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Z MD1 GI block > GI Cancer > Flashcards

GI Cancer Flashcards

0
Q

what is the pre-invasive term for severe dysplasia in the breast

A

ductal carcinoma in situ lobular carcinoma in situ

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0
Q

What staging does M1 represent in the Dukes and AJCC staging

A

Stage 4/Dukes D

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1
Q

where do sessile serrated adenomas typically arise

A

proximal colon

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2
Q

what layer breach has to happen for metastasis of the prostate

A

basal cell layer

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3
Q

what is the pre-invasive term for severe dysplasia in the glans penis

A

Erythroplasia of Queyrat

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4
Q

high risk types of HPV

A

16 and 18

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4
Q

what is the pre-invasive term for severe dysplasia in the skin

A

Bowen’s disease

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4
Q

what layer breach has to happen for metastasis of the colon

A

muscularis mucosae

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5
Q

what are the differences in macroscopic growth patterns between colorectal cancer in the proximal and distal colon

A

proximal - bulky, polypoid, exophytic distal - annular, stenosing, ulcerated

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6
Q

what are the serology hallmarks of HPV infection

A

koliocytosis p16 upregulation

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7
Q

main two causes of familial colorectal cancer

A
  • lynch syndrome - familial adenomatous polyposis
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8
Q

what is interchangeable with carcinoma in situ

A

intraepithelial neoplasia dysplasia

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10
Q

What staging does T1 represent in the Dukes and AJCC staging

A

T1

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11
Q

what is the pre-invasive term for severe dysplasia in the bladder

A

carcinoma in situ

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13
Q

what is the metaplastic result of chronic atrophic gastritis

A

intestinal metaplasia

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14
Q

what are the main histological features of sessile serrated adenoma

A
  • complex branching - boot-leg angulation and dilatation at base of crypts - elongated, vesicular nuclei, prominent nucleoli - increased atypia
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15
Q

what is attenuated variation of FAP

A

when you have

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15
Q

Explain the stages of Dukes’ classification system of colorectal cancer

A

A - invades into, but not through bowel wall B - invades through bowel wall, but not involving lymph nodes C - lymph node metastases D - distant metastasis

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16
Q

how does APC mutation lead to FAP

A

decreased cell adhesion and increased cellular proliferation

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17
Q

what layer breach has to happen for metastasis of the oesophagus

A

basement membrane

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17
Q

which two oncogenes are the most common oncogene mutations in colorectal cancer

A

K-RAS, B-RAF

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18
Q

what are the precursor lesions for colorectal carcinoma

A

adenomatous polyps

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19
Q

what does lynch syndrome cause other than higher chance of getting colorectal cancer

A
  • extracolonic cancers
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20
Q

morphology of the types of adenomatous polyps

A
  • tubular adenoma - sessile or pedunculated - villous adenoma - often large and sessile - tubulovillous adenoma - mixed features
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20
Q

what kind of genetic pathway does Lynch syndrome fall in to cause colorectal cancer

A

microsatellite instability

21
Q

which two TSG are most often associated with colorectal cancer

A

SMAD4, SMAD2 and p53

21
Q

What are the 2 staging systems of colorectal cancer

A

Dukes’ classification Australian ClinicoPathological Staging system

23
Q

what layer breach has to happen for metastasis of the breast

A

myoepithelial cell layer loss

24
Q

what are the 3 types of genetic pathways that can lead to colorectal cancer

A
  • chromosomal instability - microsatellite instability - CpG island methylator phenotype
25
Q

what is the gene mutation that causes Familial adenomatous polyposis

A

APC mutation

27
Q

what gene does HPV integrate into and effect

A

E2 gene

28
Q

what is the metaplastic result of chronic reflux oesophagitis

A

Barrets oesophagus

29
Q

difference between mild/low grade dysplasia and moderate dysplasia

A

moderate - abnormal cells go to full thickness

30
Q

what layer breach has to happen for metastasis of the cervix

A

basement membrane

31
Q

what types of cells are in the cervical transformation zone

A

squamous epithelium and glandular epithelium

32
Q

what are the dysplastic features of adenomatous polyps

A
  • crowded cells –> push up to become pseudostratified - enlarged, hyperchromatic, pseudostratified nuclei - abnormal complexity to glandular architecture - goblet cell depletion - increased mitotic count
34
Q

what is aneuploidy

A

distorted number of chromosomes with lots of switching between chromosomes

35
Q

Which TSG is implicated in breast cancer

A

Her 2

36
Q

which mutation is commonly associated with sessile serrated adenoma

A

BRAF mutation

37
Q

What staging does T3 represent in the Dukes and AJCC staging

A

Stage 2/Dukes B

38
Q

what are the main mutations of DNA mismatch repair genes in colorectal cancer

A
  • MSH2 or MLH1 - sporadic MLH1 hypermutation
40
Q

what defines epithelial cancer

A

invasion of cells across the BM

41
Q

what is the most common familial colorectal cancer syndrome

A

lynch syndrome

42
Q

criteria for identifying dysplasia of the oesophagus

A
  • surface maturation of glandular mucosa - architecture of glands –> crowding, change in shape and complexity. Glad fusion (feature of malignancy) - cytology of proliferating cells –> nuclear atypia, loss of polarity - response to inflammation and erosions/ulcers
42
Q

how many polyps do you have to have to be classed as having familial adenomatous polyposis

A

100

43
Q

where does dysplasia normally start in the epithelia

A

at the lower levels (near the stem cells)

44
Q

Barretts oesophagus is a key precursor for what

A

oesophageal adenocarcinoma

46
Q

diagnostic criteria for Barretts oesophagus

A
  • endoscopic evidence of columnar lining in oesophagus above gastroesophageal junction AND - histological evidence of intestinal metaplasia (goblet cell) in biopsies from the columnar epithelium
47
Q

what does the overexpression of genes E6 and E7 do (from HPV)

A

E6 binds p53 –> apoptotic resistant, loss of G1/S and G2/M phase cell cycle check points, genomic instability E7 binds Rb –> disrupts G1/S phase cell cycle checkpoint, compensatory upregulation of P16

48
Q

what could be the reasons for early onset colorectal cancer

A
  • familial syndromes - chronic inflammatory bowel disease
49
Q

what is the pre-invasive term for severe dysplasia in the endocervix

A

adenocarcinoma in situ

51
Q

predictors of increased malignant risk of adenomatous polyps

A
  • polyp size (>1cm) - villous morphology - high grade dysplasia (severe crowding, loss of nuclear polarity, pleomorphism, gland fusion)
52
Q

how is lynch syndrome inherited

A

autosomal dominant - inherited mutation in a DNA mismatch repair gene

53
Q

What staging does N1 represent in the Dukes and AJCC staging

A

Stage 3/Dukes C

54
Q

what does disruption of the E2 gene do on the viral plasmid

A
  • overexpression of E6 and E7 oncoproteins - loss of p53 and Rb tumour suppressor function - cell cycle can proceed despite DNA damage - loss of p53 apoptosis function
56
Q

what is the main genetic pathway that leads to sporadic colorectal cancer

A

chromosomal instability

57
Q

Colorectal cancer high risk features

A
  • high grade - T3 with localised perforation or T4 - close, indeterminate or positive margins - lymphovascular invasion -
58
Q

what is the difference between diagnosis of barrett’s oesophagus from American college of gastroenterology and from the UK/Japan

A

presence of goblet cells no required for diagnosis for Japan/UK

59
Q

where does HPV like to live

A

tropism for basal keratinocytes such as the cells of the transformation zone

60
Q

what histology do the cells within adenomatous polyps show

A
  • abnormal crypt architecture - dysplasia - no invasion beyond muscularis mucosae
61
Q

explain the stages of the Australian clinciopathological staging system

A

A - invades beyond muscularis mucosa B - invades beyond muscularis propria C - lymph node metastases D - Distant metastasis

Z MD1 GI block (18 decks)

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