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clinical oncology Flashcards

colorectal cancer: explain the molecular pathogenesis and major pathological features of colorectal carcinoma, explain the clinical presentation of and basis of screening for colorectal carcinoma, list the principles of the adenoma-carcinoma sequence, and define colorectal carcinoma staging systems (80 cards)

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1
Q

colorectal cancer location

A

major cancer in developed countries, and 4th most common cancer

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2
Q

colorectal cancer mortality

A

2nd behind lung cancer

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3
Q

colorectal cancer influences

A

environmental (diet) and genetic

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4
Q

3 functions of colon

A

extraction of water from faeces, faecal reservoir, bacterial digestion for vitamins

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5
Q

organisation of colorectal crypt of Lieberkuhn

A

proliferation at base (mesenchymal, stem, endocrine), move up to top where differentiation occurs (ECM, goblet, columnar)

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6
Q

effect of proliferation on colorectal cells

A

become vulnerable to mutations, as very high turnover

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7
Q

what gene mutation prevents cell loss in colorectum

A

APC

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8
Q

3 proliferative mechanisms to eliminate genetically defective cells

A

natural loss, DNA monitors, repair enzymes

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9
Q

define polyp and what it may be

A

any projection from a mucosal surface into a hollow viscus; may be hyperplastic, neoplastic, inflammatory, hamartomatous etc.

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10
Q

define adenoma

A

type of polyp which is a benign neoplasm of mucosal epithelial cells

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11
Q

6 colonic polyp types

A

metaplastic/hyperplastic, adenoma, juvenile, Peutz Jeghers (also with mucosal hyperpigmentation), lipomas, others

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12
Q

hyperplastic polyps: prevalence, size, malignant potential, mutation

A

very common, <0.5cm, often multiple, no malignant potential, 15% have k-ras mutation

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13
Q

histological features of hyperplastic polyp

A

well differentiated but serrated appearance

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14
Q

5 colonic adenoma types and frequency

A

tubular (>75% tubular character), tubulovillous (25-50% villous character), villous (>50% villous character), flat, serrated

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15
Q

where do colonic adenomas develop within

A

polyps

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16
Q

microscopic structure of tubular adenoma

A

columnar cells with nuclear enlargement, elongation, multilayering and loss of polarity

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17
Q

tubular adenoma activity and architecture

A

increased proliferative and decreased differentiation activity; complexity and disorganisation of architecture

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18
Q

histological features of tubular adenomas

A

increased nuclei so more poorly differentiated

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19
Q

microscopic structure of villous adenoma

A

mucinous cells with nuclear enlargement, elongation, multilayering and loss of polarity

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20
Q

villous adenoma activity and architecture

A

rarely have hypersecretory function and result in excess mucus discharge and hypokalaemia; exophytic, frond-like extensions

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21
Q

histological features of villous adenoma

A

increased nuclei so more poorly differentiated

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22
Q

define dysplasia

A

abnormal growth of cells with some features of cancer

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23
Q

describe subjective analysis of dysplasia

A

indefinite, low grade and high grade

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24
Q

low grade to high grade dysplasia

A

larger nuclei-cytoplasmic ratio etc, but architecturally similar -> huge nuclei and poor architecture and function

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25
gene mutation in adenomatous polyposis coli (APC)
5q21
26
what does site of mutation determine in APC
clinical variant e.g. classical, attenuated (fewer), Gardner (tumours outside skin also), Turcot (brain tumours also
27
colonic adenoma malignancy risk
25% of adults, with 5% becoming cancers if left (large polyps have higher risk than small polyps), with cancer staying at a curable stage for 2 years
28
location and time progression (lead time) from adenoma to carcinoma
similar distribution, with adenomas preceding cancer by 10 years
29
what decreases incidence of subsequent colorectal cancers
endoscopic removal of polyps (if many polyps, prophylactic colectomy before 30)
30
adenoma carcinoma sequence genetic pathway
APC -> K ras -> Smads -> p53 -> telomerase activation
31
what are microsatellites
repeat sequences prone to misalignment, with some coding sequences of genes which inhibit growth or apoptosis (e.g. mismatch repair genes, withrecessive genes requiring 2 hits)
32
what mutation is present in DNA repair genes in microsatellite HNPCC syndrome
germline mutation
33
adenoma-carcinoma sequence
normal (first hit e.g. APC, mismatch repair genes) -> mucosa at risk (second hit e.g. B-catenin) -> adenomas (e.g. K-ras -> p53)-> carcinomas
34
2 main pathways of colorectal cancer genetic predisposition
APC (inactivation of APC tumour suppressor genes), HNPCC (microsatellite instability)
35
why is APC especially important in colon cancer (top vs bottom of crypts of Lieberkuhn)
bottom: APC holds B-catenin in cytoplasm, and if APC turned off, B-catenin moves to nucleus and stimulates transcription cancers which increase cellular proliferation etc.; this can happen in top if mutated
36
why can p53 expression be higher in adenoma progression
p53 doesn't work properly but constantly attempted to be produced as cell aware of uncontrolled cell proliferation
37
colonic cancer location
US, eastern Europe, Australia (low in Japan, Mexico, Africa)
38
what age does colonic cancer usually affect
50-80
39
dietary factors affecting colonic cancer
high fat, low fibre, high red meat, refined carbohydrates
40
why is food and dietary factors difficult to associate with colorectal cancer
food contains carcinogens and anti-cancer agents; heat modifies chemicals; bacteria modifies food residues
41
what aspect of food (from cooking) can be associated with colorectal cancer
heterocyclic amines, which oxidises and causes mutagenesis
42
dietary deficiencies in colorectal cancer
folates (coenzyme for nucleotide synthesis and DNA methylation), MTHFR (deficiency causing DNA synthesis disruption and instability -> mutations)
43
4 anticancer food elements
vitamins C and E (ROS scavengers), isothiocyanates, polyphenols
44
what do anticancer food elements do to reduce DNA oxidation
activate MAPK, which regulates phase 2 detoxifying enzymes and reduces DNA oxidation
45
2 health foods which reduce risk of colorectal cancer
garlic associated apoptosis, green tea with EPCG-induced telomerase activity
46
colorectal cancer incidence with age
increases with age (very uncommon <40)
47
7 clinical presentations of colorectal cancer (patients may explain away these symptoms)
change in bowel habit, bleeding per rectum, unexplained iron deficient anaemia, mucus per rectum, bloating, cramps (colic), consitutional (weight loss, fatigue)
48
effect of carcinoma on lumen size
compresses
49
what may be present within larger polypoid adenomas
small carcinomas
50
distribution of colorectal cancers based on affected area
caecum/ascending colon 22%, transverse colon 11%, descending colon 6%, rectosigmoid 55%
51
microscopic structure of carcinomas
adenocarcinomas grade 1-3, mucinous carcinomas, signet ring cell, neuroendocrine
52
histological features of colonic carcinomas
poorly differentiated, invades through basement membrane
53
what is grading of colorectal cancers based on
proportion of gland differentiation relative to solid areas or nests and cords of cells without lumina (10% well, 70% moderate, 20% poor)
54
Dukes classification (basis of TNM in colon) of colorectal grading: A, B, C1, C2
A: growth limited to wall, nodes negative; B: growth beyond musc propria, nodes negative; C1: nodes positive, apical LN negative; C2: apical LN positive
55
how does diagnosis in asymptomatic patients affect prognosis
improve
56
how does rectal bleeding as presenting symtom affect prognosis
improve
57
how does bowel obstruction or perfortion affect prognosis
reduce
58
how does tumour location affect prognosis
colon better than rectum, left colon better than right
59
how does age affect prognosis
reduce if younger
60
how does high preoperative serum CEA affect prognosis
reduce
61
how does distant metastases affect prognosis
markedly reduce
62
how does depth of bowel wall penetration affect prognosis
reduce
63
how does number of regional lymph nodes involved affect prognosis
fewer improves
64
how does degree of differentiation affect prognosis
well > poor
65
how does presence of mucinous or signet ring cell affect prognosis
reduce
66
how do venous, lymphatic or perineural invasion affect prognosis
reduce
67
how does local inflammation and immunologic reaction affect prognosis
improve
68
treatment option for stage I colorectal cancer
surgery
69
treatment option for stage II colorectal cancer
surgery, 5FU
70
treatment option for stage II colorectal cancer
surgery, 5FU/leucovorin
71
treatment option for stage IV colorectal cancer
surgery, metastatectomy, chemotherapy, palliative radiotherapy
72
when is screening for high risk colon cancer conducted (6)
previous adenoma, 1st degree relative affected by colorectal cancer before the age of 45, 2 affected first degree relatives, evidence of dominant familial cancer trait including colorectal and uterine (and others), UC and Crohn’s disease, hereditable cancer families (include other sites)
73
define screening
investigating apparently healthy individuals with object of detecting unrecognised disease, or people with exceptionally high risk of developing disease, and of intervening in ways that will prevent disease occurrence or improve prognosis when it develops
74
2 criteria for screening
disease importance, known natural history of disease
75
describe disease importance in screening
condition should be important in respect to seriousness and/or frequency
76
2 reasons why natural history of disease must be known in screening
identify where screening can take place, enable effects of any intervention to be assessed
77
4 test characteristics for screening colon cancer
simple and accessible to patient, sensitive and selective, screening population should have equal acess to screening population, cost effective
78
how is the NHS screening for colon cancer done
using a FOB/FOB kit
79
what are 65-75 year old patients who tested positive in screening referred for
colonoscopy
80
what are 55-60 year old patients who tested positive in screening referred for
sigmoidoscopy

Y2 MCD Cancer (20 decks)

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