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Yr 2 Gastrointestinal > Wk 3 - Symposium 4 (Clinical): Irritable Bowel Disease (UC and CD) > Flashcards

Wk 3 - Symposium 4 (Clinical): Irritable Bowel Disease (UC and CD) Flashcards

1
Q

What is irritable bowel syndrome?

A
  • Group of disorders of the gut possibly due to inflammation and immune response
  • UC -Limited to colon and Crohn’s from mouth to anus
  • Relapsing-remitting diseases
  • Unknown cause –idiopathic
  • Triggers immune system damaging gut to lead to diarrhoea and abdominal cramps
  • Genetic, infections, immunologic, psychologic factors all investigated
  • Possible inability to limit “turn off” immune response
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2
Q

IBD is usually a…

A

relapsing-remitting disease

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3
Q

What are the types of IBD?

A
  • Ulcerative colitis
  • Crohn’s disease
    • Indeterminate colitis
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4
Q

IBD is more common in _____ (Asia and Africa/North America and Europe).

A

IBD is more common in North America and Europe.

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5
Q

What part of the GI is usually affected by ulcerative colitis?

A
  • Limited to colon
    • Backwash ileitis
  • More severe in distal colon
    • May only involve rectum
    • Caecal patch lesion
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6
Q

Describe the macroscopic features of ulcerative colitis.

A
  • Superficial mucosal ulceration
  • Pseudopolyp formation
  • Normal serosal surface
  • Confluent involvement
  • Featureless mucosa in chronic disease
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7
Q

Describe the microscopic features of ulcerative colitis?

A
  • Inflammation limited to mucosa
    • Acute & chronic inflammation
    • Cryptitis
    • Crypt abscesses
  • Inflammation evenly distributed
  • Mucosal granulomas
  • Distortion of glands
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8
Q

Describe the distribution of Crohn’s disease

A
  • May involve entire gastrointestinal tract
    • Oral ulceration
    • Perianal fistulas, abscesses
  • Classically involves terminal ileum
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9
Q

Crohn’s disease usually involves the ____ ileum.

A

Crohn’s disease usually involves the terminal ileum.

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10
Q

Describe the macroscopic features of Crohn’s disease.

A
  • Deep ulceration
    • Cobblestone mucosa
  • Bowel wall thickening & strictures
  • Abnormal serosa
    • Fat wrapping (not specific to Crohn’s but characteristic)
  • Patchy involvement
    • Skip lesions
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11
Q

Describe the microscopic features of Crohn’s disease.

A
  • Transmural inflammation – in all of bowel
    • Acute & chronic inflammation
    • Lymphoid aggregates
  • Fissuring ulceration (vs superficial in ulcerative colitis)
  • Inflammation patchy
  • Transmural granulomas
  • Neuronal hyperplasia – thickened nerves (less useful sign though)
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12
Q

What other diseases should be eliminated before making an IBD diagnosis - i.e. differential diagnosis?

A
  • Infective colitis
  • Diverticular disease
    • Sigmoid colon
  • Ischaemic colitis
  • Diversion colitis
    • Defunctioned rectum
  • Pouchitis
    • Ileal pouch post colectomy
  • Tuberculosis (vs Crohn’s disease)
    • TB mimics Crohn’s in terminal ileum (+ histo granulomas also v common in TB)
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13
Q

List some of the complications of ulcerative colitis.

A
  • Toxic megacolon (acute)
  • Dysplasia (pre-cancerous – only happens in minority but v important to monitor)
    • Longstanding disease
    • Total colonic involvement
  • Malignancy
    • Adenocarcinoma
    • 10% risk @ 20 years (total colitis)
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14
Q

What are the complications of Crohn’s disease?

A
  • Fistula formation
    • Enteroenteric
    • Enterovesical
    • Enterovaginal
    • Enterocutaneous
  • Abscess & sinus formation (in the peri-anal region)
  • Bowel obstruction (due to bowel narrowing)
    • Inflammatory stricture formation
  • Malignancy
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15
Q

List some extraintestinal complications associated with IBD.

A
  1. Liver
    • sclerosing cholangitis (esp. UC)
  2. Skin
    • erythema nodosum, pyoderma gangrenosum
  3. Joints
    • arthritis, ankylosing spondylitis
  4. Eye
    • episcleritis, uveitis, conjunctivitis
  5. Systemic amyloidosis
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16
Q

What causes IBD?

A
  • UNCERTAIN
  • Genetic factors
  • Gut microbial factors
  • Environmental factors
  • Immunological abnormalities
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17
Q

List some infective agents associated with IBD?

A
  • Mycobacteria
  • Rotavirus, chlamydia, measles virus
    • Microbial DNA identified in tissues
    • Some evidence anecdotal
  • No clear evidence for a single infective cause
  • An abnormal inflammatory reaction to normal gut flora
    • Increased mucosal permeability
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18
Q

Ulcerative colitis inflammation is usually limited to the ____ while Crohn’s is _____ inflammation.

A

Ulcerative colitis inflammation is usually limited to the mucosa while Crohn’s is transmural (ie all layers of bowel) inflammation.

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19
Q

What gene mutations are found to be involved in Crohn’s disease?

A

In Crohn’s disease particularly, there appears to be a genetic association with phenotypes. Specifically, NOD2/CARD15 mutations were found to be associated with a phenotype of Crohn’s disease which was associated in those diagnosed at a younger age, with ileal involvement, increased severity of ileal disease requiring surgical intervention/reoperation.

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20
Q

Crohn’s disease is primarily regulated by ___ and ___ mediated processes.

A

Crohn’s disease is primarily regulated by TH1 and TH17 mediated processes.

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21
Q

List some examples of cytokines associated with colonic Crohn’s.

A

Crohn’s lesions were found to have high levels of cytokines like IFN-gamma, IL-2, IL-12, and IL-18.

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22
Q

Describe the symptoms associated with intestinal inflammation (colitis vs ileitis\jejunitis).

A
  • Colitis:
    • bloody and pus-filled stools
    • tenesmus
    • urgency
  • Ileitis/Jejunitis:
    • diarrhoea
    • abdo pain
    • weight loss (or failure to growth in paeds)
    • systemic malaise
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23
Q

Malnutrition (due to malabsorption) is often more associated with ____ (Crohn’s disease/UC).

A

Malnutrition (due to malabsorption) is often more associated with Crohn’s disease.

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24
Q

What is calprotectin?

A

Calprotectin is a protein biomarker that is present in the faeces when intestinal inflammation occurs –> used in diagnosis of IBD (+ colonoscopy).

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25
Q

How is Crohn’s treated/managed?

A
  • Mild to moderate disease can be treated by oral mesalamine, immunomodulators such as thiopurines (mercaptopurines, azathioprine), methotrexate, and steroids.
  • Moderate to severe disease (including fistulizing disease) will be best treated using a combination of immunomodulators and biologics (infliximab, adalimumab, golimumab, vedolizumab) or biologics alone.
  • Generally, now avoid immunomodulators (as toxic) and give biologics.
26
Q

How is IBD treated?

A
  1. Nutritional changes/adjunct therapy
  2. Drug therapy
  3. Surgery
  4. Other
27
Q

Describe adjunctive therapy* of IBD.

*Adjunctive Therapy is therapy given in addition to the main treatment to maximize its effectiveness

A
  • Attention to diet – High fibre, “healthy diet”
  • IBS whilst in remission from UC, low fibre, use of antispasmodics –propantheline, mebeverine (antimuscarinic)
  • Avoid antimotility drugs–codeine, loperamide – precipitate paralytic ileus in active UC
  • Bile salt diarrhoea – colestyramine – binds bile salts (bile salts are irritants)
  • Antibiotics – metronidazole, ciprofloxacin
  • C. difficile colitis – metronidazole, vancomycin
28
Q

List the different drugs ‘groups’ used in IBD.

A

Can be divided into immunosuppressants and anti-inflammatory treatment.

  • Immunosuppressant
    • Antibody therapy (strongest)
    • Immunosuppressants
  • Anti-inflammatory
    • Steroids
    • Aminosalicylates

In addition to that, antibiotics, pain killers, vitamin minerals and other adjunct therapies can be used.

29
Q

What are aminosalicylates?

A

Aminosalicylates are a group of medicines used to treat inflammation of the gut that are used to treat and prevent flare-ups of ulcerative colitis.

30
Q

List some aminosalicylates.

A

Sulfasalazine, mesalazine, olsalazine, balsalazine

31
Q

How do aminosalicylates work?

A
  • Mechanism unknown
  • Possible block of inflammation, Prostaglandins, Leukotrienes, Platelet Activating Factor (PAF)
32
Q

Aminosalicylates are usually used as first-line treatment for ____ to ____ UC reducing relapse rate.

A

Aminosalicylates are usually used as first-line treatment for mild to moderate UC reducing relapse rate.

33
Q

Aminosalicylates are usually good in…

A

Maintaining remission NOT treating disease

34
Q

List some possible S/Es of aminosalicylates.

A
  • Nausea, controlled through reduced dosing
  • Ulcers of the mouth, sore mouth, loose bowel movements
  • Reduced white cell, reduced platelets
  • Rash
  • Orange urine and sweat
  • Depression in young men (effect on testosterone?)
  • Oligospermia
35
Q

What are steroids?

A

Also called corticosteroids, are anti-inflammatory medicines used to treat a range of conditions.

36
Q

List some corticosteroids.

A

Prednisolone, hydrocortisone, budesonide

37
Q

Steroids are used in UC and Crohn’s to…

A

Induce and maintain remission

38
Q

Steroids are unsuitable for ____ because of their ____.

A

Steroids are unsuitable for maintenance because of their adverse reactions.

39
Q

How do steroids work?

A

Anti-inflammatory effects are complex, but via binding to cellular glucocorticoid receptors, steroids act to inhibit inflammatory cells and suppress the expression of inflammatory mediators.

40
Q

Steroids are used in ____ IBD and unresponsive cases.

A

Steroids are used in diffuse IBD and unresponsive cases.

41
Q

What steroids are usually used in diffuse IBD?

A

Oral prednisolone and budesonide (modified release)

42
Q

Steroids can also be used in ___ and ___ disease alongside 5-ASA (aminosalicylate).

A

Steroids can also be used in refractory and moderate disease alongside 5-ASA (aminosalicylate).

43
Q

List some S/Es of corticosteroids.

A
  • Osteoporosis
  • Diabetes
  • Muscle Wasting
  • Cushing’s syndrome
  • Growth suppression
  • Infection
  • Adrenal atrophy long term (reduced with slow release budesonide)
44
Q

What immunosuppressants are used in treating IBD?

A
  • Azathioprine - in steroid dependent Crohn’s and in refractoy UC
  • Methotrexate - useful in Crohn’s
  • Calcineurin inhibitors (cyclosporin and tacrolimus) - may induce remission in steroid-resistant UC
45
Q

How does Azathioprine work?

A
  • Inhibits purine synthesis
  • Can prevent relapse
  • Mercaptopurine is the active metabolite of Aza
  • Can take weeks to months to reach peak effectiveness
46
Q

List some S/Es of Azathioprine.

A

Side effects: Nausea, vomiting, pneumonia, Herpes and diabetes, pancreatitis (1.2%)

47
Q

What is the active metabolite of azathioprine?

A

Mercaptopurine

48
Q

How does methotrexate work?

A

Methotrexate is a folate derivative that inhibits several enzymes responsible for nucleotide synthesis including dihydrofolate reductase. This inhibition leads to suppression of inflammation as well as prevention of cell division.

49
Q

How do cyclosporin and tacrolimus work (calcineurin inhibitor)?

A
  1. Both are calcineurin inhibitors that inhibit T cell activation.
  2. Its binding to the receptor cyclophilin-1 inside cells produces a complex known as cyclosporine-cyclophilin.
  3. This complex subsequently inhibits calcineurin, which in turn stops the dephosphorylation as well as the activation of the nuclear factor of activated T cells (NF-AT) that normally cause inflammatory reactions.
  4. NF-AT is a transcription factor that promotes the production of cytokines such as IL-2, IL-4, interferon-gamma and TNF-alpha, all of which are involved in the inflammatory process.
50
Q

What does antibody therapy do?

A

In general, antibody therapy works by inhibiting pro-inflammatory cytokines e.g. IL-13, IL-12 and TNFα.

51
Q

Antibody therapy in IBD is only indicated for…

A

resistant Crohn’s

52
Q

What monoclonal antibody is approved for Crohn’s disease treatment?

A

Infliximab

53
Q

How does Infliximab work?

A

Blocks pro-inflammatory cytokine TNFα

Infliximab is a IgG1κ monoclonal antibody that binds to soluble and transmembrane forms of TNF-α with high affinity to disrupt the pro-inflammatory cascade signalling. Binding of the antibody to TNF-α prevents TNF-α from interacting with its receptors.

54
Q

List some S/Es of infliximab.

A

Fever, chills, urticaria ie hives (15%), serious infection -TB (due to weakened immune system)

55
Q

Currently, only ____ is effective in decreasing the need for surgery in Crohn’s.

A

Currently, only infliximab is effective in decreasing the need for surgery in Crohn’s.

56
Q

State the main difference between the location of Crohn’s and UC.

A
  • Crohn’s - from mouth to anus ie anywhere in the GI tract
  • UC - usually in the colon and rectum (maybe caecum)
57
Q

Give an example of an important cytokine in Crohn’s disease.

A

The immune-mediated response in Crohn’s disease involves both innate and acquired mechanisms by macrophages, neutrophils, and T-cells in the intestine which promote pro-inflammatory mediators like TNF-alpha*.

*TNF is a molecule secreted by white blood cells that increases inflammation. High levels of TNF-alpha have been associated with the development of intestinal inflammation in Crohn’s disease.

58
Q

List some investigations carried out in IBD.

A
  • Blood - check anaemia, low albumin, inflammation (CRP, ESR, high platelets)
  • Stool - Calprotectin in faeces?, infection?
  • Colonoscopy - macroscopic appearance + histo
59
Q

Discuss initial anti-inflammatory treatment in IBD.

A
  • Aminoscyclates
    • 5ASA (sulfasalazine) for UC maintenance
  • Corticosteroids - prednisolone and budesonide
    • To induce remission in UC and Crohn’s
    • NOT USEFUL for maintenance due to long-term S/Es of steroids
60
Q

Describe immunosuppressant therapy for IBD.

A
  • Immunosupressants (AZA) in refractory cases (UC + Crohn’s)
  • Antibody therapy (infliximab) in resistant Crohn’s

Yr 2 Gastrointestinal (37 decks)

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