Coeliac Disease and Bowel Carcinoma Flashcards
diseases caused by malabsorption
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
malabsorption leads to
Decreased minerals and vitamins absorption, become malnourished can cause chronic issues, inflammation of bowel and no longer able to absorb properly
coeliac disease
Sensitivity to α-gliaden component of Gluten
true prevalence of coeliac disease
1 in 300
gluten sensitive enteropathy spectrum
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
aetiology of coeliac disease
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
what are the progressive changes in villi in coeliac disease
Normal healthy bowel progressive changes in villi
– Gradually completely removed
– Flat mucosa
Slower rate of absorption as less SA
impact of removing gluten on patient with coeliac disease
can reverse process
– Get a normal bowel
what investigations are used to assess bowel in coeliac disease cases
Endoscopy and biopsy to assess bowel
– Gluten free diet for a few month and repeat endoscopy to see improvement to confirm diagnosis
effect of jejunal atrophy in clinical cases of coeliac disease
- growth failure
- oral ulceration
30-40%
effect of jejunal atrophy in subclinical cases of coeliac disease
no effect
coeliac disease effects….
children mainly
but can develop with age
effect of coeliac disease on children
Don’t have absorption of nutrients in child - failure of growth, obvious in later life
effect of coeliac disease in adults
Subclinical for adults as less problems seen fully grown
No bowel symptoms
– But malabsorption - mouth ulcers as poor iron absorption
if don’t get treatment from avoiding gluten in coeliac disease
Get areas of chronic immune cell stimulation
Develop lymphoma in small bowel (like H pylori in stomach)
8 classic symptoms of coeliac disease
Weight loss Lassitude Weakness Abdominal pain/swelling Diarrhoea Aphthae/glossitis Steatorrhoea Dysphagia
(most asymptomatic or relatively small reaction to gluten)
malabsorption causes most issues
4 things that can be malabsorbed in coeliac disease cases
iron
folate
vitamin B12
fat
Suspicious of small bowel malabsorption if more than one
4 investigations for coeliac disease
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
3 areas of small bowel
duodenum
jejunum
ileum
what areas of small bowel are most effected in coeliac disease
jejunum
ileum
how can a gluten free diet help in coeliac disease (3)
Reversal of jejunal atrophy
Improved well- being
- Feel better, less immune response
Reduced risk of lymphoma
what is coeliac disease associated with
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
what does folate or combined ferritin and folate deficiency suggest
malabsorption
can lead to mouth ulcers
change in pattern of occurence of mouth ulcers can indicate
Iron or folic acid low due to mouth ulcers
- Maybe underlying bowel issue
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
colonic carcinoma prevalence
second most common malignancy in western world
- Europe and USA 10 times more common than Africa
3 causes of colonic carcinoma
Genetic difference in population
Largely due to diet
Manufacturing changes to food
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
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
polyps lead to
colonic carcinomas
aetiology of colonic carcinomas
polyps
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
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
small intestine risk of carcinoma if have intestinal polyposis
low
- Peutz-jehgers syndrome
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
well differentiated colonic carcinoma 5 year survival rate
80%
moderately differentiated colonic carcinoma 5 year survival rate
60%
poorly differentiated colonic carcinoma 5 year survival rate
25%
early diagnosis (screening) effect on survival rate of colonic carcinoma
no effect
to do with grading of disease
submucosal stage of bowel cancer 5 year survival rate
80%
muscularis stage of bowel cancer 5 year survival rate
65%
lymph nodes stage of bowel cancer 5 year survival rate
45%
liver stage of bowel cancer 5 year survival rate
5%
has spread everywhere
important to remember in terms of survival rates
better but not necessarily cured
- Good agents to treat and surgical management better
carcinoma Dukes’ Classification A
submucosal (best survival rate for bowel cancer)
carcinoma Dukes’ Classification B
muscularis
carcinoma Dukes’ Classification C
lymph nodes
carcinoma Dukes’ Classification D
liver (worst survival rate for bowel cancer)
colonic carcinoma treatment
Surgery
- Rid of lesion
Hepatic metastases
- Radiotherapy
- Chemotherapy – if spread
polyp occurence
Don’t just get one polyp
- Tendency to form a few at different stages
Screening - positive polyp test need to endoscopy regularly
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
