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NME > Coeliac Disease and IBD > Flashcards

Coeliac Disease and IBD Flashcards

1
Q

Coeliac disease is an —— small intestine enteropathy triggered by exposure to dietary —— in genetically predisposed individuals, leading to malabsorption.

A
  • immune-mediated
  • gluten
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2
Q

Gluten, specifically gliadin is a protein found in

A

wheat, barley and rye
oats can be contaminated

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3
Q

What % of the population have coeliac disease?

A

1%

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4
Q

Coeliac disease:
- which gender affected more
- occurs at what age?

A
  • F>M
  • occurs at any age
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5
Q

Coeliac disease has a higher prevalence among 1st degree relatives of patients with what disease and ———

A
  • among 1st degree relatives of patients with Crohn’s
    disease and a greater concordance in monozygotic
    (identical) twins
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6
Q

Which countries is coeliac disease most prevalent?

A

Western Europe and USA
especially in patients of Irish and Scandinavian descent

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7
Q

Ceoliac Disease: Presentation:

A
  • diarrhoea
  • steatorrhea (fatty floating stools)
  • weight loss
  • anaemia
  • vague abdominal pain

Clinical signs:
- anaemia signs: glossitis (B12 and iron deficiency,
mouth ulcers, dermatitis herpetiformis (rash)

  • 1/3 individuals asymptomatic
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8
Q

Coeliac disease vs normal bowel endoscopy

A
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9
Q

What is shown below?

A
  • dermatitis herpetiformis (itchy, vesicular rash on
    extensor surfaces)
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10
Q

Pathogenesis of Coeliac Disease:

A
  • the gluten by product gliadin, complexes with tissue
    transglutaminase (tTG) in the gut binding as an
    antigen (deaminated gliadin) to HLA-DQ2 on T cells,
    creating an immune response that results in anti-tTG
    IgA, anti-endomysial and antigliadin antibodies in the
    blood and inflammation through Natural Killer cells
  • tTG cross-reacts with epidermal Tg, hence dermatitis
    herpetiformis
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11
Q

Pathogenesis of Coeliac Disease

A
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12
Q

Coeliac Disease Histopathology:

A
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13
Q

Coeliac Disease: Diagnosis:

A
  • Serology:
    • anti-endomysial
    • IgA anti-tissue transglutaminase (IgG anti tTG in
      patients with IgA deficiency)
    • anti-gliadin antibodies
  • Endoscopy with biopsy:
    - histology of the small bowel shows raised
    intraepithelial lymphocytes, crypt hyperplasia and
    villous atrophy
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14
Q

Coeliac Disease: Treatment:

A
  • Gluten free diet (oats are fine)
  • vaccination against pneuomococcus (30% have
    reduced splenic function, more likely to get severe
    infections)
  • osteoporosis screening and prevention (1g Ca daily)
  • iron, B12, folate supplementation
  • monitor for other autoimmune disease (Graves
    disease (thyroiditis) and autoimmune hepatitis)
  • annual blood monitoring
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15
Q

Inflammatory Bowel Disease:

A
  • Crohn’s disease
  • Ulcerative colitis
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16
Q

Crohn’s disease:
- what type of ulceration
- which parts of the GI tract affected

A
  • patchy, transmural ulceration
  • affecting the bowel anywhere from mouth to anus
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17
Q

Ulcerative Colitis:
- what type of ulceration
- which parts of the GI tract affected

A
  • continous, mucosal ulceration
  • only affects the colon
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18
Q

What does the endoscopy show?

A

Cohn’s Disease
Deep ulcers
Patchy inflammation

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19
Q

What does the endoscopy show?

A

Ulcerative colitis
continuous inflammation

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20
Q

Histological features of Crohn’s disease:

A
  • transmural inflammation (all layers can be affected)
  • granulomas are seen
  • may have crypt disturbances
21
Q

Histological features of Ulcerative Colitis:

A
  • mucosal inflammation
  • crypt abscesses
  • NO GRANULOMAS
22
Q

What is the histological key feature that differs Crohn’s and ulcerative colitis?

A

Granulomas only present in Crohn’s

23
Q

What are granulomas?

A
  • aggregations of macrophages around foreign
    substances to be eliminated
24
Q

Differences between CD and UC:

A
25
Q

Crohn’s disease mostly affects what age group?

A

younger adults/children

26
Q

Crohn’s disease and smoking**

A

strong predisposition to smokers

27
Q

What three structures are seen in Crohn’s disease?**

A
  • fistulas
  • strictures
  • perianal disease
28
Q

Crohn’s disease is a penetrating disease where**

A

inflammation tracks across the bowel wall to adjacent bowel or organs and can cause localised abscess formation

29
Q

Epidemiology of CD:
- high prevalence in which countries
- high prevalence in pts of which origins
- what type of presentation (age wise)

A
  • western world
  • Ashkenzai Jews
  • bimodal presentation in teens-20s and 60-70
30
Q

What causes CD?

A
  • unknown exact cause
  • genetic, infectious, environmental, dietary, smoking,
    NSAIDs, psychological factors
  • defects in mucosal barriers, which allow entry of
    pathogens and other antigens
31
Q

What are the genetics of CD?

A
  • strong evidence for genetic predisposition
  • first degree relatives have 13-18% increased risk
  • 50% concordance in monozygotic (identical) twins**
  • no classical mendelian inheritance but polygenic
  • NOD2 (nucleotide binding domain on Chromosome
    16 is the most known varient for predisposition for
    CD**
32
Q

Crohn’s Disease:

A
  • aim is to prevent excessive surgery and short bowel
    syndrome
  • 50% of patients with CD will need surgery and 70% of
    those will need a 2nd operation within 5 years of the
    first
  • surgery may be the only treatment for drainage of
    abscesses or treatment of fibrostenotic strictures
    (where there is little inflammation but symptoms of
    bowel obstruction)
  • thiopurines, then if worsening biologics second line
    defence
  • corticosteroids for inflammation
33
Q

Crohn’s disease presentation:

A
  • diarrhoea
  • abdominal pain
  • weight loss
  • lethargy
  • peri-anal disease
34
Q

Crohn’s Investigations:

A
  • inflammatory markers
  • anaemia
  • increased faecal calprotein (qFIT)
  • low B12
  • low vit D
  • colonscopy
35
Q

Crohn’s Treatment:

A
  • corticosteroid to reduce inflammation
  • thiopurines to maintain remission
  • biologics second line
  • always check TPMT, if no TPMT then severe side
    effect of bone marrow suppression
  • thioguanine nucleotides are the active metabolites of
    thipourines which incorporate the sulphur mostly into
    the backbone of DNA, preventing unwinding
36
Q

Ulcerative colitis affects:

A
  • females
  • non-smokers***
  • bimodal age distribution; 20s and 60s
  • genetics definitely implicated
  • concordance between monozygotic twins high
  • NSAIDs can cause flares
37
Q

Ulcerative Colitis:

A
  • although only colon is affected, risk of Toxic
    Megacolon (dilatation of colon) followed by colonic
    perforation if inflammation is very severe
  • 1/3 will go into remission, 1/3 will have some
    symptoms, 1/3 will go on to more extensive disease
  • the location of disease is a risk factor
38
Q

Ulcerative Colitis: Presentation:

A
  • bloody diarrhoea
  • urgency
  • tensemus (cramping rectal pain)
  • abdominal pain lower left quadrant
39
Q

Ulcerative Colitis: Diagnosis:

A
  • colonscopy + biopsy but balanced with risk of bowel
    perforation
40
Q

Treatment of UC:

A
  • mesalazine
  • mesalazine+thiopurine+corticosteroid
    • biologics
41
Q

Mesalazines

A
  • 5-ASAs; 5-aminosalicylic acids
  • pH dependent capsules affects where in the intestine
    and colon they are released
42
Q

Thiopurines:

A
  • azathioprine, mercaptopurine
  • takes 6 weeks to act
  • metabolism is under the influence of an enzyme called thiopurine methyl transferase TPMT
43
Q

TPMT checks

A
  • thiopurine methyl transferase
  • metabolises thiopurines
  • if not present may result in prevention of DNA
    unwinding and bone marrow suppression
44
Q

Anti-TNF agents; Biologics:

A
  • block bodys natural response to tumour necrosis factor
  • infliximab
  • given acutely for patient in whom steroids are not working
  • 60%
45
Q

Treatment of Acute CD:

A
  • nil by mouth
  • IV antibiotics if there are abdominal absesses***
  • modulen (liquid diet)
  • IV hydrocortisone (corticosteroid)
  • biologics such as infliximab
46
Q

Treatment of Acute UC:

A
  • IV hydrocortisone (corticosteroid)**
  • low molecular weight heparin
  • early surgical review
  • infliximab for patients who fail steroids
47
Q

Steroids are not long term. Just for flares.

True or False?

A

True

48
Q

Case 1:
- 28 male
- 6 week history of blood diarrhoea
- mild abdo pain relieved by defecation
- weight loss (significant and unintentional)
- grandmother had Crohn’s
- gave up smoking 8 weeks ago

Bloods:
- CRP: high
- Hb: low
- Platelts: high
- MCV: low

superficial inflammation

A
  • ulcerative colitis
  • steroids
  • blood thinner to prevent clot
  • mesalazines
  • thiopurines
49
Q

Case:
- 75 F
- 1 year history of diarrhoea
- no abdo pain
- significant unintentional weight loss
- known hypothyroidism

Bloods:
- CRP: low
- Hb: low
- Platelts: high
- MCV: low

A

coeliac disease
gluten free diet

NME (52 decks)

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