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Y2 MCD Cancer > clinical oncology > Flashcards

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

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
Q

gene mutation in adenomatous polyposis coli (APC)

A

5q21

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26
Q

what does site of mutation determine in APC

A

clinical variant e.g. classical, attenuated (fewer), Gardner (tumours outside skin also), Turcot (brain tumours also

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27
Q

colonic adenoma malignancy risk

A

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

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28
Q

location and time progression (lead time) from adenoma to carcinoma

A

similar distribution, with adenomas preceding cancer by 10 years

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29
Q

what decreases incidence of subsequent colorectal cancers

A

endoscopic removal of polyps (if many polyps, prophylactic colectomy before 30)

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30
Q

adenoma carcinoma sequence genetic pathway

A

APC -> K ras -> Smads -> p53 -> telomerase activation

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31
Q

what are microsatellites

A

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)

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32
Q

what mutation is present in DNA repair genes in microsatellite HNPCC syndrome

A

germline mutation

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33
Q

adenoma-carcinoma sequence

A

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
Q

2 main pathways of colorectal cancer genetic predisposition

A

APC (inactivation of APC tumour suppressor genes), HNPCC (microsatellite instability)

35
Q

why is APC especially important in colon cancer (top vs bottom of crypts of Lieberkuhn)

A

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
Q

why can p53 expression be higher in adenoma progression

A

p53 doesn’t work properly but constantly attempted to be produced as cell aware of uncontrolled cell proliferation

37
Q

colonic cancer location

A

US, eastern Europe, Australia (low in Japan, Mexico, Africa)

38
Q

what age does colonic cancer usually affect

A

50-80

39
Q

dietary factors affecting colonic cancer

A

high fat, low fibre, high red meat, refined carbohydrates

40
Q

why is food and dietary factors difficult to associate with colorectal cancer

A

food contains carcinogens and anti-cancer agents; heat modifies chemicals; bacteria modifies food residues

41
Q

what aspect of food (from cooking) can be associated with colorectal cancer

A

heterocyclic amines, which oxidises and causes mutagenesis

42
Q

dietary deficiencies in colorectal cancer

A

folates (coenzyme for nucleotide synthesis and DNA methylation), MTHFR (deficiency causing DNA synthesis disruption and instability -> mutations)

43
Q

4 anticancer food elements

A

vitamins C and E (ROS scavengers), isothiocyanates, polyphenols

44
Q

what do anticancer food elements do to reduce DNA oxidation

A

activate MAPK, which regulates phase 2 detoxifying enzymes and reduces DNA oxidation

45
Q

2 health foods which reduce risk of colorectal cancer

A

garlic associated apoptosis, green tea with EPCG-induced telomerase activity

46
Q

colorectal cancer incidence with age

A

increases with age (very uncommon <40)

47
Q

7 clinical presentations of colorectal cancer (patients may explain away these symptoms)

A

change in bowel habit, bleeding per rectum, unexplained iron deficient anaemia, mucus per rectum, bloating, cramps (colic), consitutional (weight loss, fatigue)

48
Q

effect of carcinoma on lumen size

A

compresses

49
Q

what may be present within larger polypoid adenomas

A

small carcinomas

50
Q

distribution of colorectal cancers based on affected area

A

caecum/ascending colon 22%, transverse colon 11%, descending colon 6%, rectosigmoid 55%

51
Q

microscopic structure of carcinomas

A

adenocarcinomas grade 1-3, mucinous carcinomas, signet ring cell, neuroendocrine

52
Q

histological features of colonic carcinomas

A

poorly differentiated, invades through basement membrane

53
Q

what is grading of colorectal cancers based on

A

proportion of gland differentiation relative to solid areas or nests and cords of cells without lumina (10% well, 70% moderate, 20% poor)

54
Q

Dukes classification (basis of TNM in colon) of colorectal grading: A, B, C1, C2

A

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
Q

how does diagnosis in asymptomatic patients affect prognosis

A

improve

56
Q

how does rectal bleeding as presenting symtom affect prognosis

A

improve

57
Q

how does bowel obstruction or perfortion affect prognosis

A

reduce

58
Q

how does tumour location affect prognosis

A

colon better than rectum, left colon better than right

59
Q

how does age affect prognosis

A

reduce if younger

60
Q

how does high preoperative serum CEA affect prognosis

A

reduce

61
Q

how does distant metastases affect prognosis

A

markedly reduce

62
Q

how does depth of bowel wall penetration affect prognosis

A

reduce

63
Q

how does number of regional lymph nodes involved affect prognosis

A

fewer improves

64
Q

how does degree of differentiation affect prognosis

A

well > poor

65
Q

how does presence of mucinous or signet ring cell affect prognosis

A

reduce

66
Q

how do venous, lymphatic or perineural invasion affect prognosis

A

reduce

67
Q

how does local inflammation and immunologic reaction affect prognosis

A

improve

68
Q

treatment option for stage I colorectal cancer

A

surgery

69
Q

treatment option for stage II colorectal cancer

A

surgery, 5FU

70
Q

treatment option for stage II colorectal cancer

A

surgery, 5FU/leucovorin

71
Q

treatment option for stage IV colorectal cancer

A

surgery, metastatectomy, chemotherapy, palliative radiotherapy

72
Q

when is screening for high risk colon cancer conducted (6)

A

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
Q

define screening

A

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
Q

2 criteria for screening

A

disease importance, known natural history of disease

75
Q

describe disease importance in screening

A

condition should be important in respect to seriousness and/or frequency

76
Q

2 reasons why natural history of disease must be known in screening

A

identify where screening can take place, enable effects of any intervention to be assessed

77
Q

4 test characteristics for screening colon cancer

A

simple and accessible to patient, sensitive and selective, screening population should have equal acess to screening population, cost effective

78
Q

how is the NHS screening for colon cancer done

A

using a FOB/FOB kit

79
Q

what are 65-75 year old patients who tested positive in screening referred for

A

colonoscopy

80
Q

what are 55-60 year old patients who tested positive in screening referred for

A

sigmoidoscopy

Y2 MCD Cancer (20 decks)

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