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pathology 2 > pathology of bowel cancer > Flashcards

pathology of bowel cancer Flashcards

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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
villous
forms fingers | slightly higher risk of malignancy, usually larger
26
advanced type adenomatous polyps
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
27
adenomatous polyps mutations
usually mutates through WNT pathway | may also acquire mutations in Pi3k pathway, TP53, KRAS, SMAD4 and SMAD2
28
WNT pathway
mutations in the APC genes - increases ability to grow
29
KRAS
important to progression to carcinoma KRAS mutations are present in larger invasive adenomas is a porto-oncogene and up regulates growth factors
30
P53 alterations
also significant in the development into cancer
31
APC gene
tumour suppressor gene | helps to down regulate B-catenin and E-cadherin (WNT signalling pathway)
32
B-catenin
is a porto-oncogene and up-regulates multiple growth pathways
33
KRAS gene function
is a proto-oncogene and up regulates growth factors
34
P53 gene function
is a major TSG, regulates cell cycle and initiates senescence
35
telomerase
prevents telomere shortening and loss of multiple DNA signals
36
initial mutations in serrated/microsatellite instability pathway
mutation in mismatch repair proteins - MLH1 or MSH2 etc. | this leads to micro satellite instability, which accelerated accumulation of mutations in numerous genes
37
familial adenomatous polyposis
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
HNPCC - Lynch syndrome
autosomal dominant fewer adenomatous polyps, more than people who develop sporadic cancers mutations in mismatch repair genes results in inherited microsatellite instability
39
Lynch syndrome increases risk of developing
bowel, endometrial, bladder, gastric, and skin cancers
40
microsatelite instability
DNA can't be repaired as well which icreases likelihood of further mutations
41
2 strategies for genetic testing for Lynch syndrome is Called
Amsterdam criteria or Bethesda criteria
42
people with Lynch syndrome require
full colonoscopy every 1-2 years from age 25, plus endometrial screening for women age 25-35, bladder surveillance, gastroscopy
43
role of chronic inflammation in colorectal cancer
- 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
chronic inflammation as a response to cancer
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
early symptoms of colon cancer
bowel obstruction with seminal symptoms Melaena fecal occult blood
46
advanced colon cancer symptoms
``` local effects - bowel obstruction - perforation - severe haemorrhage systemic effects - spread to other organs - cachexia - paraneoplastic symptoms ```
47
perforation sequelae of colon cancer
tumour bursts a hole in the colon causes tumour seeding throughout the peritoneum peritonitis - fecal material throughout the peritoneum
48
sever haemorrhage and anaemia as a sequelae of colon cancer
due to erosion of the large vessels
49
cachexia
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
paraneoplastic symptoms
hormone secretion uncommon in colon cancer except in rare variants eg. nueroendocrone tumours
51
- history and examination at diagnosis of colon cancer
- personal and family history - clinical symptoms - clinical signs
52
clinical symptoms for suspicion of colon cancer
- mostly asymptomatic - altered blood in stool - melaena - pain/weight loss/bowel obstruction only when advanced
53
clinical signs for suspicion of colon cancer
- often nothing except in lower rectum | palpable mass at advanced stage
54
investigations for colon cancer
- faecal occult blood testing - imaging - endoscopy - pathology
55
imaging for colon cancer
barium studies, ultrasound, CT scan, virtual colonoscopy
56
if faecal occult blood testing is positive
referral for colonoscopy
57
if patient is symptomatic or has frank bleeding
screening FOBT is not indicated - needs diagnostic colonoscopy and biopsy
58
if small polyp is found (adenoma)
can be removed via endoscopic resection
59
if large mass is found
needs to be biopsied for histopathological diagnosis | - is it an adenoma with low grade dysplasia, high grade dyslalia or carcinoma
60
if cancer or large adenomatous polyp is found
colectomy - removal of part of the bowel - plus lymph nodes
61
clinical and pathological assessment of bowel cancer
- 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
TNM staging
T - tumour size N - lymph nodes M - metastasis
63
low stage cancer
resection means high chance of cure
64
locally advanced cancer
cure is possible but there is a risk of distant spread | chemotherapy/radiotherapy/targetted therapy may be indicated
65
high stage colon cancer
systemic disease at prevention liver/bone/brain/lung metastasis cure unlikely resection improves morbidity and survival chemotherapy restricts tumour growth and increases survival
66
ways that tumour spread
- blood - lymph - direct invasion - transcoelomic (via body cavities)
67
transcoelomic spread
when cancer spread to body cavities/peritoneum and spreads to other organs
68
pathological examination of specimen (resected tumour)
``` diagnosis of tumour type grading TNM staging assessing margins provide prognostic information ```
69
for a screening program to be worthwhile
- 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
national bowel cancer screening program
- 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
bowel cancer screening is offered to
>50 year olds | 2 yearly

pathology 2 (47 decks)

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