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MO2 > GI cancer SD > Flashcards

GI cancer SD Flashcards

1
Q

how long is the colon?

A

aprox 1.5m

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2
Q

what are the 4 regions of the colon?

A

– Ascending
– Transverse
– Descending
– Sigmoid

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3
Q

what is ascending colon linked to small intestine by?

A

the caecum

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4
Q

what joins the rectum?

A

Sigmoid colon

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5
Q

what are the functions of the colon?

A
  1. Reabsorption of fluids and some solutes
    – 2L of water enter the colon from the ileum
    – 90% reabsorbed (mainly in ascending colon)
    – Fat-soluble vitamins, e.g. vitamin K, vitamin B12, thiamine, riboflavin
    – Negligible; no significant impact on nutrition
  2. Movement of waste products for excretion
    – Movement by haustral contractions
    – Contraction of smooth muscle
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6
Q

how long does it take for waste to pass?

A

16 hours

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7
Q

what are the 4 parts that make up the histology of the colon?

A

1- mucosa- lamina propria, crypts, muscularis mucosae
2-submucosa
3-muscularis propria
4-serosa

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8
Q

what is the purpose of the 3 parts of the mucosa?

A
  • Crypts
    – Columnar colonocytes
    – Goblet cells (mucus-secreting)
    – Stem cells
  • Lamina propria
    – Connective tissue that provides
    support & immune defence
    – Lymphocytes, lymph nodules
  • Muscularis mucosae
    – 2 layers of smooth muscle
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9
Q

what is the submucosa?

A

– Connective tissue rich in blood and
lymph vessels

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10
Q

what is the purpose of the muscularis propria?

A

– Smooth muscle in three layers
(collectively the ‘taenia coli’)
– Contraction moves faeces through the
colon

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11
Q

what is the purpose of the serosa?

A

– Thin layer of mesothelial cells
– Positioning of the colon

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12
Q

what is FAP?

A
  • Inherited mutation in the APCgene
    – Formation of many polyps
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13
Q

how do you diagnose FAP?

A

Diagnosed by colonoscopy and genetic
testing
– Identification of 100+ polyps
– Sequencing of the APCgene

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14
Q

what are the risk factors for CRC?

A
  • Diet
    – ↑red meat, processed meats
    – ↓fibre, chicken & fish
  • Lack of physical activity
  • Obesity
  • Alcohol & smoking
  • Genetic predisposition
  • Protective effect of aspirin
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15
Q

where is sporadic CRC most common?

A

most common in the descending colon, sigmoid colon and rectum

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16
Q

do tumours differ by region?

A
  • Tumours differ by region
    – Ascending/transverse vs descending/
    rectal
    – mutations in KRAS (sigmoid/rectum)
    – BRAF (ascending/transverse)
    – mutually exclusive
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17
Q

what is the estimate time it takes for ademona to develop into an advanced carcinoma?

A

17 years

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18
Q

how long does it take for carcinoma to progress to metastasis ?

A

– 1.8 years from advanced
carcinoma to metastasis

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19
Q

what is the histology of CRC?

A
  • Loss of normal architecture
  • Hyperchromatic (intensely stained) cells
  • Invasion through submucosa
  • Nucleus takes up a greater proportion of the cell
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20
Q

what is the staging of colorectal cancer?

A

TNM
- tumour T1- invades submucosa
2-invades muscularis propria
3- through muscularis to pericolorectal tissues
4-penetrates to surface of visceral peritoneum/ invades or adherent to other organs

21
Q

how do we stage CRC in the UK?

A

duke stages A-D

22
Q

how does CRC metastases to the liver?

A

Liver is the most commonly affected site
– Venous drainage from the colon to the liver
– Liver mets affect 50% of CRC patients
– 20% will be resectable much better
prognosis (poor without)

23
Q

how do lungs metastases?

A
  • Lungs second-most commonly affected
    – 10-15% of CRC patients will develop lung mets
    – Rare to have lung mets alone (<10%)
    – Usually not resectable
24
Q

what is the vogelstein model?

A

Bert Vogelstein described a molecular model by which CRC could
arise, now referred to as the ‘Vogelstein model’
– Step-wise accumulation of mutations/epigenetic changes and how
they relate to tumour development
1. APCTSG, regulates Wnt signalling Mutated in ~50%
of CRC
2. KRASOncogene, drives cell growth Mutated in ~45%
3. p53TSG, ‘guardian of the genome’ Mutated in ~40%

25
Q

does ever colorectal cancer develop by vogelstein model?

A

– Vogelstein himself stressed this in his paper; it is an example
– Only 7% of tumours have mutations in all three of these genes
– Accumulation of mutations in key genes is more important than the
order

26
Q

how deos colon cancer progress with altered genes?

A

APC – loss of function (TSG)
RAS – gain of function (Oncogene) – MAPK signals and cell cycle
p53 – loss of function (TSG)
TGF-β– loss of function (Growth Suppressor)

27
Q

how do you screen for colorectal cancer?

A

Faecal Occult Blood Test
* Measure of blood (haem) in stool – frequent in CRC

28
Q

how is the faecal occult blood stool test done?

A

Hydrogen peroxide developer solution applied
* Detects pseudoperoxidase activity of haemoglobin
* Limitations
– Red meat (+ve), Cauliflower (+ve), uncooked
vegetables (+ve), Haemorrhoids (+ve)
– High vitamin C (-ve)

29
Q

how are positive faecal tests followed up?

A

sigmoidoscopy

30
Q

what is the gold standard screening approach to screening?

A

colonoscopy- detects polyps, adenomas and tumours

31
Q

what is the diet before a colonsocopy?

A

Patients required to undergo a strict diet for up to three days in advance (low fibre, only clear liquids) and bowel prep using laxatives

32
Q

how often is colonscopy screening recommended?

A

every 5-10 years

33
Q

what are the different types of endoscopy?

A

lexible sigmoidoscopy- covers the descending colon
colonoscopy- provides full coverage

34
Q

what is flexible sigmoidoscopy?

A

Similar to colonoscopy in enabling removal of polyps/adenomas and taking
biopsies
* Covers only the descending colon
– However, this is where most sporadic CRC tumours originate
– Therefore provides coverage of 70-80% of CRC cases
– Colonoscopy is preferred for colitis-associated CRC, for example

35
Q

what is the benefit of flexible sigmoidoscopy?

A
  • No sedation required
  • Reduces costs and shorter duration (10mins vs 30mins + recovery time)
36
Q

what is the main treatment stratigies for colorectal cancers?

A

remove the tumour and chemotherapy to
reduce the risk of metastases

37
Q

when does adjuvant therapy begin with colorectal cancer?

A

Adjuvant therapy normally begins ~6 weeks after surgery
– Timing depends upon post-operative wound healing and patient
age/frailty

38
Q

how does 5 FU work in GI cancer?

A

Thymidylate synthase inhibitor
Stops production of thymidine no thymidine
for DNA replication cell death

39
Q

how does leucovorin work in GI cancer?

A

Reduced form of folic acid Enhances 5-FU activity (stabilised 5-FU/thymidylate synthase complex)

40
Q

what is the purpose of oxaliplatin?

A

Platinum-based compound
Creates platinum-based DNA adducts blocks
DNA replication cytotoxic; beneficial with
Stage III tumours and beyond

41
Q

what is the purpose of capecitabine?

A

Thymidylate synthase inhibitor
Converted to 5-FU in the body; may offer
improved tolerability and reduced non-tumour
cytotoxicity

42
Q

what is the purpose of irinotecan?

A

Topoisomerase inhibitor Prevents DNA replication cytotoxic

43
Q

what are the CRC key signalling and targeted therapies?

A
  • EGFR Inhibitors
    – Target EGFR (epidermal growth factor receptor) that promotes tumour growth
  • VEGFR Inhibitors
    – Target VEGF (vascular endothelial growth factor) that promotes growth of neovasculature
  • Immunotherapy
    – Target PD-1, which is expressed on tumours to block immune response
    – PD-1 inhibition increases immune response to the tumour
    – Generally given to patients who are not responding to chemotherapy
44
Q

what role does EGFR play in crc?

A
  • EGFR Activation stimulates
    multiple downstream pathways
  • These drive cellular proliferation
    and promote cell survival (anti-
    apoptosis)
45
Q

what happens when there is mutation in pathways in CRC?

A

activates the pathways
irrespective of EGFR activity
– KRAS: ~40% of tumours
– BRAF: ~10%
– PI3K: 25%
– PTEN: <10%

46
Q

what can patients who are wild type patients recieve?

A

Cetuximab / Panitumumab - EGFR MAb’s

47
Q

what happens if there is mutant RAS?

A

therapy ineffective

48
Q

what are someVEGF MabS?

A
  • Bevacizumab (Avastin®), Aflibercept (Zaltrap®), Ramucirumab (Cyramza®),
    Regorafenib (Stivarga®).
49
Q

when may immunotherapy be used?

A

A subset of metastatic CRC patients will have genetic alterations that prevent
cells from repairing damaged DNA = High rates of DNA mutations.
– mismatch repair deficiency (dMMR)
– high microsatellite instability (MSI-H).
– Some of these mutations may lead to the production of
abnormal antigens that can be targeted by immune cells

MO2 (55 decks)

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