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Cancer > 13. Colorectal cancer > Flashcards

13. Colorectal cancer Flashcards

1
Q

What is the function of the colon?

A
  • Extracts water from faeces (slightly involved in electrolyte balance)
  • Faecal reservoir
  • Bacterial digestion of vitamins
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2
Q

How fast do the bowel cells turnover and what eliminates genetically defective cells?

A
  • 2-5 million cells die per minute
  • Proliferation renders cells very vulnerable

Protective mechanisms to eliminate cells:
• Natural loss
• DNA monitors e.g. APC (adenomatous polyposis coli)
• Repair enzymes

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3
Q

What is a polyp?

A
  • Any projection from a mucosal surface into a hollow viscus

* May be hyperplastic, neoplastic, inflammatory etc.

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4
Q

What is an adenoma?

A

Benign neoplasm of the mucosal epithelial cells

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5
Q

What are the colonic polyp types?

A
  • Meta/hyperplastic - benign and common (mucosal damage)
  • Adenomas - increase RISK of cancer
  • Juvenile
  • Peutz Jeghers
  • Lipomas
  • Others
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6
Q

Outline hyperplastic polyps?

A
  • Very common and benign
  • Not dysplastic
  • 90% of all LI polyps
  • No malignant potential
  • 15% have k-ras mutation
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7
Q

What are the colonic adenoma types?

A
  • Tubular - look like test tubes lined up (most common)
  • Villous - look like sea anemone
  • Tubulovillous - mixture of both
  • Pedunculated - like a tree
  • Sessile - like a rug on top of a carpet
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8
Q

Describe tubular adenomas

A
  • Columnar cells with some elongation, nuclear enlargement, multi-layering and loss of polarity
  • Increased proliferative activity
  • Reduced differentiation
  • Disorganised
  • Hyperchromatic - look darker on slides (increased nucleus:cytoplasm)
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9
Q

Describe villous adenomas

A
  • Mucinous cells with elongation, nuclear enlargement, multi-layering and loss of polarity
  • Exophytic, frond-like extensions
  • Rarely may have hyper-secretory function and result in excess mucus discharge and hypokalaemia
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10
Q

What is dysplasia?

A
  • Abnormal growth of cells with some features of cancer
  • Not yet cancer
  • Disorganised
  • Pseudostratification and granular hyper-chromatic dark nuclei
  • Increased nucleo-cytoplasmic ratio
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11
Q

What is familial adenomatous polyposis?

A
  • Disease in which there are thousands of polyps in the bowel
  • Cancer is inevitable - prophylactic colectomy can stop this
  • Mutation in 5q21 gene
  • Associated with APC gene
  • Site of mutation determines clinical variants
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12
Q

Does the size of a polyp change the risk of cancer?

A

Yes, large polyps have a higher risk of cancer

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13
Q

What is the incidence of cancer if a polyp is left?

A

5%

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14
Q

Mutations in what genes can increase the risk of getting polyps => adenoma carcinoma?

A
  • APC
  • k-RAS
  • Smads
  • p53
  • Telomerase activation
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15
Q

What are microsatellites, what is microsatellite instability and how is this involved in adenoma carcinomas?

A
  • Repeat sequences prone to misalignment
  • Some microsatellites are in coding sequences of genes which inhibit growth or apoptosis
  • Microsatellite instability results from impaired “mismatch repair genes”
  • DNA can’t be repaired
  • DNA damage accumulates and leads to cancer
  • Recessive gene requiring 2 hits
  • HNPCC - germ-line mutation in these genes
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16
Q

What 2 main genes pre-dispose someone to an adenoma carcinoma?

A
  • FAP - inactivation of APC tumour suppressor genes

* HNPCC - microsatellite instability

17
Q

When does an adenoma become a carcinoma?

A

When it invades the adjacent tissue

18
Q

Can cooking food be dangerous?

A
  • Yes, damaging and destroying it can release materials that may be carcinogenic
  • Includes heterocyclic amines
19
Q

What deficiencies are linked with colorectal cancer?

A
  • Folate - it is a protector of cells and destroyed by over-cooking
  • It is also a co-enzyme for nucleotide synthesis and DNA methylation
  • MTHFR mutation affects the body’s ability to use folic acid -
  • Decreased methionine synthesis leads to genomic hypomethylation and focal hypermethylation
20
Q

List some anti-cancer food elements

A
  • Vitamin C - ROS (reactive oxygen species) scavenger
  • Vitamin E - ROS scavenger
  • Isothiocyanates (cruciferous vegetables)
  • Polyphenols - green tea (activate MAPK, EGCG-induced telomerase activity)
  • Garlic - associated with apoptosis
21
Q

Outline the clinical presentation of colorectal cancer

A

• Change in bowel habit
• Rectal bleeding
• Unexplained iron deficiency anaemia
(mucus, bloating, cramps, weight loss, fatigue etc.)

22
Q

Why do people not present very often thinking they have colorectal cancer?

A
  • People ignore the symptomatic presentation

* Patient’s (and doctors) rationalise these symptoms as ‘getting old’ etc.

23
Q

Describe the distribution of colorectal cancer in the bowel?

A
  • Caecum/ascending colon - 22%
  • Transvers colon - 11%
  • Descending colon - 6%
  • Recto-sigmoid - 55%

Very similar to adenomas

24
Q

What type are almost all cancers of the large bowel?

A

Adenocarcinomas (malignant tumours of glandular epithelium)

25
Q

What are the subtypes of adenocarcinoma?

A
  • Mucinous carcinoma
  • Signet ring cell
  • Neuroendocrine (carcinoid)
26
Q

What proportion of adenocarcinomas are well, moderately or poorly differentiated?

A
  • Well differentiated - 10%
  • Moderately differentiated - 70%
  • Poorly differentiated - 20%
27
Q

Outline the Dukes classification in the staging of colorectal cancer

A

A) growth limited to wall (muscularis propria) - lymph nodes negative
B) growth beyond wall - lymph nodes negative
C1) nodes positive (but apical lymph nodes negative)
C2) apical lymph nodes positive - other nodes drain into apical lymph nodes

28
Q

Is it prognosis worse when having cancer in the colon or rectum?

A

Rectum

29
Q

How does a high serum CEA (carcinoembryonic antigen) level affect prognosis?

A

Diminished prognosis

30
Q

Is the prognosis better or worse if rectal bleeding is a presenting symptom?

A

Improved prognosis

31
Q

How does local inflammation and immunological reaction affect prognosis?

A

Improved prognosis

32
Q

Who do you screen for high risk colorectal cancer?

A

(Family) History
• Previous adenoma
• 1st relative affected before the age of 45, or 2 affected 1st relatives
• Evidence of dominant familial cancer trait e.g. colorectal, uterine etc.
• UC and Crohn’s disease

33
Q

Why does the natural history of the disease need to be known for colorectal screening?

A

To identify location of screening

34
Q

What is the current NHS screening programme for colorectal cancer?

A
  • Age 55 - faecal test to check for blood in faeces

* Positives are referred for colonoscopy (60-75 years) or sigmoidoscopy (55-60 years)

Cancer (15 decks)

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