Colonic Polyps + Colorectal Cancer Flashcards
How do you grossly characterise polyps
Flat, sessile or pedunculated on a stalk
What is a colonic polyp
Raised protrusion of colonic mucosa and that is
neoplastic OR non-neoplastic
What are the four types of colonic polyps histologically
Hyperplastic
Adenomatous
Hamartomatous
Serrated
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?
Non-your plastic
Glands
@Left:
No chance of cancer
What is the second most common type of colonic polyp
Adenomatous
What is the chance of getting cancer with adenomatous colonic polyp
Premalignant = high risk of carcinoma
Via what sequence doesn’t adenoma just polyp develop into an adenocarcinoma
Adenoma – carcinoma sequence
Explain the adenoma carcinoma sequence
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
What effect does aspirin have on carcinoma formation from colonic polyp
It stops COX – >decrease risk of carcinoma
Coloscopy revealed in adenoma. What is the theoretical risk of the adenoma to become cancer?
Look at:
Size = >2cm
Sessile growth – flat along wall, not on stock
Villous histology
What is family adenomatous polyposis
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
How do you treat a patient with family adenomatous polyposis
Remove: + rectum because of high chance of P 53 mutation and COX activity
What is Gardiner syndrome
Family adenoma just polyposis
Osteomas
Fibromatosis
What is Turcot syndrome
Family Adam just polyposis
CNS tumours = medulloblastoma + glial tumours
How does a juvenile polyposis syndrome present?
Is the risk of colorectal carcinoma?
Solitary rectal hamartoma tests polyp
That can prolapse + bleed
@Stomach, small-bowel, colon
High risk of colorectal carcinoma
What is PEUTZ-JEGHERS syndrome
How much how much is polyps throughout GI tract
+
Mucocutaneous hyperpigmentation on lips, oral mucosa, genital skin
Where does colorectal cancer arise from?
Age peak?
Incidents and mortality?
What percentage of CRC patients have a high family history?
Colonic rectal mucosa are
60–70 years
Third most common incidents + mortality
25%
Risk factors for colorectal cancer
FaT DIP
Familial cancel syndromes Tobacco use Diet = processed meat + low fibre IBD Polyps = serrated + adenomatous
Which part of bowel is more likely to be affected @ CRC? How does bowel cancer present @: – Ascending colon – Descending colon Rarely presents with what?
Recto sigmoid > ascending >descending
Asc - Fe deficiency, Exophytic mass, weight loss
Desc -
colicky pain, hematochezia, infiltrating mass,
partial obstruction
Strep Bovis bacteraemia
An Fe deficient anaemic male > 50 years old
A postmenopausal female comes into clinic. What is the suspicion?
Colo rectal cancer
What are the two molecular pathways to develop colorectal cancer
Adenoma carcinoma sequence = 80 - 85%
Microsatellite instability pathway = 10 - 15%
What are microsatellites
Repeating sequences of non-coding DNA
Explain the microsatellite instability pathway
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
Give a prototypic example of the microsatellite instability pathway
Hereditary non-polyposis colorectal cancer (HNPCC) i.e. Lynch syndrome
Autosomal dominant mutation of DNA mismatch repair enzymes
