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imed3004 COPY > Colorectal Neoplasms > Flashcards

Colorectal Neoplasms Flashcards

1
Q

What are the most common neoplasms that affect the colon/rectum?

A

Epithelial tumours (Adenomas and adenocarcinomas)

Non-epithelial (Neuroendocrine tumours, GI lymphomas, GI stromal tumours, Mesenchymal tumours)

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2
Q

What is a polyp?

A

A mass that protrudes to the lumen of the gut. It is sessile, pedunculated, and caused by abnormal mucosal proliferation. Abnormal connective tissue proliferation.

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3
Q

What are the most common types of polyps that affect the colon/rectum?

A

Adenomas

Hyperplastic polyps

*** They can be neoplastic or non-neoplastic. However, most polyps are neoplastic and most are adenomas.

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4
Q

How do neoplasms of the colon present clinically?

A

Asymptomatic

Often appear after screening (National Bowel Cancer screening programme)

Faecal Occult Blood Test (FOBT) + ve (they can cause microbleeds that appear on this test)

Incidental findings.

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5
Q

What are the types of epithelial neoplasms?

A

Tubular

Villous (they can appear villous macroscopically as well)

Tubullo-villous

Serrated

Low grade dysplasia

High grade dysplasia

All adenomas are dysplastic with no invasion (by definition)

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6
Q

How can the different types of epithelial neoplasms be differentiated?

A

They must be identified via endoscopy.

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7
Q

If adenomas are not likely to invade why are they still removed?

A

Because they are preneoplastic lesions.

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8
Q

What do dysplastic tissues look like?

A

Disordered growth, differentiation and maturation.

Individual dysplastic cells show features similar to malignant cells.

Morphological expression of disturbance of growth regulation.

They are confined to the epithelium but do not show invasion

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9
Q

What are the types of non-epithelial neoplasms that can affect the colon?

A

Leiomyoma/leiomyosarcoma

Neuroma, Schwannoma/sarcoma

Haemangioma/angiosarcoma

Lipoma/liposarcoma

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10
Q

Are non-epithelial neoplasms common in the colorectal area?

A

No

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11
Q

What are the most common colorectal carcinomas?

A

Most are adenocarcinomas (98%) and affect colorectal mucosa which is why they are glandular (Adenocarcinoma)

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12
Q

How is colorectal carcinoma?

A

Well, moderate, poor

Low and high grade

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13
Q

How common is colorectal carcinomas?

A

Incidence: 2nd most common in females and males

Mortality it is the 2nd most common lethal cancer in males after lung cancer and 3rd in females after lung and breast cancer.

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14
Q

What causes colorectal carcinomas?

A

Most are sporadic

Only 1 - 3% are familial and associated with predisposing conditions. (eg IBD)

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15
Q

How do colorectal carcinomas form?

A

Stepwise accumulation of multiple mutations.

APC-beta catenin pathway (Loss of APC gene ~85% of CRC)

Microsatellite instability pathway (Defective DNA mismatch repair genes)

Serrated pathway (BRAF mutations)

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16
Q

What genes are affected in the microsatellite instability pathway?

A

MSH2, MSH 6

MLH1

PMS1, PMS2

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17
Q

What genes are affected in the APC-beta catenin pathway?

A

Loss of APC gene

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18
Q

What mutations result in CRC via the serrated pathway?

A

BRAF mutations

19
Q

How do APC pathway lesions look different to MSI pathway lesions?

A

MSI pathway lesions follow serrated ulcerations

APC pathway adenomas appear tubular

20
Q

What kinds of neoplasms do carcinomas start as?

A

They start as adenomas.

21
Q

What evidence is there of the adenoma carcinoma sequence?

A

High prevalence of adenoma and carcinoma in similar population

Distribution of adenoma and carcinoma in colorectum is similar

Early invasive carcinoma shows residual adenoma

Risk of carcinoma related to number of adenomas

Surveillance programmes that detect and remove adenomas result in reduction of the incidence of carcinomas

22
Q

What age has the highest rate of CRC?

A

Peak incidence 60 - 70 except in familial cases

23
Q

What kind of diet is associated with higher rates of CRC?

A

High calorie

Low fiber

Refined carbs

Red meat

Reduced protective micronutrients

24
Q

What is the clinical presentation of colorectal neoplasms?

A

Fatigue, anaemia, weakness

Bleeding PR, altered bowel habits

Screening

Metastatic disease

25
Q

What is the most common site for colorectal metastases?

A

The liver due to portal vein

26
Q

What familial syndromes are associated with CRC?

A

Familial Adenomatous Polyposis syndrome (FAP): <1% of cases

Lynch syndrome (aka Hereditary nonpolyposis colorectal carcinoma): ~3% of cases

Others

27
Q

What is lynch syndrome? (Mode of inheritance)

A

Autosomal dominant disorder

28
Q

Which genes are affected by Lynch syndrome?

A

Same genes as the microsatellite instability pathway of CRC: MLH1, MSH2, MSH6, PMS2 or mutations in adjacent genes.

MSI cancer accounts for ~3%

29
Q

What is the most common site of cancer?

A

Rectosigmoid region accounts for approximately 55% of cancers

30
Q

What does multiple carcinomas/adenomas in 1 person’s colon indicate?

A

A familial syndrome

31
Q

How does location of the neoplasm indicate its morphology and invasion?

A

Proximal tumours tend to be polypoid and exophytic

Distal tumours tend to be ulcers, annular strictures, with proximal dilatation.

Distal tumours tend to invade into submucosa into muscle then into serosa.

32
Q

How are colorectal carcinomas staged?

A

T1: submucosa

T2: Muscularis propria layer

T3: Peritoneum/serosa

T4: Other organs

33
Q

How do colorectal cancers invade?

A

Direct invasion to adjacent structures

Blood vessels - liver

Lymphatics - lymph nodes

34
Q

How is CRC diagnosed?

A

Clinical, endoscopic, and radiological features

Confirmed via endoscopic biopsies

35
Q

What pathological assessments are conducted in CRC by pathologists?

A

Pre-treatment diagnosis confirmation.

Prognostication: staging

Therapy: mutational analysis K-Ras, N-Ras

Response to treatment assessment

Genetic and familial syndromes

Microsatellite status: Lynch syndrome, prognostication and response to treatment.

36
Q

What are neuroendocrine tumours called? Are they malignant and if so how dangerous are they?

A

Carcinoid. They are all considered malignant. Most are low grade though few are high grade.

37
Q

What is the most common site of neuroendocrine tumours?

A

Appendix is the most common site

after that the small intestine, rectum, stomach, and colon

38
Q

Can GIST tumours be detected in the intestines and colon?

A

Yes less commonly than the stomach though.

39
Q

What mutations lead to GIST?

A

80% are in CD117 (C-kit the receptor tyrosine kinase)

10% are in PDGFRA (Platelet Derived Growth Factor Receptor Alpha)

40
Q

What is the malignant potential of GIST?

A

High and low risk malignant potential

41
Q

Which cells are involved in GIST tumours?

A

Interstitial cells of Cajal (ICC) or precursors - special cells of the gut wall coordinating peristalsis

42
Q

What percentage of GIT malignancies are lymphomas?

A

1 - 4%

43
Q

What are the types of lymphomas that can affect the GIT?

A

B cell lymphomas in marginal zone. (MALT), diffuse large B cell lymphomas (DLBCL), Burkitt lymphomas, Mantle cell lymphoma, and others

T cell lymphomas: Associated with malabsorption syndromes.

imed3004 COPY (50 decks)

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