Colonic Polyps + Colorectal Cancer

Question 0

How do you grossly characterise polyps

Answer 0

Flat, sessile or pedunculated on a stalk

Question 1

What is a colonic polyp

Answer 1

Raised protrusion of colonic mucosa and that is

neoplastic OR non-neoplastic

Question 2

What are the four types of colonic polyps histologically

Answer 2

Hyperplastic
Adenomatous
Hamartomatous
Serrated

Question 3

Is hyperplastic a neoplastic or non-neoplastic?
What is there hyperplasia of?
Where in the GI tract does this occur?
What is the risk of malignancy?

Answer 3

Non-your plastic
Glands
@Left:
No chance of cancer

Question 4

What is the second most common type of colonic polyp

Answer 4

Adenomatous

Question 5

What is the chance of getting cancer with adenomatous colonic polyp

Answer 5

Premalignant = high risk of carcinoma

Question 6

Via what sequence doesn’t adenoma just polyp develop into an adenocarcinoma

Answer 6

Adenoma – carcinoma sequence

Question 7

Explain the adenoma carcinoma sequence

Answer 7

Normal = no risk of polyp – >

(Somatic/sporadic mutation)

APC gene mutation =
⬇️INTERcellular adhesion + ⬆️proliferation =
risk of polyp formation - both copies of tumour suppressor genes knocked out ->

KRAS mutation = unregulated INTRAcell. signal transduction - actually forms the polyp – >

P 53 mutation + ⬆️ COX expression = Carcinoma

Question 8

What effect does aspirin have on carcinoma formation from colonic polyp

Answer 8

It stops COX – >decrease risk of carcinoma

Question 9

Coloscopy revealed in adenoma. What is the theoretical risk of the adenoma to become cancer?

Answer 9

Look at:

Size = >2cm
Sessile growth – flat along wall, not on stock
Villous histology

Question 10

What is family adenomatous polyposis

Answer 10

A.D. this order – >knock out APC gene – >
⬆️p(many many many polyps) – >

Progress to KRAS mutation = actually MAKE many many many polyps – >Increased risk of carcinoma

Question 11

How do you treat a patient with family adenomatous polyposis

Answer 11

Remove: + rectum because of high chance of P 53 mutation and COX activity

Question 12

What is Gardiner syndrome

Answer 12

Family adenoma just polyposis
Osteomas
Fibromatosis

Question 13

What is Turcot syndrome

Answer 13

Family Adam just polyposis

CNS tumours = medulloblastoma + glial tumours

Question 14

How does a juvenile polyposis syndrome present?

Is the risk of colorectal carcinoma?

Answer 14

Solitary rectal hamartoma tests polyp

That can prolapse + bleed

@Stomach, small-bowel, colon

High risk of colorectal carcinoma

Question 15

What is PEUTZ-JEGHERS syndrome

Answer 15

How much how much is polyps throughout GI tract

+

Mucocutaneous hyperpigmentation on lips, oral mucosa, genital skin

Question 16

Where does colorectal cancer arise from?
Age peak?
Incidents and mortality?
What percentage of CRC patients have a high family history?

Answer 16

Colonic rectal mucosa are
60–70 years
Third most common incidents + mortality

25%

Question 17

Risk factors for colorectal cancer

Answer 17

FaT DIP

Familial cancel syndromes
Tobacco use
Diet = processed meat + low fibre
IBD
Polyps = serrated + adenomatous

Question 18

Which part of bowel is more likely to be affected @ CRC?
How does bowel cancer present @:
– Ascending colon
– Descending colon
Rarely presents with what?

Answer 18

Recto sigmoid > ascending >descending

Asc - Fe deficiency, Exophytic mass, weight loss
Desc -
colicky pain, hematochezia, infiltrating mass,
partial obstruction

Strep Bovis bacteraemia

Question 19

An Fe deficient anaemic male > 50 years old

A postmenopausal female comes into clinic. What is the suspicion?

Answer 19

Colo rectal cancer

Question 20

What are the two molecular pathways to develop colorectal cancer

Answer 20

Adenoma carcinoma sequence = 80 - 85%

Microsatellite instability pathway = 10 - 15%

Question 21

What are microsatellites

Answer 21

Repeating sequences of non-coding DNA

Question 22

Explain the microsatellite instability pathway

Answer 22

Cell division we copy microsatellite exactly the way they are – >

@Defect in the DNA copy mechanism I.e. problem in DNA repair mismatch enzymes– >

Copy DNA over and over again = mutations accumulate – >

can’t maintain stability of microsatellites

Question 23

Give a prototypic example of the microsatellite instability pathway

Answer 23

Hereditary non-polyposis colorectal cancer (HNPCC) i.e. Lynch syndrome

Autosomal dominant mutation of DNA mismatch repair enzymes

Question 24

What three cancers is there an increased risk of with Lynch syndrome/HNPCC

Answer 24

Colorectal

Endometrial

Ovarian

Question 25

What age group do the screen for colorectal cancer?

What do we use in order to screen?

Answer 25

> 50 years

Colonoscopy/
flexible sigmoidoscopy/
stool occult blood test

Question 26

What do you see on barium enema x-ray @ CRC?

Tumour marker for CRC?

Answer 26

Apple core lesion

CEA tumour marker = good for monitor recurrence
NOT USEFUL for screening THOUGH!!!!

Question 27

What molecular pathways are left-sided cancers and right-sided cancer is associated with?

Answer 27

Left = adenoma carcinoma

Right = microsatellite instability pathway

Question 28

How do you left-sided cancers grow?
How do you right-sided cancers grow?

How did they present?

Answer 28

Left = napkin ring lesion
Squeeze on lumen as if a ring squeezes on Newman
Stool calibre = thin + blood streaked + LLQ pain

Right = raised lesion @Colonic mucosa surface
Fe deficient anaemia