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Semester 4 (NME) > Colon > Flashcards

Colon Flashcards

1
Q

Where is the most common metastasis site for colon cancer?

A

Liver

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2
Q

Lower 1/3 of rectum is different to the rest of the colon and rectum how?

A

Bypasses portal circulation (blood drainage)

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3
Q

What are the two sub-types of inflammatory bowel disease? (IBD)
(What is the cause of each)

A

Crohns and ulcerative colitis

Both are autoimmune- genetic/ environmental factors

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4
Q

Name a big environmental risk factor for crohns disease?

A

Smoking

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5
Q

IBD affects people most commonly at what age?

A

15-45

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6
Q

Ulcerative colitis affects which area’s of the GI tract?

A

Sigmoid colon and rectum

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7
Q

Crohns affects which part of the GI tract?

A

All of it

Although doesn’t often affect rectum

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8
Q

Mouth ulcers are a specific symptom of which type of IBD?

A

Crohns

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9
Q

Crohns and ulcerative colitis show what patterns in the location of their inflammation?

A

Crohns: ‘Skip lesions’

Ulcerative colitis: “Continuous”

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10
Q

What are the symptoms of IBD?

A 
Recurrent diarrhoea (can be bloody- more likely UC)
Weight loss/ extreme tiredness
Abdominal pain (more common in crohns)
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11
Q

What is the difference in the depth of inflammation of UC/ crohns?

A

UC: Just submucosal
Crohns: Transmural (through whole bowel wall)- Can lead to peritonitis-shock-death

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12
Q

What is the treatment for ulcerative colitis?

A

Mesalazine (first line)- reduce inflam
Steroids for flare up
Infliximab/ Ciclosporin
Azathioprine (Immunosupressant)

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13
Q

What effect does IBD (especially UC) have on the hasutra?

A

Flattens them out (inflam)

‘Leadpipe appearance’

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14
Q

How would you diagnosis IBD?

A

Colonoscopy

Can do biopsy to exclude malignancy

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15
Q

How do you differentiate when taking a history between IBD and bowel cancer?

A

AGE (single biggest factor- either side of 50)

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16
Q

What are the types of symptoms in IBS?

A

Constipation- Give laxative

Diarrhea- Give immodium (loperimide) / buscapan

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17
Q

What are the paracolic gutters?

A

Between colon and posterolat abdominal wall, immediatly lateral to ascending and decending colons. They allow spread of material from one part of peritoneal cavity to another (cancer/ infection)

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18
Q

What is the transverse mesocolon?

A

A fold of peritoneum connecting transverse colon with post abdo wall.
Attached to pancreas and greater ommentum

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19
Q

What is the marginal artery?

A

An anastamoses between R/Mid/ L coeliac arteries

it’s continuous

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20
Q

What is McBurney’s point?

A

Base of the appendix, often site of pain in appendicitis

1/3 of distance on line from ASIS to umbilicus

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21
Q

What is appendicitis and how does it’s incidence change with age?

A

Inflammation of the appendix due to lumen obstruction

Incidence decreases with age as lumen size also decreases with age

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22
Q

What is the rectosigmoid junction?

A

Teniae coli dissapear and replaced by longitudinal smooth muscle of rectum

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23
Q

What is the pectinate (dentate) line in the rectum?

A

Line which divides lower 1/3 and upper 2/3 of the rectum. Above the line no pain is felt but the lower 1/3 can feel pain

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24
Q

Where are anal valves/ sinus’ located?

A

Valves are located in a circle around the pectinate line, with each valve having a sinus just superior to it

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25
Q

How does the rectum differ to the rest of the colon?

A

it has no sacculations (haustra) or omental appendices, it follows the curve of the sacrum and enters the rectal ampulla then into the anal canal

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26
Q

What is a portal system?

A

Where a capillary bed drains into another capillary bed without first going through the heart
(So liver receives both oxygenated and deoxygenated blood)

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27
Q

How and where does the hepatic portal vein form?

A

Formed by union of sup mesenteric vein and splenic vein

Forms post to pancreas

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28
Q

How does the HPV travel to the liver? What structures does it travel with?

A

Through the hepatoduodenal ligament

Along with hepatic artery proper and bile duct

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29
Q

What is the function of the HPV and how does it enter the liver?

A

Drains all abdo viscera into liver

Divides into R/L branches before entering liver parenchyma

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30
Q

What are the 4 portal/ systemic anastamoses? What 3 pathologies are 3 of them linked with?

A

Submucosa of oesophagus (oesophageal varicies)
Submucosa of anal canal (haemorrhoids/ piles)
Paraumbilical region (caput medusae)
Transperitoneal veins

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31
Q

How are pathologies caused in the sites of anastamoses of the systemic and portal systems?

A

Portal hypertension leads to engourgement of these veins and then bleeding

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32
Q

What are haustra?

A

Bulging pouches in the colon caused by taniae coli contraction

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33
Q

Where do each of the three major GI tract lymph drainage sites lead to?

A

Coeliac/ sup mesenteric/ inf mesenteric LN’s drain to:

Intestinal trunks > cisterna chyli > Thoracic duct > L subclavian

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34
Q

Where is the cisterna chyli found?

A

Dilation of lymph vessel

Post to AA @ L1/L2

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35
Q

ALL splanchnic nerves are what type?

A

Preganglionic

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36
Q

What are the two diiferent types of splanchnic nerves and where do they arise from?

A

Sympathetic: From thoracic/ lumbar/ sacral sympathetic trunks > prevertebral plexus ganglion
Parasympathetic: From pelvis (ant rami S2-S4) to an extension of prevertebral plexus (hypogastric/ pelvic plexi)

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37
Q

How does villi differ in the Li and SI?

A

LI has deep crypts but no villi

LI secretes lots of mucus but no digestive enzymes

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38
Q

Which epithelial cells are found in the SI but not the LI?

A

Enterocytes/ enteroendocrine cells/ paneth cells

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39
Q

Why can broad spectrum AB’s be dangerous in the colon?

A

Kills good bacteria resulting in less competition for bad bacteria- can possibly lead to clostridium difficile infection

40
Q

What are the 3 layers of the mucosa in the GI tract?

A

Epithelium
Lamina propria (BV’s etc- loose connective tissue)
Muscularis mucosa- Double layer SM

41
Q

What lies deep to the muscosa in the GI tract?

A

Submucosa (loose connective tissue with larger BV’s/ lymph/ nerve)
Can contain mucus secreting glands

42
Q

What lies deep to the submuscosa in the GI tract?

A 
Muscularis propria (aka externa)
Has inner (circular) and outer (longitudinal) smooth muscle layers for peristalsis
In colon longitudinal muscle become tenaie coli
43
Q

What lies deep to the muscularis propria in the GI tract?

A

Adventia

This is the outermost layer and is connective tissue covered by peritoneum. Also has vessels/ nerves

44
Q

What is the main function of the LI?

A

Re-absorption of water

although the majority of water absorbed in SI

45
Q

What is the compostion of feces?

A

75% water
5% bacteria
20% indigestible material/ dead cells

46
Q

Where are bile salts absorbed?

A

In the terminal ileum (some in the caecum)

(the sent back to liver to be put back into bile)-

47
Q

What are the most common bacteria in the colon?

A

Mainly anaerobes:

Enterocossus faecalis/ bacterioides fragilis/ escherichia coli

48
Q

What are the functions of bacteria in the colon?

A

Vitamin K synth (50% of total)
Biotin synthesis (water solube vit for glucose metabolism)
Vitamin B5 synth (water sol vit for steroid synthesis)
Converts bilirubin to urobilogens/ stercobilogens
Breaks down peptides (producing waste)

49
Q

What is vitamin K needed for?

A

Production of 4 clotting factors (incl prothrombin)

remember it is lipid soluble so needs fat in the diet in order to be absorbed

50
Q

What is vitB5 and what is it needed for?

A

Synthesised by colon bacteria

Used for neurotransmitter and steroid synthesis

51
Q

How is bilrubin processed by the colon?

A

Converted to urobilogens and stercobilagens by colonic bacteria
Some U+S then goes into blood and out via kidneys.
Most is converted by O2 to urobilns and stercobilins

52
Q

What gives poo it’s colour?

A

Urobilns and stercobilins

53
Q

Break down of peptides by colonic bacteria produces what?

A

1) Ammonium ions (absorbed by colon, send to liver for conversion to non-toxic then out via kidneys)
2) Indole and skatole (give faeces it’s odour)
3) Hydrogen sulphide (H2S)- Gives rotten egg smell

54
Q

What are mass movements?

A

3-4 times per day for 10-30mins
Push from transverse colon right to rectum, inducing need for defecation. Stimulated by distension of duodenum Chyme can travel 30-80% colon length

55
Q

What is haustral churning?

A

Mixing of chyme in adjacent haustra

56
Q

The majority of colorectal tumours are of what type?

A

Adenocarcinoma (from polyps)

57
Q

What are the three most common cancers in the UK?

A

1) Breast
2) Lung
3) Colorectal

58
Q

What are the two biggest cancer killers in the UK?

A

1) Lung
2) Colorectal
(20% colorectal have metastasis on presentation)

59
Q

What is the distribution of colorectal cancer between the colon and the rectum?

A

70% colon

30% rectum

60
Q

What is the most common site for colorectal cancer?

A

Over 70% are lower descending/ sigmoid/ rectum

61
Q

What is the lifetime risk and 10yr survival rate for colorectal cancer?

A

1 in 20

10yr Survival is 57%

62
Q

What is the most common age of presentation of colorectal cancer?

A

60-65

63
Q

What are the risk factors for colorectal cancer?

A

FHx under age 60/ genetics (FAP)
IBD/ UC/ Crohns
Sedentary/ alcohol/ smoking/ low fibre intake
Diabetes/ nullparity

64
Q

What is the common series of acquired mutations in colorectal cancer?

A

c-ki-ras mutation (becomes ademoa)
APC loss (in-siu carcinoma)
DCC loss
p53 loss (invasive carcinoma)

65
Q

Where is the APC gene located?

A

5q21

66
Q

Where is the p53 gene located?

A

17p13

67
Q

What are the most common S+S of colorectal cancer?

A 
Change in bowel habits >6wks
Loose stools
Rectal bleeding/ iron deficiency anaemia
Weight loss
Jaundice and hepatomegaly if mets
68
Q

How is colorectal cancer diagnosed?

A

Colonoscopy/ DRE
Do FBC/LFT
Dukes and TNM to stage

69
Q

What is the NICE recommended chemo treatment for colorectal cancer?

A

FOLFOX
Folinic acid: Is an adjuvant (enhancer) of 5-FU
5-Flurouracil (irreversibly inhibits thymidylate synthase)
Oxiliplatin

70
Q

What are the surgical treatment options for colorectal cancer?

A 
Subtotal colectomy (remove LI, preserve rectum)
Local excision (remove local wall- early stage)
R/L hemicolectomy
71
Q

What is an adenoma?

A

Benign tissue of epithelial glandular origin

72
Q

What are the three common polyp types seen in the colon?

A

1- Hyperplastic- from hyperplasia 2- Inflammatory
(1+2 are most common and unlikely to become malignant)
3- Adenoma (pre-malignant polps)

73
Q

What are the three subtypes of adenoma in the colon?

A

Tubular (75%)- most common and not malig likely
Tubulovilous (15%)- Mix of 1 + 3
Vilous (10%)- Mostly in rectal area, high malignancy risk, most commonly sessile (flat) and non-pedunculated

74
Q

What featured of polyps increase their likelihood of becoming malignant?

A

Large size
Villous
Sessile (flat)

75
Q

What is FAP?

A

Familial adenomatous polyposis (~1% CRC)
Rare autosomal dominant APC mutation
100/1000’s polyps form by age 16, turn malig by age 35

76
Q

What % of CRC’s have mutations in the APC gene?

A

80-90%

77
Q

What is attenuated FAP?

A

Develops later in life (44yo) with less (

78
Q

What is HNPCC (aka lynch syndrome)?

A

Hereditary non-polyposis colon cancer (3% of all CRC)
Few polyps but fast progession to malig
Often mutations in DNA repair genes (hMSH1/2)
Presents earlier than sporadic CRC

79
Q

What is Wnt?

A

A signalling molecule that causes cell growth

It binds to a frizzled (FZD) receptor and through ‘dishevelled (DVL)’ protein stops degradation of ‘B-catenin)

80
Q

What is B-catenin?

A

A signal molecule that when levels rise binds to TCT transcription factor which increases cell proliferation by upregulating MYC and CYCLIN D1 genes

81
Q

How does APC normally affect cell growth?

A

APC gene is a tumour suppressor
Together with GSK3B and other molecules it forms a complex which degrades ‘B-catenin’ by tagging it for phosphorylation and this limits cell growth

82
Q

How does a mutation resulting in loss of the APC gene affect cells?

A

It means the complex which degrades ‘B-Catenin’ doesn’t form, this increases ‘B-catenin’ levels and increases cell proliferation by up-regulating transcription of MYC and CYCLIN D1 proteins

83
Q

What are the different dukes stages?

And 5yr survival rate

A

A: In submucosa and muscle wall only- 90%
B: Breached muscle layer and wall (but no LN’s)- 70%
C1: Spread to immediate (pericolic) LN’s -35%
C2: Spread to higher (mesenteric) LN’s
D: Distal visceral mets - 5%

84
Q

Most CRC’s are diagnosed when they are at which stage?

A

B

85
Q

Faecal occult blood screening is offered to all those aged…?
What does a +ve result mean?

A

60-75
(looks for hidden blood)
2% of +ve results are cancer, 30% are polyps

86
Q

How is a faecal occult blood test performed?

A

Stool and H2O2 are placed on paper

Haem in blood breaks down H2O2 so therefore blood is present

87
Q

What is a paracrine hormone?

A

Only has effect in immediate vicinity

88
Q

What are the two types of gut movements?

A

Segmentation- Mixing (Circular muscle)

Peristalsis- Propulsion + mass effect (longitudinal muscle)

89
Q

What is the histological compostition of smooth muscle fibres in the GI tract?

A

Unstriated, irregular actin/ myosin pattern, long and thin in bundles of ~5000 fibres

90
Q

What are slow waves and what is their frequency in different parts of the GI tract?

A

Regular contractions of gut
Stomach- 3/min Duodenum= 20/min Ileum= 10/min
Colon = 7/min

91
Q

What is the role of interstitial cells of cajal? (ICC)

A

Integrate SM activity and act as pacemaker cells

92
Q

What is interdigestion?

A

Digestion between meals

93
Q

What are long reflexes?

A

Extrinsic nerves where PNS acts with ENS (So there is both ENS and CNS involvement)

94
Q

What is the difference in SNS/PNS action on the GI tract in terms of mechanism?

A

SNS- acts direct on SM

PNS- acts indirectly on myenteric/ submucosal plexi

95
Q

What are short reflexes?

A

Enteric NS only!

Often local distension = increased local motility

Semester 4 (NME) (24 decks)

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