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BPT Oncology > Colorectal Cancer > Flashcards

Colorectal Cancer Flashcards

1
Q

How common is colorectal?

A

2nd most common in men and women

9% of cancer dx

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2
Q

What is the medium age of dx?

A

68 men, 72 women

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3
Q

In which age group is incidence increasing?

A

Those <50

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4
Q

What is the percentage 5 year survival of stage 1 vs 4

A

98.6 vs 13.4

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5
Q

When is FOBT given?

A

Second yearly for those 50-74

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6
Q

What is the percentage of positive FOBT have cancer?

A

1:29

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7
Q

What are risk factors?

A 
IBD
Previous abdominopelvic radiation 
Obesity
Diabetes and insulin resistance
Meat consumption 
Family history
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8
Q

Which IBD subgroup is highest risk?

A

USC with PSC

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9
Q

When should screening begin post abdopelvic radiation?

A

5 years after or at aged 30

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10
Q

What are the molecular subtypes?

A

CMS1 - MSI-immune
CMS2 - canonical
CMS3 - metabolic
CMS4 - Mesenchymal

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11
Q

What percentage of CRC are from genetic syndromes?

A

5%

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12
Q

What are the main genetic syndrome and what are the genes?

A

Polyposis syndrome inc FAP. APC gene

Lynch syndrome (Hereditary non-polyposis coli HNPCC). Loss of MLH1, MSH2, PMS2 or MSH6 - microsatellite instability

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13
Q

How do you differentiate familiar and sporadic lynch

A

Loss at normal tissue for loss of MLH1

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14
Q

What does deficiency in mismatch repair mean for outcomes

A

Better outcomes with deficient over proficient

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15
Q

Why are liver mets common in colon ca?

A

Colon is drained by portal vein

Cf to rectal cancer where lung mets are more common

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16
Q

How many LNs should be resected?

A

14

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17
Q

What is the rectum?

A

Below the peritoneal reflection

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18
Q

When do you get chemoradiotherapy in rectal?

A

Neoadjuvant

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19
Q

In which stages do you give adjuvant therapy in CRC?

A

Stage three and high risk stage 2

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20
Q

What is high risk stage 2 disease?

A

T4 (extending into peritoneum)
Presenting with obstruction or perforation
Inadequate node sampling
Presence of lymhovascular or perineural invasion

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21
Q

What are the T types?

A

Tx - cannot be assessed
T0 - no primary
Tis - carcinoma in situ, intraepithelial or invasion of lamina propria
T1 - invasion of submucosa
T2 - invasion of muscular propria
T3 - through muscularis propria into pericolorectal tissues
T4a - penetrates surface of visceral peritoneum
T4b - in invades or adherent to other organs or structures

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22
Q

What are the N classes?

A 
Nx - cannot be assessed
N0 - no LN mets 
N1 - Mets in 1-3 regional LNs 
N1a - mets in one regional LN
N1b - mets in 2-3 regional LN
N1c - tumour deposit in subserosa, mesentery, or nonperitonealised pericolic or perirectal tissues without region LN mets 
N2 - mets in 4 or more regional LNs 
N2a - mets in 4-6 regional LNs 
N2b - mets in 7 or more regional LNs
23
Q

What are the M classes?

A

M0 - no distant mets
M1 - distant mets
M1a - mets confined to one organ site (eg liver, lung, nonregional LN)
M1b - mets in more than one organ/site or the peritoneam

24
Q

What are the stages in relation to TNM?

A 
0 - Tis 
I - T1/2
IIA/IIB/IIC - T3/T4a/T4b
III - T1-4 + N1-2b
IV - Any T, any N with M1a or 1b
25
Q

What is the aim of adjuvant chemo?

A

Cure - mop up micro-metastasis

26
Q

What adjuvant chemo is used?

A

Fluoropyrimidine (either 5FU or capecitabine) and oxaliplatin
ie FOLFOX or CAPOX

27
Q

How long do you give adjuvant chemo?

A

3 in lower risk (T1-3, N1), 6 in higher (T4 and/or N2)

28
Q

What does the presence of post-op circulating tumour DNA mean?

A

Recurrence is inevitable

29
Q

What percentage of CRC express CEA?

A

70%

30
Q

How do you surveil post curative treatment?

A

No Australia guidelines - follow US:

Full colonoscopy if not already had one then at 3 years then 5 yearly
Exam w CEA 3monthly for three years then 6 monthly
CT CAP annually for three years

31
Q

What percentage of CRC presents with metastatic disease?

A

25%

32
Q

When is mutational status important?

A

Metastatic disease

33
Q

What are the implications of the different mutations?

A

RAS/RAF - predictive of response to EGFR directed therapy
BRAF - poor responders, rapid development of chemotherapy resistance and nodal spread
MMR status - MSI-H do poorly

34
Q

Which agents are used with EGFR positive?

A

Cetuximab

Panitumimab

35
Q

How is stage 4b managed?

A

Metastatic chemotherapy - FOLFOX and FOLIFIRI

No surgery

36
Q

Which vascular endothelial growth factor inhibitor is used?

A

Bevacizumab

37
Q

When are targeted therapies used?

A

Metastatic disease

Not in adjuvant therapy

38
Q

What is the 5 year survival of M1a disease?

A

as high as 40%

39
Q

How long is neoadjuvant therapy given in M1a?

A

3 months

40
Q

What side CRC is poorer prognosis?

A

Right

41
Q

What met CRC benefits from anti-EGFR therapy?

A

Left-sided RAS wildtype

cetuximab & panitumimab

42
Q

Which mutations are more common on which side?

A

BRAF - right side

RAS/RAF - left side

43
Q

What is hte mechanism of fluoropyrimidines (5FU)

A

Inhibit thymidine synthesis - metaabolites incorportted into DNA - apoptosis

44
Q

What is FOLFIRI?

A

5FU w irinotecan

45
Q

What is FOLFOX?

A

5FU w oxaliplatin

46
Q

What are the toxicities of fluoropyridines?

A

Mucocitis - oral to anus
N/V
Coronary artery vasospasm
Myelosuppression

47
Q

What is the variation in fluoropyrimidine metabolism?

A

Deficiency in enzyme dihydropyrimidine dehydrogenase
Present in 2-8% of population
Presents with early myelosuppression and bad mucositis
Antedote present

48
Q

What is the toxicity of irinotecan?

A

Diarrhoea, myelosuppression and fatigue

UAT181 enzyme metabolises SN-38 - deficiency in this (also in Gilbert’s syndrome) can lead to fatal toxicity with myelosuppresion

49
Q

What is the toxicity of oxaliplatin?

A

Peripheral neuropathy - cumulative effect, irreversible
Cold dysaesthesia
Fatigue
Infusion reactions

50
Q

What are the EGFR inhibitors?

A

Cetuximab and panitumimab

51
Q

What are the the VEG-F inhibitors?

A

Bevacizumab only one available in Aus

52
Q

When is bevacizumab used?

A

R sided RAS/RAF mCRC

53
Q

What are some side effects of bevacizumab?

A

HTN, proteinuria, thromboembolism, wound breakdown

BPT Oncology (17 decks)

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