occurs in 2-8% - can cause fatal toxicity (early myelosuppresion & severe mucositis)

18
Q

Toxicities of irinotecan (3)

A

Diarrhoea, myelosuppression, fatigue

UAT18 metabolises SN-38 which is active metabolite

Deficiency of UAT181 is seen in Gilbert’s and can lead to fatal toxicity (myelosuppression)

19
Q

Toxicities of oxaliplatin (4)

A

Peripheral neuropathy (predominantly sensory), cold dysaesthesia, fatigue and infusion reactions

20
Q

Unique toxicities of RAS/RAF/HER2 mutations with EGFR inhibitors?

A

Confers resistance
HypoMg (due to renal loss of Mg)
Cutaneous acneform rash

21
Q

Toxicities of bevacizumab (5)

A

Hypertension
Wound breakdown/impaired healing
GI perforation
Proteinuria
Thromboembolic events
Reversible posterior leukoencephalopathy

22
Q

Mechanism of action of enzalutamide

A

Androgen receptor (AR) antagonist

CYP3A4 + CYP2C9 inducer

23
Q

Mechanisms of resistance in CRPC (6)

A

AR amplification
AR mutation
AR splice varirants
Altered activity of AR coactivators
Intra-tumoral androgen synthesis
Aberrant kinase activation

24
Q

Definition of castrate level of testosterone

A

<1.7nmol/L

25
Q

Management of metastatic castrate sensitive prostate cancer (mCSPC)

A

Androgen deprivation therapy (ADT)

(1) GnRH agonists - gosereline, leuprolide
- Can have initial clinical flare phenomenon due to increase in LH and testosterone

(2) GnRH antagonists - degarelix
- Rapid reduction in serum testosterone, avoid clinical flare phenomenon
- Increased local injection site reactions
- Lower risk of CV side effects

(3) Bilateral orchidectomy

MAJOR CHANGE - intensification therapy - upfront use of docetaxel/abiraterone/enzalutamide/local RTx - increases OS
- CHAARTED study - docetaxel in CSPC - improved survival

26
Q

Management of metastatic castrate resistant prostate cancer (mCRPC)

A

(1) Chemotherapy
- Docetaxel/cabazitaxel

(2) Androgen receptor targeted therapies
- Abiraterone/enzalutamide

(3) Immunotherapy (e.g. sipuleucel)
- Modest effect

(4) Radiopharmaceuticals (Lu-PSMA)
- Lutetium-PSMA

(5) PARP inhibitors

27
Q

Mechanism of docetaxel/cabazitaxel & side-effects/toxicities associated

A

Taxane therapy

Stabilises microtubules during mitosis/interphase leading to mitotic arrest/cell death

Toxicities of docetaxel: sensory/motor PN, cytopenias, hypersensitivity reactions

Toxicities of cabazitaxel: diarrhoea, cytopenias, sensory/motor PN (but less than with docetaxel)

28
Q

Mechanism of abiraterone & toxicities

A

Androgen biosynthesis inhibitor
- Inhibits 17-alpha-hydroxylase and lyase which coverts ACTH to DHEA

Increases mineralocorticoid hormone production

Side effects: hypertension, hypokalaemia, peripheral oedema [[all related to increased mineralocorticoid ]] + transaminitis

Co-administered with prednisolone

29
Q

ALK mutation

A

Translocation, chromosomal rearrangement mutation
Localted on short arm of Chr 2
Alectanib - alk targeted therapy

30
Q

Stage IV NSCLC

A

Includes unilateral pleural effusion, contralateral lung involvement or other mets

Asian, non-smoker, female
EGFR mutation

PDL1 status - pembrolizumab

In NSCLC - KRAS mutations most prevalent genomic driver
> Sotorasib irreversibly inhibits KRAS

31
Q

Osimertinib

A

3rd generation EGFR TKI
Excellent CNS penetration

Toxicities: skin + diarrhoea, pneumonitis 2% (cannot combine with immunotherapy)

32
Q

Ipilimumab MoA?

A

CTLA-4 inhibitor

33
Q

Bevacizumab MoA?

A

Anti-VEGF

34
Q

Ramucirumab MoA?

A

Anti-VEGFR

35
Q

Cetuximab MoA?

A

Anti-EGFR
Chimeric
Head and neck cancer
Metastatic left sided KRASwt CRC

36
Q

General side effects of tyrosine kinase inhibitors?

A

Most - cardiotoxicity, hepatotoxicity, pulmonary toxicity

Most - fatigue, diarrhoea, mucositis, nausea, LFT derangement

Many - QTc prolongation, endocrine (thyroid, sugars)

EGFR (including BRAF inhibition) - dermatologic toxicity

VEGF - hypertension, impaired wound healing, GI perforation, proteinuria

37
Q

What tumour marker is falsely elevated in smokers?

A

CEA

38
Q

Example of CDK4/6 inhibitors?

A

Palbociclib, ribociclib

39
Q

Radiosensitive neoplasms (for spinal cord compressions)?

A

Lymphoma
Myeloma
Small cell lung cancer
Germ cell tumours
Prostate cancer
Breast cancer

40
Q

Radioresistant neoplasms (for spinal cord compressions)?

A

Melanoma
Renal cell
NSCLC
GI cancers
Sarcoma

41
Q

Cord compression tumour grading?

A

FRACP Written Exam 2023 (20 decks)

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