clinical oncology 2: colorectal cancer Flashcards
epidemiology of colorectal cancer:
- 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
what are the functions of the colon?
extract water from faeces
- faecal resevoir
- bacterial digestion eg for vitamin B & K
what is the microanatomy of the colon?
IMAGE 1 crypts of Lieberkuhn
why is the colon particuarly susceptible to cancer?
very high turnover of cells -> proliferation renders cells vulnerable
what is a polyp?
any projection from a mucosal surface into a hollow viscus
- may be hyperplastic, neoplastic, inflammatory, hamartomatous etc
what is an adenoma?
benign neoplasm of mucosal epithelial cells
what are the types of colonic polyps?
- metaplastic/hyperplastic
- adenomas
- juvenile
- peutz jeghers
- lipomas
what are hyperplastic polyps?
very common benign polyps
- 90% of all polyps
- <5mm
- cells well ordered
- multiple polyps often present IMAGE 2
what are the types of colonic adenomas?
cell type: tubular / villous
protrusion: pedunculated / sessile
IMAGE 3
what are tubular adenomas?
columnar cells with signs of dysplasia
(nuclear enlargement, multilayering, loss of polarity, increased proliferation, decreased differentiation, architectural disorganisation)
what are villous adenomas?
mucinous cells with signs of dysplasia
(same as tubular + exophytic, frond-like extensions)
- rarely may be hypersecretory -> hypokalaemia
what is dysplasia?
‘bad growth’ - abnormal growth of cells with some features of cancer
how does ulcerative colitis affect the risk of colorectal cancer and why?
increases risk
- UC causes increased proliferation of cells in attempt to repair damage & inflammation damages basement membrane -> invasion is easier
outline the adeno-carcinoma sequence:
IMAGE 4
what mutation causes APC?
- 5q21 mutation
- site of mutation determines clinical variants
- many patients have prophylactic colectomy <30
what genetic conditions predispose to colorectal cancer?
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)
how does colorectal cancer present clinically?
- change in bowel habit
- bleeding PR
- iron deficient anaemia
- mucus PR
- bloating
- cramps
- weight loss, fatigue etc
where do colorectal cancers usually occur?
signmoid colon or rectum
- others distributed fairly evenly
what is the Duke’s classification?
first staging system that proved staging a cancer can improve its management
- TNM classification used nowadays
how does the Duke’s classification work?
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
when are patients screened for colorectal cancer?
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)
what is population screening?
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
