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BDS2 BAMS > Coeliac Disease and Bowel Carcinoma > Flashcards

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
Q

colorectal carcinoma prevalence

A

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
Q

colonic carcinoma prevalence

A

second most common malignancy in western world

- Europe and USA 10 times more common than Africa

27
Q

3 causes of colonic carcinoma

A

Genetic difference in population

Largely due to diet

Manufacturing changes to food

28
Q

symptoms of colonic carcinoma

A

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
Q

screening for colonic carcinoma

A

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
Q

polyps lead to

A

colonic carcinomas

31
Q

aetiology of colonic carcinomas

A

polyps

32
Q

features of polyps

A

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
Q

8 risk factors leading to colonic carcinoma

A

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
Q

small intestine risk of carcinoma if have intestinal polyposis

A

low

- Peutz-jehgers syndrome

35
Q

large intestine risk of carcinoma if have intestinal polyposis

A 
high
- Gardiners syndrome 
- Cowden’s syndrome
Mucosal polyps around mouth and continuous through gut 
Can become carcinomas in colon
36
Q

well differentiated colonic carcinoma 5 year survival rate

A

80%

37
Q

moderately differentiated colonic carcinoma 5 year survival rate

A

60%

38
Q

poorly differentiated colonic carcinoma 5 year survival rate

A

25%

39
Q

early diagnosis (screening) effect on survival rate of colonic carcinoma

A

no effect

to do with grading of disease

40
Q

submucosal stage of bowel cancer 5 year survival rate

A

80%

41
Q

muscularis stage of bowel cancer 5 year survival rate

A

65%

42
Q

lymph nodes stage of bowel cancer 5 year survival rate

A

45%

43
Q

liver stage of bowel cancer 5 year survival rate

A

5%

has spread everywhere

44
Q

important to remember in terms of survival rates

A

better but not necessarily cured

- Good agents to treat and surgical management better

45
Q

carcinoma Dukes’ Classification A

A

submucosal (best survival rate for bowel cancer)

46
Q

carcinoma Dukes’ Classification B

A

muscularis

47
Q

carcinoma Dukes’ Classification C

A

lymph nodes

48
Q

carcinoma Dukes’ Classification D

A

liver (worst survival rate for bowel cancer)

49
Q

colonic carcinoma treatment

A

Surgery
- Rid of lesion

Hepatic metastases

  • Radiotherapy
  • Chemotherapy – if spread
50
Q

polyp occurence

A

Don’t just get one polyp
- Tendency to form a few at different stages

Screening - positive polyp test need to endoscopy regularly

51
Q

colon cancer screening

A

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

BDS2 BAMS (54 decks)

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