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Year 2 - MCD Cancer > CasaD - Colorectal Cancer > Flashcards

CasaD - Colorectal Cancer Flashcards

1
Q

Cancer Epidemology?

A

MAJOR cancer of the developed world

• 4th most common world-wide

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2
Q

Causative factors of colorectal cancer?

A

Environment (diet)
&
Genetic factors

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3
Q

Function of the colon?

A

Extraction of water from faeces
• electrolyte balance

Faecal reservoir
• evolutionary advantage

Bacterial digestion for vitamin
• e.g. B & K

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4
Q

Anatomy of the colorectal?

A

Smooth folded mucosa
• w. THICK muscle layer

Cancer type = adenocarcinoma (glandular)

Cells divide in the crypts of Lieberkuhn
• and are shunted UP

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5
Q

Explain how Turnover causes the development of colorectal cancer

A

Turnover:
• 2-5m cells per minute die in the colon
• = high proliferation rate (cells are vulnerable to mutation)

APC mutation PREVENTS cell loss and causes cell proliferation

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6
Q

What normal protective mechanisms does the colorectal have in regards to turnover?

A 
Normal protective mechanisms include: 
 – natural loss
 – DNA monitors
& 
 – repair enzymes
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7
Q

Define polyp

A

Polyp = any projection from a mucosal surface into a hollow viscus

& may be:
hyperplastic, neoplastic, inflammatory, hamartomatous etc.

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8
Q

Define adenoma

A

A benign neoplasm of the mucosal epithelial cells

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9
Q

What different colonic polyp types can there be

A

Polyp types include:
• Metaplastic /hyperplastic

  • Adenomas
  • Juvenile, Peutz Jeghers, lipomas, others – (don’t need to know much about these)
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10
Q

Explain HYPERPLASTIC polyps

A

 Very common growths <0.5cm

 Constitute 90% of all colon polyps

 Often come in multiples

 They have NO malignant potential
• but 15% have a K-Ras mutation

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11
Q

What are the different colonic adenoma types?

A

Tubular
– 90% adenomas (>75% tubular)

Tubulovillous
– 10% adenoma (25-50% villous)

Villous
– (>50% villous).

Other
– flat, serrated

The more villous, the worse

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12
Q

Relationship with colorectal cancer and villous?

A

The MORE villous = the WORSE

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13
Q

Anatomy of the 2 types of adenoma?

A

Adenomas on a stalk
• pedunculated

Flat & raised adenoma
• sessile

BOTH can be tubular, villour etc.

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14
Q

Tubular microstructure of adenomas?

A

COLUMNAR cells with:
• nuclear enlargement
• elongation
• multi-layering and loss of polarity

 Proliferation increases
 Reduced differentiation
Complexity/disorganisation of architecture

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15
Q

Villous microstructure of adenomas?

A

MUCINOUS cells with
• nuclear enlargement
• elongation
• multi-layering and loss of polarity

 Exophytic
– front-like extensions
 Rarely, may hyper-secrete resulting in excess mucus discharge and hypokalaemia.

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16
Q

Define dysplasia

A

Abnormal growth of cells with SOME features of cancer

(i.e. UC leads to dysplasia)

Indefinite
• has both HIGH & LOW-grade

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17
Q

APC?

A

Adenomatous Polyposis

18
Q

Explain APC

A

APC/FAP (familial adenomatous polyposis)

o 5q21 gene mutation

o Site of mutation determines clinical variants
– i.e. classic, attenuated, Gardner, Turcot

o Many patients of FAP have a prophylactic colectomy

19
Q

Epidemology of colonic adenomas?

A

25% of adults have adenomas at age 50 –> 5% become cancers if left.
• adenomas precede carcinomas by about 15 years

Larger polyps have a greater chance of becoming cancerous than smaller polyps.

Cancers stay at a curable stage for about 2 years.

20
Q

Progression from adenoma to carcinoma?

A

Most colorectal cancers arise from adenomas
• with 10-30% of CRCs having a residual adenoma

Endoscopic removal of polyps DECREASES the incidence of subsequent CRC

21
Q

Genetic pathways in colorectal cancer?

•

A

(1) Adenoma Carcinoma Sequence

(2) Microsatellite Instability

22
Q

Explain (1) in genetic pathways in Colorectal Cancer

A

Adenoma Carcinoma Sequence

  • APC = best known genes that is damaged
  • Others = K-Ras, Smads, p53, telomerase activation
23
Q

Explain (2) in genetic pathways in Colorectal Cancer

A

Microsatellite Instability

Microsatellites are repeat sequences prone to misalignment
• some microsatellites are in coding sequences of genes which inhibit growth or apoptosis

Mismatch repair genes
• are recessive genes requiring 2 hits (loss of this greatly increases chances of CRC)
• HNPCC – Hereditary Non-Polyposis Colorectal Cancer – germ-line mutations

24
Q

2 main pathways for genetic predisposition for colorectal cancer?

A

FAP
• inactivation of APC TSG

HNPCC
• microsatellite instability

25
Q

Dietary factors that predispose to colonic carcinoma?

A

High fat
Low fibre
High red meat
Refined carbohydrates

High oC cooking can modify chemicals further in the food
• induce mutagenic chemicals

26
Q

Explain HCAs

A

Heterocyclic Amines

These include PhIP
• PhIP is oxidised
• turns into N-OH-PhIP + deoxyguanosine
• This then turns MUTAGENESIS

27
Q

Explain 2 specific dietary deficiencies that can lead to colorectal cancer

A

Dietary deficiencies:

FOLATES:
 Folates are co-enzymes needed for nucleotide synthesis and DNA methylation

MTHFR – Methylenetetrahydrofolate Reductase:
 Deficiency leads to disruption in DNA synthesis causing DNA instability –> mutation.
 Decreased methionine synthesis leads to genomic hypomethylation and focal hypermethylation –> gene activating & silencing effects

28
Q

Food can also have anti-carcinogenic elements - what are these?

A

Vitamin C and E
– ROS scavengers

Isothiocyanates
– cruciferous vegetables

Polyphenols 
 – green tea and fruit juice
 –  can activate MAPK pathways --> regulating phase 2 metabolisms to detoxify enzymes as well as other genes = thus reduce DNA oxidation
 – EGCG-induced telomerase activity
 – Garlic associated apoptosis
29
Q

Clinical presentation of colorectal cancer?

A

 Change in bowel habit

Pre-rectal bleeding
– Patients & doctors rationalise these symptoms as getting old!

 Unexplained iron deficient anaemia

 Other
– mucus pre-rectal production, bloating, cramps (“colic”), weight loss and fatigue

30
Q

Macroscopic features of colorectal cancer?

A

Small carcinomas may present w. larger polypoid adenomas

• pedunculated OR sessile

31
Q

Distribution of colon cancer around the colon?

A

Caecum/ascending colon
- 22%

Transverse colon
- 11%

Descending colon
- 6%

Recto-sigmoid
- 55%

32
Q

Microscopic features of carcinomas?

A

Almost all are adenocarcinomas:
 Mucinous carcinoma
 Signet ring cell carcinoma
 Neuroendocrine carcinoma (rare).

33
Q

How is colorectal cancer graded?

A

Defined by the proportion of gland differentiation relative to solid areas or nests and cords of cells without lumina:

o 10% = well differentiated
o 70% = moderately differentiated
o 20% = poorly differentiated.

34
Q

Explain the Dukes Classification

A

Dukes A
• growth limited to mucosa/submusoca
• nodes negative

Dukes B
• growth beyond Muscularis propria
• nodes negative

Dukes C1
• nodes positive
• apical lymph node negative

Dukes C2
• apical lymph nodes (LN) positive

Apical lymph nodes – highest lymph node to have been removed. If +ve, chance of spread to lymph.

The scale has a worse prognosis as you go down A –> C2.

35
Q

Clinical features affecting prognosis?

A

 Diagnosis of asymptomatic patients
+ve

 Rectal bleeding as presenting symptom
+ve

 Bowel obstruction
-ve

 Tumour location
±ve

 Age <30
-ve

 Preoperative serum CEA (high)
-ve

 Distant metastasis
-ve

36
Q

Pathological features affecting prognosis?

A

 Decreased bowel wall penetration
+ve

 Decreased regional LN involvement
+ve

 Poor differentiation
-ve

 Mucinous/signed ring cell type
-ve

 Venous invasion
-ve

 Lymphatic invasion
-ve

 Peri-neural invasion
-ve

 Local inflammation and immunologic reaction
+ve

37
Q

Treatment options for colorectal cancer?

A

Grade 1
• surgery

Grade 2
• surgery
• 5FU

Grade 3
• surgery
• 5FU/Leucovorin

Grade 4
• surgery
• metastatectomy/ chemo/ palliative RT

38
Q

Screeing prerequisities for those at HIGH RISK for Colon Cancer?

A

 Previous adenoma

 1st degree relative affected by CRC before age 45

 Two affected 1st degree relatives

 Evidence of dominant familial cancer trait

 UC and Crohn’s disease

 Heritable cancer families

39
Q

NHS screening for colon cancer?

A

They look for FOB – Faecal Occult Blood.
• from 55+, a FOB test kit is send to people

If positive, an endoscopy is performed
• 55-60yo = sigmoidoscopy
• 60+ = full colonoscopy

40
Q

A 76 year old man presents with new onset rectal bleeding to the GP:

A/ Haemorrhoids must be excluded in the first instance
B/ Factor 5 leiden abnormalities are the likely cause
C/ The GP should reassure and send the patient home
D/ Colorectal malignancy must be excluded in the first instance
E/ Crohn’s disease must be excluded in the first instance

A

D

41
Q

With respect to the aetiology of colorectal adenocarcinoma:

A/ Many carcinomas are derived from adenomas
B/ Adenomas are invasive tumours
C/ Ulcerative colitis is the underlying cause in many cases
D/ Many carcinomas are derived from hyperplastic polyps
E/ Angiodysplasia is the underlying cause in many cases

A

A

Year 2 - MCD Cancer (14 decks)

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