WEEK 4 - Inflammatory Bowel Conditions Flashcards

1
Q

What are the differences between Crohn’s Disease and Ulcerative Colitis?

A

UC: colon only, continuous retrograde inflammation beginning at rectum, mucosal inflammation, no granulomas, crypt distortion, loss of haustra , pseudopolyps

CD: anywhere (mouth to anus), discontinuous inflammation (skip lesions), transmural inflammation, granulomas may be present, extracolonic disease (abscesses, fistulae, perianal disease), thickened wall, “cobble stoning”

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2
Q

What is chronic inflammation?

A

Inflammation doesn’t resolve normally - prolonged inflammatory response.
Lack of clear resolution.
Inflammation is self perpetuating.
Persistent.
Damage of tissue.
New connective tissue formation (scarring, fibrosis).
Granuloma formations in CD

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3
Q

What is ulcerative colitis?

A

Diffuse inflammation of the mucous membrane of the colon.
Confined to colon only.
Clinical manifestations vary with location, extent and severity of disease.

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4
Q

What is ulcerative proctitis?

A

Inflammation confined to the rectum.
Main symptom = passing fresh blood of blood stained mucous.
May have diarrhoea, normal stools or constipation.
Inflammation can causes urgent need to pass stool.
Tenesmus - feeling of incomplete stool excretion.

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5
Q

What is left sided colitis (distal colitis)?

A

Inflammation starts in the rectum and extends up through the left side of the colon up to the splenic flexure.
Symptoms = bloody diarrhoea, mucous, pain in L) side of abdo, urgency, tenesmus.

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6
Q

What is pancolitis?

A

Inflammation of an extensive length of the colon.

Symptoms = frequent diarrhoea with blood, mucous, sometimes pus, severe abdo cramps & pain, tenesmus, weight loss.

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7
Q

What is acute severe ulcerative colitis?

A

Very severe diarrhoea with blood, mucous, sometimes pus.
Severe abdo cramps & pain, tenesmus, weight loss.
Nocturnal diarrhoea.
Medical emergency - usually requires hospitalisation.

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8
Q

What are complications of ulcerative colitis?

A
Change of structure & function of bowel 
Anaemia 
Haemorrhage
Perforation
Toxic megacolon
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9
Q

What is Crohn’s Disease?

A

Affects any part of the GIT from mouth to anus.
Most common = terminal ileum (1st) then colonic (2nd).
Patchy inflammation, skip lesions.
Inflammation of the bowel wall.
Clinical manifestations vary with extent, severity of disease & complications.

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10
Q

What are S&S of terminal ileo and ileo-caecal Crohn’s disease?

A

Right lower abdo pain
Impaired bile salt absorption
Impaired vit B12 absorption
Diarrhoea or constipation

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11
Q

What are S&S of small bowel Crohn’s disease?

A

Abdo pain and diarrhoea.

The diarrhoea is unlikely to be blood stained as blood will be degraded by digestive processes.

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12
Q

What are S&S of colonic Crohn’s disease?

A

Blood stained diarrhoea.
Frequent bowel actions, especially if sigmoid & rectum involves.
Often called Crohn’s colitis.

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13
Q

What are S&S of penetrating Crohn’s disease?

A
Anal fissures
Skin tags
Fistulas 
Abscesses
Perforation
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14
Q

What is stricturing Crohn’s disease?

A

Ongoing episodes of inflammation & healing - fibrotic tissue - stricture.
Symptoms = cramping abdo pain, nausea, abdo bloating, constipation, loud bowel noises.
Strictures can lead to partial or complete bowel obstruction.
Solutions: dilatation, strictureplasty, bowel resection.

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15
Q

What are complications of IBD?

A
Malnutrition 
Osteoporosis 
Anaemia
Fatigue
IBS
Psychosocial
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16
Q

What are extra-colonic manifestations of IBD?

A
Joint: arthritis, arthralgias
Ankylosing spondylitis 
Primary sclerosing cholangitis
Eye inflammation 
Renal/biliary stones 
Skin: erythema nodosum, pyoderma gangrenosum
17
Q

What are risk factors for IBD?

A

Largely unknown
Ethnicity: Jewish, Caucasian, developed countries
Age: 26-30, typical onset 20s
Smoking: Crohn’s disease, protective factor in ulcerative colitis
Crohn’s disease: more common in females and younger children than UC
Genetic influences are stronger in CD than UC

18
Q

What does the aetiology of IBD depend on ?

A

Environmental factors
Genetic predisposition
Gut microbiota
Host immune response (innate/adaptive)

19
Q

What is the pathophysiology of IBD?

A
  1. Altered microbiota (less diverse?), over abundance of pro-inflammatory flora.
  2. Degradation & loss of mucosal layers (loss of protective mechanisms)
  3. Loss of epithelial junctions - leaky gut
  4. ? Disordered response to micro flora by TLR & antigen presenting cells
  5. Over expression of pro inflammatory cytokines (phagocytes, neutrophils, macrophages) & production of prostaglandins (pain)
  6. Activation, differentiation & proliferation of lymphocytes
    - vasodilation (redness & swelling)
    - increase in vascular permeability
    - tethering & extravasation of WCs
    - leakage of plasma (swelling)
20
Q

What’s the difference between infectious gastroenteritis & IBD?

A

Time course of illness:
Gastroenteritis = common & short lived, abrupt onset, symptoms worse at onset, history of contacts.
IBD = onset more gradual & insidious with crescendo or fluctuating pattern, symptoms longer than initially acknowledged.

21
Q

What do diagnostic investigations examine to determine whether it’s IBD?

A

Organic vs. functional
Inflammation acute or chronic?
Is there damage or structural change?

22
Q

What is IBS (irritable bowel syndrome) ?

A

Functional gastrointestinal disorder
Disturbance in bowel function affecting sensorimotor function of the gut
More common
Without alarm bells or abnormal blood tests
Has some similar symptoms to IBD

23
Q

What is involved in the diagnosis & assessment of IBD?

A
Clinical presentation
Blood examination (FBE, biochemical, inflammatory markers, iron studies, coeliac antibody testing)
Stool testing (culture, faecal calprotectin)
Imaging (abdo X-ray, CT, MRI, US)
Endoscopy & histology
24
Q

How do you manage IBD?

A

Goals:
Treat acute disease …
- reduce or control intestinal inflammation
- mucosal healing
- minimise side effects & long term adverse effects
- eliminate symptoms
Improve & maintain General well being & quality of life
Correct nutrition deficiencies
Maintain steroid free remission
Prevent disease progression & complications

Type/location/severity of disease/existing complications/risk factors will direct type of treatment & mode of delivery

25
Q

What is the pyramid model of treatment for IBD?

A

Bottom to top:

  1. 5-ASA or sulfasalazine
  2. Prednisone or budesonide
  3. Immunomodulators
  4. Biological agents
  5. Surgery
26
Q

What are 5-ASAs used for ?

A

More useful in mild/moderate UC than CD
Oral and rectal
Act locally
Prevent prostaglandin production

27
Q

What are corticosteroids used for?

A

Used for active diseases, not maintenance of remission
IV, oral, rectal
Act systemically or local
Act on multiple inflammatory pathways, induce anti-inflammatory substances & processes
Multiple side effects with long term use

28
Q

What are calcineurin inhibitors used for? (Cyclosporine, tacrolimus)

A

Inhibit the proliferation of lymphocytes

29
Q

What are immunomodulators used for ? (Thiopurines - azathioprine/mercaptopurine antimetabolites-methotrexate)

A

Immunosuppressants

30
Q

What are biological therapies used for ?

A

Monoclonal antibodies - bind to and neutralise cytokines or block the movement of lymphocytes.
CD:
Infliximab/adalimumab (anti TNF alpha)
Vedolizumab (leukocyte trafficking agent)
Ustekinumab (anti IL12 and IL23)
UC:
Infliximab, adalimumab, golimumab (anti TNF alpha), vedolizumab