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104 Theme 1 - The Alimentary System > Bowel cancer > Flashcards

Bowel cancer Flashcards

1
Q

Why use the term Bowel Cancer?

A
  • It is the language the public understands
  • Terminology was devised following survey of the public prior to the introduction of the Bowel Cancer Screening Programme
  • For the purpose of public understanding bowel cancer only applies to the large intestine i.e. to colon and rectal cancer
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2
Q

What are the Key Facts about Bowel Cancer ?

A
  • Bowel cancer is the third most common cancer in women after breast and lung cancer
  • Bowel cancer is the third most common cancer in men after prostate and lung cancer
  • High incidence of bowel cancer in western world; low incidence in Asia and Central Africa
  • Bowel cancer affects men and women equally
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3
Q

What are the Risk Factors for Bowel Cancer ?

A
  1. Bowel cancer is believed to be an environmental disease and potentially preventable
  2. Longstanding ulcerative colitis
  3. Crohn’s disease; to a lesser extend than UC
  4. Presence of adenoma in the large bowel
  5. Previous history of bowel cancer surgery
  6. Family history of bowel cancer
  7. Old age – older people are also at risk of cancer in other organs besides bowel cancer
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4
Q

1.Bowel cancer is believed to be an environmental disease and potentially preventable, therefore which behaviours can affect the risk of bowel cancer?

A

a) Individuals who migrate from a low risk area to a high risk area increase their risk of developing bowel cancer e.g. Japanese who migrated to the USA acquired the risk of their host country
b) Foods rich in red meat & fat increase the risk of bowel cancer
c) Food rich in vegetables, fruit & fibre reduces the risk of bowel cancer by ↑ faecal bulk & reduces transit

time

d) Physical activity & low BMI are associated with low risk of bowel cancer

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5
Q

Which diet reduces the risk of bowel cancer?

A

Diet rich in high fibre, fruit & vegies reduces the risk of bowel cancer

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6
Q

How does high fibre diet reduce bowel cancer?

A
  • By increasing the formation of short chain fatty acids which promote healthy gut micro-organisms and reduces the proliferation of potentially neoplastic cells
  • Increasing stool bulk reduces transit time and potential carcinogens in the stool have a shorter contact with the bowel mucosa
  • High fibre diet reduces formation of secondary bile acids which are potentially carcinogenic
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7
Q

What is a polyp?

A

•A polyp is a protruding growth into a hollow viscus; can be benign, adenoma or malignant

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8
Q

What are the 2 types of polyp?

A

•In bowel cancer screening a polyp is either ‘innocent’ or precancerous. If the cancer is polypoid, do not use the term polyp

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9
Q

What are adenomas?

A

•Most polyps in the large bowel are adenomas i.e. pre-cancerous lesions and consist of dysplastic epithelium

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10
Q

What does this show?

A
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11
Q

What is dysplasia?

A

•Dysplasia (Greek: dys = bad; plasis = formation); the cells have morphological features of cancer but without invasion of the surrounding tissue

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12
Q

What are the 2 types of dysplasia?

A
  • Low grade dysplasia – early precancerous features
  • High grade dysplasia – advanced precancerous features with high risk of invasion if not removed
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13
Q

How is polyp type confirmed?

A

•Whether a polyp is benign (hyperplastic), dysplastic (adenoma) or cancerous, the diagnosis can only be confirmed on microscopic examination by the pathologist

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14
Q

What are the pathological features of the different types of polyps ?

A
  • Hyperplastic consists of numerous goblet cells when compared to normal mucosa; has a lace - like pattern
  • Tubular adenoma has test tube-like appearance
  • Villous adenoma has finger-like appearance
  • Tubulovillous adenoma has a mixture of tubular and villous features

Pathology reporting: Tubular adenoma with

low or high grade dysplasia

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15
Q

Label the type of polyps

A
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16
Q

What is the Adenoma-Carcinoma Sequence?

A
  • This is a stepwise progression from normal mucosa to adenoma to cancer
  • Morphological features i.e. macroscopic and histological features are also mirrored at genetic level where there are stepwise genetic alterations
  • Carcinoma of the bowel is a classic example of multistep carcinogenesis both phenotypically (morphologically) and genetically
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17
Q

What is the evidence for Adenoma - Carcinoma Sequence?

A

•Observational studies have shown that most sporadic cancers which are not genetically determined arise from adenomas and this is supported by the following evidence:

1) Populations which have a high prevalence of adenomas have a high prevalence of cancer
2) Distribution of adenomas in the large bowel mirrors the distribution of bowel cancer i.e. 60% of the cancer arise in the left colon and rectum and most adenomas arise in this region; this is the rationale for bowel cancer screening using flexible sigmoidoscopy

Peak incidence of polyps predates the development of cancer e.g. peak age for adenomas is around 60years, median age for bowel cancer is 71years

4) Residual adenoma is found in most cases of early invasive cancer
5) Risk of cancer is directly related to the number of polyps e.g. patients with Familial Adenomatous Polyposis have high risk of cancer
6) Programmes which follow-up patients and remove adenomas reduce the incidence of bowel cancer

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18
Q

What is Familial Adenomatous Polyposis (FAP)?

A
  • Patients with FAP have hundreds to thousands of polyps in large bowel, 500 – 2500
  • A minimum of 100 polyps is required to make diagnosis FAP
  • The polyps are dysplastic and therefore called adenomas
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19
Q
  • FAP is associated with _____% risk of development of cancer by age of 30
  • Patients undergo prophylactic colectomy around the age of ___
  • FAP contributes to ____% of bowel cancer
A

100%

20

1%

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20
Q

What is the genetics of FAP in Bowel Cancer?

A
  • Hereditary autosomal dominant condition
  • The defective gene is on Chr 5q21 known as the APC gene (Adenomatous Polyposis Coli)
  • Patients acquire the first abnormal gene in utero as a germ cell mutation known as the ‘first hit’
  • To develop polyps they acquire the second genetic abnormality in the somatic cells known as the ‘second hit’
  • The ‘second hit’ paves the way for the development of polyps from a young age throughout the teens
  • Patients have no polyps at birth and require ‘ the second hit’ to develop polyps
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21
Q

What does this show?

A

Early Multiple Adenomas in FAP

22
Q

What does this show?

A

Advanced Multiple Adenomas in FAP

23
Q

What is the Two Hit Hypothesis in Hereditary and Sporadic Bowel Cancer?

A
  • In FAP the patient is born with a single genetic abnormality (first hit ) and acquires the second genetic abnormality ( second hit) after birth to develop adenomas then cancer
  • In sporadic bowel cancer the person acquires the two hits in somatic cells to develop adenomas then cancer
  • The two hit hypothesis was proposed by Knudson to explain hereditary retinoblastoma, cancer of the eye in children and is applicable to most cancers
24
Q

How does the second hit lead to heterozygosity?

A
  • The mutation of the APC gene is important in the initiation of bowel cancer
  • With one copy of abnormal gene, the cells are heterozygous
  • The loss of the second set of normal genetic material during the ‘second hit’ leads to loss of heterozyosity and cells will acquire two identical copies of abnormal genes i.e. become homozygous for the cancer gene
  • After the second hit the cells acquire more genetic abnormalities to progress with adenoma-carcinoma sequence
25
Q

How does the progress from normal muscosa to cancer happen?

A

To progress from normal mucosa to adenoma to cancer genetic abnormalities are acquired in a stepwise fashion
( Fearon & Vogelstein model)

26
Q

Complete the table on the progress from normal muscosa to cancer

A
27
Q

Name the genetic abnormalities associated with bowel cancer

A
  • Lynch Syndrome (previously Hereditary Non-polyposis Colorectal Cancer (HNPCC)
  • Familial adenomatous polyposis (FAP)
  • Attenuated FAP - less than 100 adenomas
  • Familial Colorectal Cancer Type X (FCCX)
  • MUTYH Associated Polyposis (MAP)
  • Serrated Polyposis Syndrome
  • Hamartomatous Polyposis Syndrome
28
Q

What is Lynch Syndrome (LS) Hereditary non-Polyposis Colorectal Cancer (HNPCC)?

A
  • Familial cancer affecting predominantly the caecum and right colon, before the age of 50
  • Associated with endometrial, small bowel and cancer of the urinary tract; it is important when asking about family history of cancer not to concentrate just on large bowel cancer
  • There are no precursor polyps hence the name
  • Bowel cancer from young patients and advanced cancers are routinely tested for Lynch Syndrome genetic mutations whether they have a family history of cancer or not
29
Q

•Lynch Syndrome accounts for ____% of bowel cancer

A

2-3%

30
Q

What does this show?

A

LS Cancer involving the Caecum

31
Q

What are the genetics of Lynch Syndrome?

A
  • During replication the DNA base pairs can mismatch e.g. Guanine – Thymine instead of Guanine – Cytosine
  • There are mismatch repair genes which act as ‘spell checkers’ and correct these mismatches
  • Without the repairs the errors accumulate and create microsatellites
  • Microsatellites are tandem repeat of nucleotides in the DNA of an individual and are fixed for life
  • Errors due to mismatch in the DNA leads to expansion and contractions of these repeat nucleotides causing what is termed as microsatellite instability – a hallmark of defective mismatch repair
  • There are several mismatch repair genes
  • At least 4 genes are involved in LS and these are routinely tested for in bowel cancer
  • MSH2 (2p16) and MLH1 (3p21) genes account for 30% of the Lynch Syndrome
  • PMS1 and PMS2 are the other genes involved in Lynch Syndrome
32
Q

Are the genetics of lynch syndrome similar or different to FAP?

A

Different

33
Q

What is the similarity between the genetics of lynch syndrome and FAP?

A

•Similar to FAP individuals inherit the defective copy of the mismatch repair gene in utero (first hit) and acquire the second copy during life (second hit) and develop cancer

34
Q

What is the Amsterdam Criteria?

A
  • Three or more relatives with LS-associated cancer ( bowel cancer or cancer of the endometrium, small bowel, ureter or renal pelvis) plus all of the following:
  • One affected patient should be a first-degree relative of the other two;
  • Two or more successive generations should be affected;
  • Cancer in one or more affected relatives should be diagnosed before the age of 50 years;
  • Familial adenomatous polyposis should be excluded in any cases of colorectal cancer;
  • Tumours should be verified by pathological examination
35
Q

What are the symptoms of bowel cancer?

A
  • Can be asymptomatic and detected during screening
  • Change in bowel habit: constipation alternating with diarrhoea due an obstructive cancer
  • Bleeding from the rectum
  • Anaemia especially with cancers of the caecum due to slow occult blood loss
  • Abdominal pain due to obstruction
36
Q

What would the presenting symptom be for these patients?

A
37
Q

How is bowel cancer diagnosed?

A
  • History and clinical examination
  • Flexible sigmoidoscopy and colonoscopy with biopsy and histological examination
  • CT Colonography for patients who cannot tolerate colonoscopy
  • Staging CT scan for distal metastasis
  • MRI for rectal cancer to assess local spread
38
Q

What are the pathological catagories of bowel cancer?

A
  • Histologically adenocarcinoma
  • Graded as well, moderate & poorly differentiated
  • Well differentiated (A) resembles normal colonic mucosa (B)
  • Moderately differentiated most common (C)
  • Poorly differentiated (D) minimal or no glandular differentiation
39
Q

How is bowel cancer staged?

A
  • TNM is important for assessing prognosis of bowel cancer and making treatment decisions
  • TNM used in Radiology and Pathology
  • T = Tumour; assesses depth of invasion of the bowel wall
  • N = Lymph node metastasis
  • M = Distant metastasis to liver of lung
  • Bowel wall consists of mucosa to the end of external muscularis propria
40
Q

What is the T stage for this?

A

T1 = Invasion of the submucosa; the muscularis propria is clear

41
Q

What is the T stage for this?

A

T2= Involves of the muscularis propria without full thickness invasion – in this case there is invasion of the inner layer and not the external layer

42
Q

What is the T stage for this?

A

T3 = Invasion of the full thickness of the bowel wall but not the serosa

43
Q

What is the T stage for this?

A

T4 = the cancer has gone through the bowel wall and is present on the serosa

44
Q

What is the TNM stage?

A

Cancer which has invaded the full thickness of the bowel with lymph node metastasis is staged as T3 N1

45
Q

What does this show?

A

Liver metastasis from bowel cancer = M1

46
Q

What is Bowel Cancer Screening (BCS)?

A
  • Screening means looking for early signs of disease in ‘healthy’ people
  • Bowel screening can prevent cancer by detecting polyps before they turn into cancer
  • Will detect early cancers at a curable stage
47
Q

What methods are Used for bowel cancer screening?

A
  • Stool test or faecal Immunochemical Test (FIT)
  • Flexible sigmoidoscopy (FS)
  • Colonoscopy is ideal, but requires sedation, expertise ; associated with 1-2% risk of perforation
  • Colonoscopy used for screening in the USA
  • In the UK : Flexible sigmoidoscopy at 55years then FIT from 60-74years every two years
  • Sigmoidoscopy detects polyps and cancers in the rectum and left colon
48
Q

What is the Faecal Immunochemical Test (FIT)?

A
  • Testing for occult blood i.e. hidden blood in the stool, not visible to the naked eye
  • FIT is an antibody-antigen reaction; the reagent contains an antibody specific to human blood
  • Positive test does not mean one has bowel cancer
  • Haemorrhoids & inflammation can cause a positive test
49
Q

What is the science behind the stool test?

A
  • Ulcerating cancers bleed silently
  • Trauma to large polyps due to friction with stool also causes bleeding
  • The participants receive a stool kit
  • The test is done in the privacy of their own home
  • The stool kit is send to the lab
  • The resultant an anti gen-antibody reaction is read by machine
50
Q

What happens after a positive stool test ?

A
  • If positive – the patient will be referred for colonoscopy
  • Colonoscopy will detect:

– polyps ( benign and precancerous)

–early cancers

–and advanced cancers

•FIT does not detect non-bleeding polyps or non-bleeding cancers and the test is repeated every two years in people with negative tests

104 Theme 1 - The Alimentary System (17 decks)

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