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pathology 2 > pathology of bowel cancer > Flashcards

pathology of bowel cancer Flashcards

1
Q

variation

A

colon and rectum have similar diseases but different treatment
small bowel has similar spectrum of disease but adenocarcinoma is less common
low grade neuroendocrine tumours are more common in the appendix

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2
Q

lymphoma is the bowel

A

almost always non-hodgkin

B and T cell lymphomas

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3
Q

adenocarcinoma

A

malignant epithelial tumour forming glands

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4
Q

types of bowel cancer

A 
carcinoma
lymphoma
neuroendocrine disorders
GIST 
sarcomas
metastases from other organs
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5
Q

risk factors for bowel cancer

A

obesity
diet high in processed meat, red meat and alcohol
sedentary lifestyle
inflammatory bowel disease
risk of smoking is unclear
some benefit with longterm NSAIDS eg. low dose aspirin

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6
Q

four classes of regulatory genes

A
  • growth promoting proto-oncogenes - gain of function
  • growth inhibiting tumour suppressor genes - loss of function
  • genes that regulate cell death - pro apoptotic
  • genes involved in DNA repair
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7
Q

mucosa at risk

A

macroscopically norma

histologically mild, hard to identify abnormalities

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8
Q

adenoma

A

macroscopically small polyp
histologically low grade dysplasia
acquisition of additional mutations
benign

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9
Q

advanced adenoma

A

high grade dysplasia
larger irregular polyps
acquisition of additional mutation and overexpression of various growth factors

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10
Q

carcinoma

A

acquires ability to invade bowel wall and lymph vascular spaces
becomes less well differentiated

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11
Q

serrated adenomas

A

macroscopically small polyp
histologically serrated architecture
parallel pathway toward bowel cancer
progress directly to carcinoma

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12
Q

mechanisms of genetic instability in colon cancers

A
  1. chromosomal instability
  2. micro satellite instability
  3. defective DNA polymerase proofreading
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13
Q

chromosomal instability

A

results In high levels of somatic copy number alterations and DNA gains/amplifications or losses/deletions

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14
Q

micro satellite instability

A

due to defective DNA mismatch repair
leads to high mutation rate
most of these tumours show CpG island hypermethylation

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15
Q

defective DNA polymerase proofreading

A

very high mutation rate affecting large numbers of genes

most of these are silent passenger mutations, with some mutations occurring in driver genes

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16
Q

dysplasia

A

cellular atipica in absence of invasion
can occur in squamous or glandular epithelium
reflects underlying cellular and molecular changes
increase the risk of subsequent development of cancer

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17
Q

adenoma in the tubular GIT

A

have pre malignant potential

show dysplasia and/or molecular changes in key cancer genes

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18
Q

serrated polyps

A

colorectal neoplasms that have serrated/saw tooth glands
historically thought to be benign, we know know that a proportion of these lesions progress to cancer via the MSI/serrated pathway

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19
Q

types of serrated polyps

A

hyperplastic polyp
sessile serrated lesion
traditional serrated adenoma

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20
Q

hyperplastic polyp

A

small, sessile (done like_ or flat lesion, serrated glands in superficial portion of crypt, often rich in goblet cells
more common in the left colon

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21
Q

sessile serrated lesion

A

ill-defined, dome-like, small, often have a mucus cap imparting a cloud like appearance on endoscopy, serrations involve full depth of crypt, usually don’t have conventional dysplastic nuclei, but sometimes can

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22
Q

traditional serrated adenoma

A

larger
exophytic polyp
serrated epithelium with conventional cytological featured of dysplasia

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23
Q

adenomatous polyps

A

colorectal neoplasms that have dysplastic glands
macroscopically, polypoid, flat or depressed
larger = higher risk
small ones can be removed endoscopically
are benign

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24
Q

types of adenomatous polyps

A

tubular
tubulovillous
villous
advanced

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25
Q

villous

A

forms fingers

slightly higher risk of malignancy, usually larger

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26
Q

advanced type adenomatous polyps

A

are usually large, can’t be removed endoscopically, always show areas of high grade dysplasia, often have higher mutation burden and foci of early invasive carcinoma

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27
Q

adenomatous polyps mutations

A

usually mutates through WNT pathway

may also acquire mutations in Pi3k pathway, TP53, KRAS, SMAD4 and SMAD2

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28
Q

WNT pathway

A

mutations in the APC genes - increases ability to grow

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29
Q

KRAS

A

important to progression to carcinoma
KRAS mutations are present in larger invasive adenomas
is a porto-oncogene and up regulates growth factors

30
Q

P53 alterations

A

also significant in the development into cancer

31
Q

APC gene

A

tumour suppressor gene

helps to down regulate B-catenin and E-cadherin (WNT signalling pathway)

32
Q

B-catenin

A

is a porto-oncogene and up-regulates multiple growth pathways

33
Q

KRAS gene function

A

is a proto-oncogene and up regulates growth factors

34
Q

P53 gene function

A

is a major TSG, regulates cell cycle and initiates senescence

35
Q

telomerase

A

prevents telomere shortening and loss of multiple DNA signals

36
Q

initial mutations in serrated/microsatellite instability pathway

A

mutation in mismatch repair proteins - MLH1 or MSH2 etc.

this leads to micro satellite instability, which accelerated accumulation of mutations in numerous genes

37
Q

familial adenomatous polyposis

A

autosomal dominant
100% risk of colon by age 40
mutation in APC gene at 5q21
carpet of >100 adenomas increases the probability of second, third hits
prophylactic total colectomy at age 25, screening of relatives

38
Q

HNPCC - Lynch syndrome

A

autosomal dominant
fewer adenomatous polyps, more than people who develop sporadic cancers
mutations in mismatch repair genes
results in inherited microsatellite instability

39
Q

Lynch syndrome increases risk of developing

A

bowel, endometrial, bladder, gastric, and skin cancers

40
Q

microsatelite instability

A

DNA can’t be repaired as well which icreases likelihood of further mutations

41
Q

2 strategies for genetic testing for Lynch syndrome is Called

A

Amsterdam criteria or Bethesda criteria

42
Q

people with Lynch syndrome require

A

full colonoscopy every 1-2 years from age 25, plus endometrial screening for women age 25-35, bladder surveillance, gastroscopy

43
Q

role of chronic inflammation in colorectal cancer

A
  • driver of dysplasia
    inflammatory bowel disease increases risk of bowel cancer due to repeated cycles of inflammation, ulceration and epithelial damage leasing to increased turnover of epithelium and higher chance of mutations occurring
44
Q

chronic inflammation as a response to cancer

A

CRC triggers a host immune response
more inflammation within a tumour means the body has recognised cancer as non-self and is attacking the tumour cells
implication for prognosis and potential for immunotherapy

45
Q

early symptoms of colon cancer

A

bowel obstruction with seminal symptoms
Melaena
fecal occult blood

46
Q

advanced colon cancer symptoms

A 
local effects 
- bowel obstruction 
- perforation
- severe haemorrhage 
systemic effects 
- spread to other organs 
- cachexia 
- paraneoplastic symptoms
47
Q

perforation sequelae of colon cancer

A

tumour bursts a hole in the colon
causes tumour seeding throughout the peritoneum
peritonitis - fecal material throughout the peritoneum

48
Q

sever haemorrhage and anaemia as a sequelae of colon cancer

A

due to erosion of the large vessels

49
Q

cachexia

A

loss of body mass
nausea, viminting, loss of appetite, loss of weight
metabolic and systemic proinflammatory changes resulting in muscle and adipose tissue atrophy, loss of appetite, insulin resistance etc.

50
Q

paraneoplastic symptoms

A

hormone secretion
uncommon in colon cancer except in rare variants
eg. nueroendocrone tumours

51
Q
  • history and examination at diagnosis of colon cancer
A
  • personal and family history
  • clinical symptoms
  • clinical signs
52
Q

clinical symptoms for suspicion of colon cancer

A
  • mostly asymptomatic
  • altered blood in stool - melaena
  • pain/weight loss/bowel obstruction only when advanced
53
Q

clinical signs for suspicion of colon cancer

A
  • often nothing except in lower rectum

palpable mass at advanced stage

54
Q

investigations for colon cancer

A
  • faecal occult blood testing
  • imaging
  • endoscopy
  • pathology
55
Q

imaging for colon cancer

A

barium studies, ultrasound, CT scan, virtual colonoscopy

56
Q

if faecal occult blood testing is positive

A

referral for colonoscopy

57
Q

if patient is symptomatic or has frank bleeding

A

screening FOBT is not indicated - needs diagnostic colonoscopy and biopsy

58
Q

if small polyp is found (adenoma)

A

can be removed via endoscopic resection

59
Q

if large mass is found

A

needs to be biopsied for histopathological diagnosis

- is it an adenoma with low grade dysplasia, high grade dyslalia or carcinoma

60
Q

if cancer or large adenomatous polyp is found

A

colectomy - removal of part of the bowel - plus lymph nodes

61
Q

clinical and pathological assessment of bowel cancer

A
  • how advanced
  • has it or is it likely to spread to other sites
  • does the patient need further treatment
  • what is th e likely prognosis
62
Q

TNM staging

A

T - tumour size
N - lymph nodes
M - metastasis

63
Q

low stage cancer

A

resection means high chance of cure

64
Q

locally advanced cancer

A

cure is possible but there is a risk of distant spread

chemotherapy/radiotherapy/targetted therapy may be indicated

65
Q

high stage colon cancer

A

systemic disease at prevention
liver/bone/brain/lung metastasis
cure unlikely
resection improves morbidity and survival
chemotherapy restricts tumour growth and increases survival

66
Q

ways that tumour spread

A
  • blood
  • lymph
  • direct invasion
  • transcoelomic (via body cavities)
67
Q

transcoelomic spread

A

when cancer spread to body cavities/peritoneum and spreads to other organs

68
Q

pathological examination of specimen (resected tumour)

A 
diagnosis of tumour type 
grading 
TNM staging 
assessing margins 
provide prognostic information
69
Q

for a screening program to be worthwhile

A
  • disease must have serious consequence
  • disease must have a detectable preclinical period before it becomes clinically apparent and during which is can be detected by a screening test
  • the test must be sensitive and specific - not too many false positives or false nagative results
  • the test must be safe
  • effective treatment exists
  • treatment is more effective when started earlier
70
Q

national bowel cancer screening program

A
  • offered to the general population - normal risk level
  • looking for faecal occult blood which is present due to microscopic haemorrhage from cancer or precancerous lesions
  • patient puts sample in container and sends it back to be tested
  • immunochemical test for globin from blood
71
Q

bowel cancer screening is offered to

A

> 50 year olds

2 yearly

pathology 2 (47 decks)

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