Colorectal Cancer Flashcards

1
Q

What are the histological layers of the GI tract from the inside out?

A
  1. Mucosa
  2. Submucosa
  3. Muscularis propria
  4. Subserosa
  5. Serosa - adventitia, peritoneum
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2
Q

What type of cancer are the vast majority of colorectal cancers and how common is it in the UK?

A
  1. Adenocarcinoma

2. 3rd most common cancer in the UK

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3
Q

In which age group is colorectal cancer usually found?

A

Uncommon <40, 86% in those >60.

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4
Q

What is significant in the history of someone presenting with colorectal cancer?

A
  1. FHx of colorectal cancer
  2. PMHx of colorectal cancer, previous polyps >1cm with high grade dysplasia
  3. Long standing - Crohn’s and ulcerative colitis, DM, immunosuppression, radiation exposure to the abdomen.
  4. Smoking, obesity, processed red meat, low fibre, alcohol.
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5
Q

What is the defect in Lynch syndrome and what is the inheritance pattern?

A
  1. Microsatellite instability - germline mutation in DNA mismatch repair genes (80% lifetime risk of colorectal cancer)
  2. Autosomal dominant (3% of colorectal cancers)
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6
Q

Which cancers does Lynch syndrome predispose to?

A

Endometrial (most common in women), ovarian, and GIT cancers (colorectal most common in men).

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7
Q

What is the surveillance for people with Lynch syndrome?

A

Colonoscopic surveillance at least every other year from 25 years old.

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8
Q

Where does Lynch syndrome colorectal cancer arise in the colon and how well differentiated are the cells?

A
  1. Right side of colon

2. Moor poorly differentiated

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9
Q

What is familial adenomatous polyposis?

A

Hundreds of adenomatous polyps develop in the colon during the 2nd to 3rd decade of life.

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10
Q

At what age is adenocarcinoma development inevitable in familial adenomatous polyposis?

A

35 years

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11
Q

What is the defect in familial adenomatous polyposis and what is the inheritance pattern?

A
  1. Germline mutation in APC gene (tumour suppressor)

2. Autosomal dominant

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12
Q

What is the surveillance and management for familial adenomatous polyposis?

A
  1. Surveillance sigmoidoscopy from 12 years

2. Prophylactic total bowel removal (panproctocolectomy) <25 years

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13
Q

Which cancers is familial adenomatous polyposis most associated with?

A

Small bowel, gastric, and thyroid cancers

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14
Q

What are the two main inherited disorders which increase your risk of developing colorectal cancer?

A
  1. Lynch syndrome

2. Familial adenomatous polyposis

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15
Q

What is the main protective factor for colorectal cancer?

A
  1. Vegetarian and high fibre diet

2. Daily aspirin use

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16
Q

What are colorectal adenomas?

A

Polyps derived from the epithelial cells lining the mucosa.

17
Q

What is the epidemiology for colorectal adenomas?

A
  1. Very common

2. Incidence increases with age such that at 60, they are found in 20% of the population.

18
Q

What are the two main types of polyp?

A
  1. Pedunculated (attached to mucosa by stalk)

2. Sessile (attached to mucosa by a broad base)

19
Q

What are the factors associated with a greater risk of progression from a polyp to a malignancy?

A

Increasing size, high grade dysplasia, histological type (villous > tubular).

20
Q

What are the features of colorectal dysplasia and how is it graded?

A
  1. Disordered growth
  2. Increase in nuclear:cytoplasmic ratio
  3. Premalignant - left untreated may become malignant
  4. Graded as low or high
21
Q

What is an adenoma?

A

A benign tumour of glandular epithelium which does not have malignant potential (except in the GI tract).

22
Q

What is the pathway for the majority of colorectal cancers?

A

Chromosomal instability pathway

23
Q

What is the progression of the chromosomal instability pathway?

A

Normal mucosa - adenoma - invasive adenocarcinoma

24
Q

What causes the progression of cancer in the chromosomal instability pathway?

A

Accumulation of mutation in these growth-regulating genes:

  1. Inappropriate activation of proto-oncogenes (K-ras)
  2. Inactivation of tumour suppressor genes (APC, both copes must be activated, two-hit hypothesis)
25
Q

How are mutations acquired by patients in the adenoma-carcinoma pathway of colorectal cancer?

A
  1. Sporadic throughout life (majority)

2. Germline mutation in APC with 2nd hit (FAP)

26
Q

What is the microsatellite instability pathway for colorectal cancer?

A

Cancers arise from serrated polyps, polyps acquired sporadic mutations which accumulate to cause carcinoma.

27
Q

What is the national screening programme for colorectal cancer?

A
  1. Faecal occult blood test every 2 years between 60-74 years old - colonoscopy if +ve, detects at early stage.
  2. One-off flexisig performed at age 55 - detect adenomatous polyps for removal, preventing progression.
28
Q

What is this a presentation of?
Bleeding/mucus PR, altered bowel habit (looser), constipation in obstruction, tenesmus, PR mass. Weight loss, night sweats, fever.

A

Left sided colorectal cancer

29
Q

What is this a presentation of?
Right-sided abdominal mass, vague symptoms, weight loss, iron deficiency anaemia, occult bleeding, abdominal pain, obstruction unlikely.

A

Right-sided colorectal cancer

30
Q

What is this a presentation of?

Jaundice from hepatic metastases, anorexia, weight loss, ascites, pneumaturia/recurrent UTIs due to colovesical fistula.

A

Metastatic colorectal cancer

31
Q

How is a suspected colorectal cancer investigated?

A
  1. FBC (microcytic iron deficiency anaemia), U&Es, LFTs, calcium, CEA (monitor for relapse, not diagnostic).
  2. Colonoscopy - full bowel prep and laxatives (histology/biopsy/resection)
  3. CT colonography if cannot tolerate colonoscopy.
  4. CT/MRI CAP if cancer confirmed to assess invasion.
32
Q

Why is staging a colorectal cancer important?

A

Single most important pathological prognostic indicator.

33
Q

What are the stages of T in TNM for colorectal cancer?

A

T1 - into submucosa but not muscularis propria
T2 - submucosa and muscularis propria but not subserosa
T3 - subserosa but not serosa
T4 - through serosal surface

34
Q

What is the Duke’s staging criteria?

A
Colorectal cancer:
A. Invades submucosa and/or muscularis propria but not beyond.
B. Into subserosa/beyond
C. Involves lymph nodes
D. Distant metastasis deposits
35
Q

What is the management of dysplastic polyps/carcinoma in situ in colorectal cancer?

A

Colonoscopic excision is curative if the margins are clear.

36
Q

What is the surgical management of stage I-III colorectal adenocarcinomas?

A

Laparoscopic:

  1. Right hemicolectomy - caecal, ascending and proximal transverse colon.
  2. Left hemicolectomy - distal transverse and descending colon.
  3. High anterior resection - sigmoid tumours.
  4. Anterior resection - low sigmoid or high rectal tumours.
  5. Abdominal-perineal (AP) resection and colostomy for very low rectal tumours.
  6. Total mesorectal excision for rectal cancers in combination with anterior/AP resection.
37
Q

What is the FOLFOX regime and what is it used for?

A
  1. Fluorouracil, folinic acid, oxaplatin.

2. Medical management of colorectal cancer.

38
Q

What is the management for metastatic colorectal cancer?

A
  1. Surgery with liver resection may be curative if confined to single lobe.
  2. Chemotherapy and endoscopic stenting in palliation.
  3. Radiotherapy mostly used in palliation.
39
Q

What is the prognosis of colorectal cancer based on Duke’s staging?

A
5-year survival:
A. 95%
B. 80%
C. 65%
D. 5% (20% if resectable)