Pathology - large tubes Flashcards

1
Q

whats a polyp

A

small growths of tissue in the colon

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2
Q

hsito characterization of polyps

A

flat
sessile
pedunculated
based on protrusion into colonic lumen

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3
Q

describe a hyperplastic polyp

A

non neoplastic

general smaller and in the rectosigmoid area

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4
Q

what are most common type of polyp

A

hyperplastic
smaller
rectosigmoid
non neoplastic

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5
Q

list the non neoplastic types of polyps

A

hamartomatous

hyperplastic

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6
Q

list the neoplastic types of polyps

A

adenomatous

serrated

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7
Q

tuular adenomatous polyp malig risk

A

lower than villous

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8
Q

villous adenomatous polyp maligi risk

A

higher than tubular

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9
Q

describe a hamartomatous poly

A

tissue of origin - frowths of normal colonic tissue with distorted architected
solitary lesions
no signi risk of mali transformation
non neoplastic

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10
Q

lsit two syndromes associated with hamartomatous polyps

A

peutz jegher

juvenile polyposis

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11
Q

list syndromes associated with adenomatous polys

A

FAP
gardner
turcot

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12
Q

BRAF mutations and polyps

A

serrated

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13
Q

describe serrated polyps

A

premalignant
CpG methylation phenotype pathway with microsatellite intability
saw tooth of crypts on biopsy

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14
Q

what is responsible for 20% of sporadic colorectal cancer

A
serrated poly
CpG methylation phenotype pathway with microsatellite instability
sawtooth crypts
premaligi
BRAF mutation
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15
Q

inheritance pattern of familial adenomatous polyposis

A

AD

APC gene on 5q

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16
Q

chromosome of FAP

A

chromosome 5q with APC

TWO HIT HYPOTHESIS

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17
Q

when do polyps start in FAP and who cares

A

start after puberty

100% progress to colorectal cancer unless resected

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18
Q
FAP
osseous tumours/osteosarcoma
soft tissue tumours/desmoid tumour
hypertrophy of retinal pigment epithelium
impacted/supernumerary teeth
A

gardner syndrome

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19
Q

describe gardner syndroem

A
AD
supernumerary/impacted teeth
hypertrophy of retinal pigment epithelium
soft tissue tumour/desmoid tumor
osseous tumors/osteosarcoma
FAP
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20
Q

FAP

malignant CNS tumor - astrocytoma, medulloblastoma

A

Turcot syndrome

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21
Q

describe turcot syndrome

A

AR
FAP
malignant CNS tumour - astrocytoma, medulloblastoma

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22
Q
numerous hamartomas in the small bowel
hyperpigmented buccal mucosa
lips
hands
genitalia
A

peutz jegher

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23
Q

inheritance patter of peutz jegher

A

AD

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24
Q

describe peutz jegher

A

multiple hamartous polys mainly in small bowel
hyperpigmentation of lips, mucosa, hands, genitals
increased risk of colorectaol , breast, stomach, small bowe, pancreatic cancers

25
Q

increased cancer risk with peutz jegher

A
colorectal
stomach
breast
small bowel
pancreatic
26
Q

child less than five

hamartomatosu polyps in colong, stomach, small bowel

A

juvenile polyposis syndrome

27
Q

describe juvenile polyposis syndrome

A

AD
child less than five
hamartomatous polyps in colon, stomach, small bowel

28
Q

list the syndromes associated with colon poyls and their pattern fo inhertiance

A
FAP - AD
Gardner - AD
Turcot - AR
Peutz jegher - AD
Juvenile Polyposis - AD
Lynch syndrome - AD
29
Q

what is lynch syndrome

A

AD mutuation of DNA mismatch repair genes with subsequent microsatellite instability

30
Q

increased risk fo what in juvenile polyposis syndrome

A

colorectal cancer

pJ: colorectal, breast, stomach, small bowel, pancreatic cancer increased risk

31
Q

what portion fo the colon is always involved in lynch syndrome

A

the proximal colon

32
Q

what type of cancer is lynch syndrome associated with

A

colorectal
breast
ovarian
skin

colorectal
breast
ovarian
skin

33
Q

how do you identify lynch syndrome in families

A

3-2-1 rule
3 relative with Lynch syndrome-associated cancers (colorectal, breast, ovarian skin) across 2 generations, 1 that msut be diagnosed before 50 years old

34
Q

when should you suspect thers some lynch syndrome going on.

A

breast/ovarian/colorectal/skin cancer in 3 family members in 2 generations with at least one of them diagnosed before 50 years old.

35
Q

what is the second most common cause of cancer-related death in men and women

A

colorectal cancer

36
Q

typical patient in colorectal cancer

A

> 50 years old

25% have familial history

37
Q

risk factors for colorectal cancer

A
adenomatous polyp
serrated polyp
familial cancer syndromes
IBD - UC
tobacco use
diset of processed meats with low fibre
38
Q

low fibre

A

and processed meats - colorectal

diverticulosis

39
Q

most common site fo colorectal cancer

A

rectosigmoid > ascending > descending @ FA

descending @ goljan

40
Q

exophytic mass
iron deificiency anaemia
weight los

A

right sided colon cancer

41
Q

colicky pain
infiltrating mass
obstruction
hematochezia

A

LS colon cancer

42
Q

hematochezia

A

diverticulosis
LS colon cancer
angiodysplasia

43
Q

apple core lesion

A

colon cancer

44
Q

streptococcus bovis endocarditis

A

colon cancer

45
Q

when should you be suspicious of colon cancer

A

old man with fe def aneamia

post meno women with fe def anaemia

46
Q

describe screening for colon cancer

A

after 50 years old

flexible sigmoidoscopy, stool occult blood test (not as good)

47
Q

what is good marker for monitoring reoccurrence but not screeing colon cancer

A

CEA

48
Q

CEA

A

marker for watching recurrence of colon cancer, but not screeing

49
Q

list order of gene events that underlie the pathogenesis of colorectal cancer

A

APC - KRAS - p53/DCC

50
Q

how much of colorectal cancer is due to the microsatellite instability pathway

A

15

51
Q

describe the microsatellite instability pathway and colorectal cancer

A

DNA mismatch repair gene mustsaions - mutatiosn accumulate but no definced morphologic corrleates
seen at Lynch syndrome and sporadic

52
Q

describe the APC/beta-catenint correlation with the pathogenesis of colorectal cancer

A

associated with 85% of spiradics.

schromsoonaml sintailiton

53
Q

normal colon – ? – colon at risk

A

loss of APC: decreased intercellular adhesion and increased proliferation

54
Q

normal colon – colon at risk – ? – adenoma

A

KRAS mutation: unregulated intracellular signal transduction

55
Q

normal colon – colon at risk – adenoma – ? – carcinoma

A

loss of tumour suppressor gene(s) p53 and DCC

increased tumorigenesis

56
Q

gene associated with decreased intracellular adhesion and increased proliferation in CRC

A

loss fo APC

57
Q

gene associated with unregulated intracellular signal transduction in CRC

A

loss of KRAS

58
Q

gene associated with increase tumorigenesis in CRC

A

loss of tumor suppresses p53 or DCC