Coeliac Disease and Bowel Carcinoma Flashcards

1
Q

diseases caused by malabsorption

A

pernicious anaemia
- intrinsic factor and vitamin B12 at end of ileum (disease caused by Crohn’s or carcinoma)

coeliac disease (small bowel)

crohn’s disease (small bowel)

infections

tumors

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2
Q

malabsorption leads to

A

Decreased minerals and vitamins absorption, become malnourished can cause chronic issues, inflammation of bowel and no longer able to absorb properly

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3
Q

coeliac disease

A

Sensitivity to α-gliaden component of Gluten

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4
Q

true prevalence of coeliac disease

A

1 in 300

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5
Q

gluten sensitive enteropathy spectrum

A

Some foods not enough to cause clinical symptoms

Wide range of foods can cause issues

  • wheat > barley > spelt > rye > kamut > oats
  • Oats generally OK but can be contaminated in the factory
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6
Q

aetiology of coeliac disease

A

genetic (DQw2)
T lymphocytes
Villous atrophy

Wheat being cut up
– Different components absorbed
Cytokines react
– Attacks and causes damage to epithelial cells on surface of bowel
– Inflamed bowel
– Lose villi which increase SA
Malabsorption due to combination of inflammation and reduction in SA

Gluten sensitivity enteropathy
– Wasting away of bowel wall

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7
Q

what are the progressive changes in villi in coeliac disease

A

Normal healthy bowel progressive changes in villi
– Gradually completely removed
– Flat mucosa
Slower rate of absorption as less SA

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8
Q

impact of removing gluten on patient with coeliac disease

A

can reverse process

– Get a normal bowel

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9
Q

what investigations are used to assess bowel in coeliac disease cases

A

Endoscopy and biopsy to assess bowel

– Gluten free diet for a few month and repeat endoscopy to see improvement to confirm diagnosis

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10
Q

effect of jejunal atrophy in clinical cases of coeliac disease

A
  • growth failure
  • oral ulceration

30-40%

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11
Q

effect of jejunal atrophy in subclinical cases of coeliac disease

A

no effect

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12
Q

coeliac disease effects….

A

children mainly

but can develop with age

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13
Q

effect of coeliac disease on children

A

Don’t have absorption of nutrients in child - failure of growth, obvious in later life

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14
Q

effect of coeliac disease in adults

A

Subclinical for adults as less problems seen fully grown

No bowel symptoms
– But malabsorption - mouth ulcers as poor iron absorption

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15
Q

if don’t get treatment from avoiding gluten in coeliac disease

A

Get areas of chronic immune cell stimulation

Develop lymphoma in small bowel (like H pylori in stomach)

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16
Q

8 classic symptoms of coeliac disease

A
Weight loss
Lassitude
Weakness
Abdominal pain/swelling 
Diarrhoea
Aphthae/glossitis
Steatorrhoea
Dysphagia

(most asymptomatic or relatively small reaction to gluten)
malabsorption causes most issues

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17
Q

4 things that can be malabsorbed in coeliac disease cases

A

iron

folate

vitamin B12

fat

Suspicious of small bowel malabsorption if more than one

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18
Q

4 investigations for coeliac disease

A

Jejunal biopsy (grab biopsy through endoscopy, capsule take section out)

  • Capsule
  • Endoscope – best test

Faecal fat

Haematinics

Autoantibodies – look for antibodies associated with coeliac disease in blood
- Serum transglutaminase
- Anti-gliadin/anti-endomyseal antibodies
Cheap, very sensitive but not very specific, can show positive when don’t have disease
Negative = don’t have disease
Positive = do other tests, all positive then have but if they return negative then false positive result

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19
Q

3 areas of small bowel

A

duodenum
jejunum
ileum

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20
Q

what areas of small bowel are most effected in coeliac disease

A

jejunum

ileum

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21
Q

how can a gluten free diet help in coeliac disease (3)

A

Reversal of jejunal atrophy

Improved well- being
- Feel better, less immune response

Reduced risk of lymphoma

22
Q

what is coeliac disease associated with

A

dermatitis herpetiformis: antibody mediated problems in response to gluten - reaction

  • Oral disease
  • Blisters on skin, shoulders and back
  • Granular IgA deposit in skin and mucosa
23
Q

what does folate or combined ferritin and folate deficiency suggest

A

malabsorption

can lead to mouth ulcers

24
Q

change in pattern of occurence of mouth ulcers can indicate

A

Iron or folic acid low due to mouth ulcers

- Maybe underlying bowel issue

25
colorectal carcinoma prevalence
Used to biggest killer in Scotland Largely genetic based disease - Some families very strong Relatively young effected (40-50) Clear pattern - dominant genetic tendency to have bowel cancer Easily treated if caught early on - Catch tumour before malignant can keep disease under control - Blocked bowel with large tumour
26
colonic carcinoma prevalence
second most common malignancy in western world | - Europe and USA 10 times more common than Africa
27
3 causes of colonic carcinoma
Genetic difference in population Largely due to diet Manufacturing changes to food
28
symptoms of colonic carcinoma
None Anaemia Rectal blood loss - Shouldn’t occur if healthy Predictive risk of symptoms of bowel cancer from range of symptoms - Vague things - need advanced disease for some to show - Need to use practical other ways to ID
29
screening for colonic carcinoma
FOB Barium enema Endoscopy CT/MRI scan Carcinoembryonic antigen (CEA) All adults in the UK over 50 invited - FOB sample by post - 5 year repeat if negative - Endoscopy if positive
30
polyps lead to
colonic carcinomas
31
aetiology of colonic carcinomas
polyps
32
features of polyps
May be pedunculated or flat Most will bleed due to irritation to malignancy - Bigger and bigger become malignant If polyps found on endoscopy, screening interval reduced Blood cells coming out of bowel due to polyps ID then do endoscopy and treat before the spread - Get irritated by food passing over - Leak red blood cells into bowel - RBC pass out of mucosa - Can be removed without long term consequences if caught early mouth polyps the same
33
8 risk factors leading to colonic carcinoma
Diet - high fibre - high fat - high meat - Low veg High smoking Alcohol no difference (does increase mouth cancer risk) Low exercise Genetic – P53 in 75% Ulcerative colitis Intestinal polyps - All the way through lead to certain diseases Family history of bowel cancer – get checked regularly
34
small intestine risk of carcinoma if have intestinal polyposis
low | - Peutz-jehgers syndrome
35
large intestine risk of carcinoma if have intestinal polyposis
``` high - Gardiners syndrome - Cowden’s syndrome Mucosal polyps around mouth and continuous through gut Can become carcinomas in colon ```
36
well differentiated colonic carcinoma 5 year survival rate
80%
37
moderately differentiated colonic carcinoma 5 year survival rate
60%
38
poorly differentiated colonic carcinoma 5 year survival rate
25%
39
early diagnosis (screening) effect on survival rate of colonic carcinoma
no effect to do with grading of disease
40
submucosal stage of bowel cancer 5 year survival rate
80%
41
muscularis stage of bowel cancer 5 year survival rate
65%
42
lymph nodes stage of bowel cancer 5 year survival rate
45%
43
liver stage of bowel cancer 5 year survival rate
5% has spread everywhere
44
important to remember in terms of survival rates
better but not necessarily cured | - Good agents to treat and surgical management better
45
carcinoma Dukes' Classification A
submucosal (best survival rate for bowel cancer)
46
carcinoma Dukes' Classification B
muscularis
47
carcinoma Dukes' Classification C
lymph nodes
48
carcinoma Dukes' Classification D
liver (worst survival rate for bowel cancer)
49
colonic carcinoma treatment
Surgery - Rid of lesion Hepatic metastases - Radiotherapy - Chemotherapy – if spread
50
polyp occurence
Don’t just get one polyp - Tendency to form a few at different stages Screening - positive polyp test need to endoscopy regularly
51
colon cancer screening
over 50, every 5 years if negative, endoscopy if positive, FOB sample by post - Dentist can encourage ``` FOB test in stool in Scotland Endoscopy in England Barium enema CT/MRI scan Carcinoembryonic angina (CEA) ``` Do regularly every few years to pick up early