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BPT Oncology > Colorectal Cancer > Flashcards

Colorectal Cancer Flashcards

1
Q

How is FOBT done?

A

second yearly test for 50-74 year olds

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2
Q

What does the FOBT measure?

A

human globin in stool

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3
Q

What is the most common cause of positive FOBT?

A

haemorrhoids, diverticular disease

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4
Q

What are the risk factors for colorectal cancer?

A

FHx, inflammatory bowel disease, previous abdominopelvic radiation, obesity, diabetes, meat consumption

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5
Q

What percentage of colorectal cancer is due to genetic syndromes?

A

5%

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6
Q

What are the polyposis syndromes?

A

FAP and MUTYH-associated polyposis

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7
Q

What is the pathogenesis of FAP?

A

loss of APC gene on chromosome 5 (autosomal dominant)

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8
Q

What is the pathogenesis of lynch syndrome?

A

loss of MLH1, MSH2, PMS2 or MSH6 leading to microsatellite instability - can be sporadic or hereditary

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9
Q

What is the risk of developing colorectal cancer in FAP?

A

90%

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10
Q

What is the risk of developing colorectal gene if MLH1 deficient?

A

50%

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11
Q

Which type of colorectal cancer can use immunotherapy?

A

mismatch repair deficient colorectal cancer because of the development of neoantigens

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12
Q

What is the management for T3 and above rectal cancer?

A

neoadjuvant therapy - either radiotherapy or chemoradiotherapy, to prevent local spread and improve chance of an R0 resection or to achieve complete pathological response

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13
Q

How is colorectal cancer staged?

A

T - tumour - where it is in relation to the bowel wall
N - regional lymph nodes
M - metastases

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14
Q

What is the role of adjuvant chemotherapy/

A

to ‘mop up’ micro-metastatic disease before it establishes as metastatic disease

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15
Q

What is the recommended treatment for stage 3 CRC?

A

adjuvant chemotherapy with a fluoropyrimidine (5FU or capecitabine) and oxaliplatin

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16
Q

What is ctDNA?

A

a blood test which assess the presence of circulating tumour DNA in those who’ve had a curative procedure -> maybe will be used to escalate or de-escalate therapy in locally advanced rectal cancer

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17
Q

What is the follow up for colorectal cancer?

A

colonoscopy at conclusion of treatment, 3 years, then 5 yearly
physical exam and CEA 3 monthly for 3 years then 6 monthly
CTCAP annually for 3 years

18
Q

What percentage of colorectal cancer presents as denovo metastatic disease?

A

25%

19
Q

What precentage of patients with local disease will relapse with metastatic disease?

A

50%

20
Q

What is predictive of response to EGFR directed therapy in metastatic CRC?

A

absence of RAS/RAF mutations

21
Q

What is the prognosis for BRAF positive patients with CRC?

A

poor - rapidly develop chemotherapy resistance

22
Q

Is MMR deficient status a good or bad prognostic sign?

A

good prognosis in stage 1-3 but bad prognosis in stage 4

23
Q

What is the management in stage 4b CRC?

A

palliative intent chemotherapy
often no role for surgery
combined with a targeted agent - a vascular endothelial growth factor inhibitor or endothelial growth factor receptor

24
Q

Is there any role for targeted agents in adjuvant treatment?

A

no

25
Q

What are the most common sites of metastases in CRC?

A

liver, lung, peritoneum

26
Q

What is oligometastatic disease?

A

metastases to one visceral organ

27
Q

What is the difference between management for M1a (oligometastatic) and M1b disease?

A

can use neoadjuvant therapy and aggressive surgical therapy for oligometastatic

28
Q

Is right sided disease or left sided disease more aggressive?

A

R sided

29
Q

What mutation is more common in right sided disease?

A

BRAF

30
Q

What mutation is more common in left sided disease?

A

RAS/RAF

31
Q

What are the common toxicities with fluoropyrimidine chemotherapy?

A

mucositis, diarrhoea, nausea, vomiting, coronary artery vasospasm, myelosuppression

32
Q

How is fluoropyrimidine metabolised?

A

by dihydropyrimidine dehydrogenase - deficient in 8% of the population - potential for fatal toxicity, manifests as early myelosuppression and bad mucositis - can lead to perforation and death

33
Q

What are the fluoropyrimidines?

A

5FU and capecitabine

34
Q

What is in FOLFIRINOX?

A

5FU and oxaliplatin plus irinotecan

35
Q

What is the mechanism of action of fluoropyrimidines?

A

thymidine synthetase inhibition

36
Q

What is the mechanism of action of irinotecan?

A

inhibits topoisomerase-1

37
Q

How is irinotecan metabolised?

A

the active metabolite SN-38 is metabolised by UAT181 - if deficient then irinotecan can cause fatal toxicity

38
Q

What are the toxicities of oxaliplatin?

A

peripheral neuropathy, cold dysaesthesia, fatigue, infusion reactions

39
Q

What mutations confer resistance to EGFR inhibitors?

A

RAS/RAF/HER2

40
Q

What are the toxicities of EGFR inhibitors?

A

hypomagnesia and cutaneous acneform rash

41
Q

What are the toxicities of VEG-F inhibitor?

A

hypertension, wound breakdown/impaired healing, GI perforation, proteinuria, thromboembolic events

BPT Oncology (10 decks)

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