GI Neoplasia Flashcards

1
Q

what is interchangeable with carcinoma in situ?

A

intraepithelial neoplasia

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2
Q

malignancy is defined by?

A

invasion/metastasis

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3
Q

aneuploidy?

A

more than 2 chromosomes, inappropriate numbers: chromosomal instability

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4
Q

proto-oncogenes need one or two hits?

A

one hit

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5
Q

how many hits for TSGs?

A

two hit

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6
Q

P53 active between which cell phases?

A

G1 and S

G2 and M

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7
Q

RBactive between which cell phases?

A

G1 and S

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8
Q

carcinoma is cancer of?

A

epithelium

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9
Q

sarcoma is cancer of?

A

mesenchymal

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10
Q

dysplasia signs? 3

A

disordered
premalignant lesion
mutations

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11
Q

cancer is defined by?

A

invasion and breach of basement membrane to stroma

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12
Q

bone is a common site for breast and prostate possibly due to?

A

similar micro environment

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13
Q

example of physiological metaplasia?

A

cervical transformation zone during menstrual cycle

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14
Q

pathological metaplasia in oesophagus?

A

barrett’s oesophagus due to chronic GORD

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15
Q

HPV is only on cervix?

A

ubiquitous: >150 serotypes

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16
Q

What are the high risk cancer HPVs?

A

16 and 18

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17
Q

What are the low risk cancer HPVs?

A

6 and 11

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18
Q

what part of HPV genes leads to cervical cancer?

A

E2 gene disruption during viral genome integration leads to too much E6, E7 then loss of p53 and Rb tumour suppressors

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19
Q

What does HPV E6 and E7 oncoproteins do?

A

inhibits tumour suppressor protein

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20
Q

cervix intraepithelial neoplasia increased risk are which 2 categories?

A

ClN2 and ClN3

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21
Q

diagnostic criteria for Barrett’s oesophagus?

A

endoscopic evidence of columnar

histo: metaplasia (goblet cells)

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22
Q

what gives you an increased 10% lifetime risk of oseophageal adenocarcinoma?

A

Barrett’s oesophagus

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23
Q

What is the most common familial colorectal cancer syndrome?

A

Lynch Syndrome

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24
Q

gland fusion or fusion with lamina propria is a feature of?

A

malignancy

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25
Q

what happens to nucleus of dysplastic cells?

A

loss of polarity

nuclear atypia

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26
Q

dysplastic changes to basement membrane?

A

separation of basal cell layer

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27
Q

fused glands in mucosa indicates what?

A

lamina propria invasion

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28
Q

what is a pre-invasive term for severe dysplasia?

A

carcinoma in situ

29
Q

is there metaplastic precursor in breast ductal carcinoma in situ?

A

Nope.

30
Q

breach in what = invasive carcinoma for cervix?

A

basement membrane

31
Q

breach in what = invasive carcinoma for prostate?

A

basal cell layer loss

32
Q

breach in what = invasive carcinoma for breast?

A

myoepithelial cell layer loss

33
Q

breach in what = invasive carcinoma for oesophagus?

A

basement membrane

34
Q

breach in what = invasive carcinoma for colon?

A

muscularis mucosae

35
Q

4 ways of carcinoma spread?

A

direct
lymphatic
vascular
perineural

36
Q

what are adenomatous dysplastic polyps?

A

precursor lesions

37
Q

Are Tubular adenoma/villous adenoma invasive? what are their features

A

nope. precursor, no invasion
Tubular: sessile/pedunculated
Villous: large/sessile

38
Q

if the polyp is >1cm and high grade dysplasia then what?

A

increased risk of malignancy

39
Q

cancer risk if you have Familial adenomatous polyposis?

A

100%

40
Q

cancer risk if you have lynch syndrome?

A

70-80%

41
Q

Familial adenomatous polyposis recessive or dominant?

A

dominant

42
Q

where are the lymphatics in the colon?

A

not in the lamina propria

43
Q

how to treat adenomatous polyps?

A

complete excision

44
Q

are adenomatous polyps invasive?

A

no invasion beyond muscularis mucosae

45
Q

are hyperplastic polyps benign? or malignant?

A

benign

46
Q

at what point do you get colorectal adenocarcinoma?

A

invasion beyond muscularis mucosae

47
Q

what happens to stroma witth colorectal adenocarcinoma?

A

desmoplastic stromal reaction

48
Q

3 colorectal cancer pathways

A
Chromosomal instability
microsatellite instability (MSI)
CpG island methylator phenotype (CIMP)
49
Q

which TSGs are lost in carcinoma?

A

p53

SMAD4/SMAD2

50
Q

which proto-oncogenes are lost in carcinoma?

A

K-RAS

51
Q

what is the most common familial colorectal cancer syndrome?

A

Lynch Syndrome

52
Q

Lynch Syndrome dominant or recessive? onset of cancer?

A

dominant

mean age 45

53
Q

extracolonic cancers in Lynch Syndrome?

A

yes
endometrium
renal pelvis

54
Q

2 things in micro satellite instability pathway?

A

defective DNA mismatch repair

widespread mutations in DNA micro satellites

55
Q

where do sessile serrated adenoma/polyps usually arise?

A

proximal colon

56
Q

sessile serrated adenoma/polyps easy or heard to detect?

A

hard to detect at colonoscopy

57
Q

what is serrated in sessile serrated adenoma/polyps ?

A

elongation and serration of crypts

58
Q

How do colorectal cancers grow in:
1. proximal colon
2. distal colon
why?

A
  1. bulky, polypoid: due to more liquid stool

2. annular, stenosing, ulcerated: due to more solid stool

59
Q

invasion assessment of colon cancer. 4 things

A

muscularis muscosae
lymph nodes
infiltration of adjacent organs
perforation into peritoneal cavity

60
Q
Australian staging for colorectal cancer:
ACPS A
ACPS B
ACPS C
ACPS D
A

ACPS A: beyond muscularis mucosae
ACPS B: beyond muscularis propria
ACPS C: lymph node metastasis
ACPS D: distant metastase

61
Q

TMN staging is?

A

Tumour invasion Tis, T1,2,3,4
Node metastases: N0,1,2
M etastases: Mx, M0,1

62
Q

what organ is common site of metastases for colorectal cancer?

A

liver cause of portal system

63
Q

neoadjuvant therapy is? Grade 1 is best or worse?

A

pre-operative chemoradiotherapy

grade 1 is complete tumour destruction

64
Q

early onset cancer should raise suspicion of?

A

underlying syndrome

65
Q

2 things that dysplasia has histologically:

A

nuclear atypia

disordered growth

66
Q

complete excision of dysplasia will cure?

A

yes

67
Q

Cetuximab and panitumumab block what?

A

EGFR signalling

68
Q

K-RAS and B-RAF mutation predicts what?

A

poor response to EGFR-targeted therapy so need to screen before targeted therapy

69
Q

Colorectal sequence:

A
normal, then get first hit (APC)
dysplastic
early adenoma (K-RAS)
intermediate adenoma (SMAD4)
late adenoma (p53)
carcinoma
metastasis