clinical oncology 2: colorectal cancer Flashcards Preview

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Flashcards in clinical oncology 2: colorectal cancer Deck (22)
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1
Q

epidemiology of colorectal cancer:

A
  • 4th most common cancer overall
  • 2nd most common cancer cause of death (behind lung cancer)
  • 25% adults have adenomas by 50 -> 5% become colorectal cancer
2
Q

what are the functions of the colon?

A

extract water from faeces

  • faecal resevoir
  • bacterial digestion eg for vitamin B & K
3
Q

what is the microanatomy of the colon?

A

IMAGE 1 crypts of Lieberkuhn

4
Q

why is the colon particuarly susceptible to cancer?

A

very high turnover of cells -> proliferation renders cells vulnerable

5
Q

what is a polyp?

A

any projection from a mucosal surface into a hollow viscus
- may be hyperplastic, neoplastic, inflammatory, hamartomatous etc

6
Q

what is an adenoma?

A

benign neoplasm of mucosal epithelial cells

7
Q

what are the types of colonic polyps?

A
  • metaplastic/hyperplastic
  • adenomas
  • juvenile
  • peutz jeghers
  • lipomas
8
Q

what are hyperplastic polyps?

A

very common benign polyps

  • 90% of all polyps
  • <5mm
  • cells well ordered
  • multiple polyps often present IMAGE 2
9
Q

what are the types of colonic adenomas?

A

cell type: tubular / villous
protrusion: pedunculated / sessile
IMAGE 3

10
Q

what are tubular adenomas?

A

columnar cells with signs of dysplasia
(nuclear enlargement, multilayering, loss of polarity, increased proliferation, decreased differentiation, architectural disorganisation)

11
Q

what are villous adenomas?

A

mucinous cells with signs of dysplasia
(same as tubular + exophytic, frond-like extensions)
- rarely may be hypersecretory -> hypokalaemia

12
Q

what is dysplasia?

A

‘bad growth’ - abnormal growth of cells with some features of cancer

13
Q

how does ulcerative colitis affect the risk of colorectal cancer and why?

A

increases risk
- UC causes increased proliferation of cells in attempt to repair damage & inflammation damages basement membrane -> invasion is easier

14
Q

outline the adeno-carcinoma sequence:

A

IMAGE 4

15
Q

what mutation causes APC?

A
  • 5q21 mutation
  • site of mutation determines clinical variants
  • many patients have prophylactic colectomy <30
16
Q

what genetic conditions predispose to colorectal cancer?

A

FAP (familial adenomatous polyposis): inactivation of APC tumour suppressor genes
HNPCC (hereditary non-polyposis colorectal cancer): due to microsatellite instability
(microsatellites are repeat sequences prone to misalignment, often mismatch repair genes)

17
Q

how does colorectal cancer present clinically?

A
  • change in bowel habit
  • bleeding PR
  • iron deficient anaemia
  • mucus PR
  • bloating
  • cramps
  • weight loss, fatigue etc
18
Q

where do colorectal cancers usually occur?

A

signmoid colon or rectum

- others distributed fairly evenly

19
Q

what is the Duke’s classification?

A

first staging system that proved staging a cancer can improve its management
- TNM classification used nowadays

20
Q

how does the Duke’s classification work?

A

Duke’s A: growth limited to wall (muscularis propria), nodes negative
Duke’s B: growth beyond muscularis propria, nodes negative
Duke’s C1: nodes positive, apical lymph node negative
Duke’s C2: apical lymph node positive

21
Q

when are patients screened for colorectal cancer?

A

if deemed high-risk ie if they have:

  • had a previous adenoma
  • a close relative affected by colorectal cancer <45
  • 2 close relatives ever affected by colorectal cancer
  • evidence of a dominant familial cancer trait
  • UC/Crohn’s
  • heritable cancer within the family (including other sites)
22
Q

what is population screening?

A

the practice of investigating apparently healthy individuals with the object of detecting unrecognised disease or a high risk of developing disease, and of interviewing in ways that will prevent the occurrence of disease or improve the prognosis when it develops