Crohn’s Disease and Ulcerative Colitis Flashcards by niamh ritchie

significant diseases of GI

Oesophagus and upper GI

Malabsorption

Pernicious anaemia
Coeliac disease
Crohn’s disease

Large bowel

Inflammatory bowel disease (IBD)
Cohn’s disease
Ulcerative Colitis

Colonic Ca

Infections

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incidence of inflammatory bowel disease

20 times more in Western Societies
- Increasing

White > Black

age: 15-25, 50-80

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gender ratio for Crohn’s

male > female

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gender ratio for Ulcerative Colitis

female > male

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aetiology of inflammatory bowel diseases

Immunological

Psychological
- Chronically anxious more at risk

Smoking
- Less risk but benefit lost by increase CV disease risk

Genetic

Mystery
- Complex pattern of inherited and environmental and psychological changes
- Change in gut pathology
Likely more than one cause in population
- Clinical manifestation the same but aetiology of changes in mucosa are different

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aetiology of Crohn’s disease

Granulomatous inflammation – varied aetiology
- Collection of multinucleated giant cells in clump and resistant to removal by phagocytosis (surrounded by immune cells)

Tissue causes immune stimulation body is unable to deal with (alike TB) and generalised chronic inflammation

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cause of Crohn’s disease

unknown

Food intolerance
- Irritation to immune system caused by something passing through the gut

Persisting viral infection/immune activation

Recurrent viral infection
Infectious agent passed to people in right susceptibility causes problems

? Infection with Mycobacteria (paratuberculosis)

Johne’s disease
-Problem in cattle which is similar to Crohn’s

Hard to find and ID agents

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M.paratuberculoisis cycle

Mycobacteria causes disease in cow
Happen in farm 
Dairy passed into industry 
Treated incorrectly 
Passed to humans

Incidence of both diseases increased similarly

Gap in time of 10 years
Zoonotic infection from cow to people

Pasteurisation of milk
- Good at getting rid of pathogens
But not M.paratubercolosis
- Only way is by UHT milk

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Crohn’s disease impact on bowel surface

Lumps (should be smooth)

areas of oedema, caused by granulomas washed into lymphatics carried away into tissue fluid, preventing draining of lymphatics
Cobble stoning of mucosa

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how are the lumps formed in Crohn’s disease

Block lymphatics cause oedema and lump

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crohn’s disease sites

can be ID anywhere
- can be in certain sections and skip lesions

(colitis in colon)

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3 common Crohn’s disease sites

Mouth

Ileocecal region - small to large

rectal

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ulcerative colitis sites

only colonic disease
- Ascending, sigmoid, descending
Starts at rectum and works way up
- Continuous inflammation up the way

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what is ulcerative colitis

Ulcers in colon
- Like mouth ulcers

Change in bowel activity

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features of ulcerative colitis

Disease continuous

Rectum always involved (bottom up)

Anal fissures 25%

Ileum involved 10%
- Small bowel involved in small number

Mucosa granulomas & Ulcers

Vascular

Serosa normal

Superficial inflammation
Only areas affected are top layers
a featureless colon with complete loss of haustration, total blurring of the normal vascular pattern, and agranular-likemucosadevelops.

ulcerative colitis thereisa continuous, diffuse granular mucosal pattern, with or without superadded ulceration; i

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features of Crohn’s disease

Discontinuous

Rectum involved 50%

Anal fissures 75%

Ileum involved 30%

Mucosa cobbled and fissures
- Due to lymphatic blockage

Non-vascular

Serosa inflamed
- Entire thickness of bowel wall inflamed

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microscopic features of ulcerative colitis

Granular Mucosal

Vascular more blood vessels

Mucosal abscesses

microscopic features of Crohn’s disease

Transmural
- full thickness effected

Oedematous
- blocking lymphatics

granulomas
- Drainage is deep
Biopsy to show it is a challenge

Clinical features and signs of Crohn’s disease

Oedema

Perioral erythema

red inflammatory changed
Swollen lips (can just be one or both)

Inflammation
Swelling
Oedema of bowel wall
- narrower lumen so problem with passing bowel contents

All though bowel wall so abscesses can form
Outside or inside
End up with inflammation causing a fistula
- hole between two loops of bowel, connection,
- bacteria spread

full thickness inflammation, granuloma formation and oedema

Crohn’s colitis is characterised by discrete ulcers with intervening normal mucosa.

ulcerative colitis effect on mucosa

Normal tissue
– Secretory mucosa
– Thin layer of serosa tissue

In UC distorted picture but not extended to outside

Bottom area largely normal
superficial

ulcerative colitis there is a continuous, diffuse granular mucosal pattern, with or without superadded ulceration

a featureless colon with complete loss of haustration, total blurring of the normal vascular pattern, and agranular-likemucosadevelops.

when taking a biopsy of a UC site what can a perforation cause

peritonitis

ease of management of UC

Straightforward to manage

Easy access
Take away colon = remove symptoms as only site effected

Bottom up (limited disease)

ulcerative colitis symptoms (3)

Diarrhoea
Abdominal pain
PR Bleeding

crohn’s disease symptoms

Depend on site effected
– Tend not to be painful but mouth can be

Colonic disease – same as UC

Small bowel disease

Pain - obstruction
Narrower tube so easier to block
Malabsorption – anal disease

Mouth

Change in appearance
Orofacial granulomatosis
Gingivitis

colonic crohn's disease symptoms

same as UC Diarrhoea Abdominal pain PR Bleeding

small bowel Crohn's disease symptoms

Pain - obstruction - Narrower tube so easier to block - Malabsorption – anal disease

mouth Crohn's disease symptoms

Change in appearance - Orofacial granulomatosis - Gingivitis

orofacial granulomatosis

Not a single condition - Granuloma formation blocks lymphatics Lip and oral swelling then noted from other causes increased capillary leakage

triggers of orofacial granulomatosis

Food preservative and additives – benzoate/Sorbate/cinnamon - Benefit to miss additives in some people – exclusion diet - Responsive after 3 months then potential success Some have no identifiable trigger

children and orofacial granulomatosis

common in 6-13 year olds can be very localised or wider issue with Crohn's disease - need to investigate - need GA in endoscopy higher risk of perforating bowel in children so Assess how they grow - normal function= grow normally - malabsorption will not Younger Get OFG more likely to get Crohn's disease

5 clinical features of OFG

lip swelling angular cheilitis - inflamed at corners of mouth, mouth tissue sitting incorrectly cobble stoning ulceration microscopic granulomas

6 investigation for inflammatory bowel disease

Inflammatory process happening in body raised in Crohn’s Blood tests - Anaemia, CRP (c reactive protein), ESR Faecal Calprotectin Endoscopy Leukocyte Scan Barium Studies Bullet Endoscopy

bullet endoscopy for IBD investigations

- Swallow capsule - Photo inside bowel - Send to radio by receiver - Picture whole bowel But if miss area of interest cannot retake as works its way out

faecal calprotein for IBD investigation

- Released in inflammation - Bowel mucosal cells released into bowel, whether bowel is inflammed or not If small areas of disease – not a lot produced so hard to tell Significant area – can see higher than normal Stool sample analysed - Bleeding into bowel then RBC in stool

complication of ulcertaive colitis

developing carcinoma - Risk increases with time (not as big now due to awareness and screening) - Depends on time rather than disease activity Judgement as to whether Colectomy is justified - Attitude to risk - Carcinoma surveillance potential

2 treatment pathways for IBD

medical treatment | surgical treatment

medical treatments for IBD

immunosuppressive - Get rid of inflammation (Suppress immune system) Systemic Steroids(Prednisolone) ``` Local Steroids (rectal administered – colorectal disease) - Work topically on surface of bowel ``` Anti-inflammatory drugs - 5-ASA based drugs – Pentasa, mesalazine, sulphasalazine - topical Non Steroid immunosuppressants - Azathioprine - Methotrexate Anti TNFα therapy - Infliximab, adalimumab (‘biological’ drugs)

Anti TNFα therapy - Infliximab, adalimumab (‘biological’ drugs) for IBD treatment

- Manufactured antibodies against specific antigens e.g. TNF α - Immune response for disease not generated - Disease better controlled (inflammation where shouldn’t be) but infection response effected

topical medical treatments for IBD

Local Steroids (rectal administered – colorectal disease) Anti-inflammatory drugs - 5-ASA based drugs – Pentasa, mesalazine, sulphasalazine

systemic medical treatment for IBD

Systemic Steroids(Prednisolone) - Easy treatment but can cause problem in patients (children stop growing) - Pass straight through

oral issues for IBD

Oral lesion in Crohn’s – Orofacial granulomatosis Oral ulceration - ulcers worse when ulcerative colitis worse - Worse by low iron, b12 or folic acid - Inflamed bowel traumatised by food - bleed, lower store and malabsorption in small bowel of iron or folic acid or surgical removal of part of small bowel so less able to absorb - Not able to absorb enough nutrient to maintain life Haematinic deficiency caused by malabsorption or intestinal bleeding - B12 deficient - ileocecal area effected commonly in crohn’s, site of absorption so get pernicious anaemia

what can make oral ulcers worse

Worse by low iron, b12 or folic acid - Inflamed bowel traumatised by food - bleed, lower store and malabsorption in small bowel of iron or folic acid or surgical removal of part of small bowel so less able to absorb - Not able to absorb enough nutrient to maintain life - ulcers worse when ulcerative colitis worse