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3702 > Inflammatory Bowel Disease > Flashcards

Inflammatory Bowel Disease Flashcards

1
Q

What is IBD?

A

Common feature chronic inflammatory diseases of the lower intestine.

Results from a breakdown of the homeostatic balance between mucosal immunity and the gut microflora.

Dysregulated immune response is directed against the normal non pathogenic microflora of the GI tract.

IBD = UC and CD

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2
Q

What are some contributing factors to IBD?

A

Environmental factors

Genetic predisposition

Gut microflora

Host immune response

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3
Q

What is ulcerative colitis?

A

Always involves the rectum and inflammation can extends continuously throughout the colon.

Only affects the colon and only affects the mucosa of the gut wall (shown in blue in the diagram).

Common in young adults15-25 and second peak in 6th decade.

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4
Q

What are the symptoms of ulcerative colitis?

A

Bloody diarrhoea

Fever

Passage of mucus

Episodic cramps

Anorexia

Nausea

Abdominal pain

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5
Q

What is the pathophysiology of UC?

A

Activation of CD4+ Th2 cells leads to inflammation and the influx of neutrophils, plasma cells and eosinophils in the colon.

Chronic inflammation results in ulceration with loss of goblet cells and the formation of abscesses.

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6
Q

What is Crohn’s disease?

A

Chronic transmural inflammation – i.e. involves all layers of the gut wall.

Not region specific i.e. can affect any region of the GI tract.

Small intestine involvement.

Distribution is asymmetric and discontinuous with segmental; “skip lesions”.

Common in young adults 15-30, second peak in the 6th decade.

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7
Q

What are the symptoms of Crohn’s disease?

A

Recurrent mild diarrhoea.

Cramps and fevers lasting for days or weeks.

Fatigue.

Non specific symptoms which may not involve diarrhoea.

Can result in malabsorption.

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8
Q

Explain the pathology of Crohn’s disease:

A

Loss of tolerance to intestinal microflora.

Th1 involvement – release of IL-12, TNF-alpha, INF-gamma.

Leads to expression of matrix metalloproteinases which cause the damage to the tissue.

Results in damage to the gut wall.

Can result in abscesses, strictures, fissures and fistula which can require surgery.

In some cases can require the creation of a stoma.

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9
Q

How do you distinguish IBD from IBS?

A

IBD is associated with greater inflammatory activity than functional digestive disorders such as irritable bowel syndrome.

Calprotectin is a neutrophil derived protein - acts as a GI specific inflammatory biomarker.

Presence of calprotectin in faecal matter can help distinguish between IBD, other causes of GI inflammation and IBS.

Detected via an ELISA.

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10
Q

How would a diagnosis of IBD be carried out?

A

Identify symptoms

Look for clinical signs.

Objective measures:

Blood tests. 
C-reactive protein [CRP].
Erythrocyte sedimentation rate [ESR].
Haemoglobin concentration.
Serum albumin.

Faecal calprotectin analysis.

Sigmoidoscopy or colonoscopy for mucosal assessment.

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11
Q

How would you treat IBD?

A

Therapeutic goal is to induce and maintain remission by the use of drugs that will suppress the immune response.

Agents aimed at reduction of symptoms:

Analgesic (not NSAIDs).
Anti-cholinergic.
Anti-diarrhoeal.

Immunosuppressants:

Corticosteroids.
Aminosalicylates.
Ciclosporin.

Antimetabolites:

Azathioprine.
6-mercaptopurine.
Methotrexate.

Biologics:

TNF-α - Infliximab, Adalimumab, Golimumab.
Intergrin α4Beta7 cell adhesion molecule - Vedolizumab.
IL-12 / IL-23 - Ustekinumab.

JAK inhibitors:

JAK1 / JAK 3 -Tofacitinib.

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12
Q

How would you treat ulcerative colitis?

A

Therapy depends on disease location and severity.

Aminosalicylates are used first line.

Proctitis and Proctosigmoiditis / left sided colitis -Topical agents (suppository or enema) would be used initially.

Oral therapy in combination with a topical agent used for Extensive.

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13
Q

What is the step up treatment for ulcerative colitis?

A

Aminosalicylates - / + corticosteroid

Ciclosporin (acute serious)

TNF-α (moderate / severe)

Vedolizumab (moderate / severe)

Tofacitinib (moderate / severe)

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14
Q

What is the step up treatment for Crohn’s disease?

A

Corticosteroid or aminosalicylate 1st presentation

+ azathioprine or mercaptopurine

TNF-α (moderate / severe)

Ustekinumab or Vedolizumab (moderate / severe)

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15
Q

How would you maintain remission in ulcerative colitis?

A

Mild to moderate disease:

Oral aminosalicylate.
Azathioprine or 6-mercaptopurine if remission is not maintained by aminosalicylate.

Acute severe disease:

Azathioprine or 6-mercaptopurine.
biologics if non-biologics are contraindicated or ineffective.

Important to maintain therapy to reduce the risk of relapse

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16
Q

How would you maintain remission in Crohn’s disease?

A

Some choose not to have maintenance therapy.

For those who do choose maintenance therapy the choice of therapy is dictated by that used to induce remission.

E,g, Azathioprine / 6-mercaptoethanol if corticosteroids induced remission.

Methotrexate.

Biologic.

N.B. not a corticosteroid.

After surgery - azathioprine + metronidazole for 3 months.

17
Q

What are severe symptoms of UC?

A

Bowel movements (no. per day) - 6 or more plus at least one of the features of systemic upset.

Visible blood in stools.

Pyrexia (temperature greater than37.8°C).

Pulse rate greater than90 bpm.

Anaemia.

Erythrocyte sedimentation rate above 30 mm/hour.

18
Q

What is the IBD treatment pathway?

A

Diagnosis.

Multidisciplinary provision of information and support.

Inducing remission.

Maintaining remission.

Monitoring treatment and bone health.

Surveillance.

19
Q

What are the overall aims of drug treatment of IBD?

A

Induce remission.

Maintain remission.

Control symptoms.

Limit drug toxicity.

Modify disease progression.

Limit/avoid complications.

20
Q

What are the main treatment options for UC and CD: inducing remission

A

UC:

Aminosalicylates.
Corticosteroids.
Ciclosporin.
Infliximab, adalimumab, golimumab.
Vedolizumab.
Ustekinumab.
Tofacitinib.
CD:
Aminosalicylates.
Corticosteroids.
Infliximab, adalimumab, golimumab.
Vedolizumab.
Ustekinumab.
21
Q

Why are aminosalicylates used for treatment?

A

5-ASA (mesalazine) is the active component.

5-ASA is unstable in acidic conditions - oral preparations are formulated to withstand the acidic conditions of the stomach.

Active 5-ASA is released in the colon or ileum to exert its anti inflammatory effect topically.

Formulation choice is important and is influenced by the site of disease.

22
Q

What counselling points should be given with aminosalicylates?

A

Common side effects include: diarrhoea, headache, leucopenia, nausea, rash.

Rare side effects: agranulocytosis, neutropenia, pancreatitis.

Report any unexplained bleeding, bruising, purpura, sore throat, fever or malaise that happens during treatment.

Renal function will need checking before starting treatment, at 3 months and then annually.

23
Q

What are the types of topical (rectal) aminosalicylates?

A

Often used in conjunction with oral treatment.

Suppositories - reach rectum.

Foam enemas - reach rectum and sigmoid colon.

Liquid enemas - reach rectum and rectosigmoid colon.

24
Q

Why are corticosteroids used for treatment?

A

Aim to rapidly achieve remission but limit exposure.

IV, oral and rectal formulations.

IV should be used in severe disease.

Budesonide associated with less systemic absorption.

Using rectal steroids also minimises systemic absorption.

Not used to maintain remission.

25
Q

What counselling points should be given with corticosteroids?

A

If effective then steroids are gradually reduced, so need to ensure patient is confident with regimen.

Ensure patients are aware of side effects of long term use of corticosteroids:

Adrenal suppression, Cushing’s, osteoporosis, thin skin, fluid retention, diabetes etc.

Monitoring needed for early signs of adverse effects

26
Q

Why is ciclosporin used for treatment?

A

Only used (rarely) in Ulcerative Colitis (not Crohn’s).

Used in acute severe active UC unresponsive to IV steroids after 72hrs or if symptoms worsen on steroids (but unlicensed).

Given by intravenous infusion initially.

Can take up to 14 days for response.

If no response - colectomy surgery.

If effective may be converted to oral therapy for 3-6 months (unlicensed).

Side effects limit long term use so usually used as a ‘bridge’ to treatment with azathioprine or as a last stage before surgery.

27
Q

What counselling points should be given with ciclosporin?

A

Key side effects:

Renal and hepatic impairment.
Hypertension.
Infections (consider PCP prophylaxis).
Electrolyte disturbances (K, Mg).

Monitoring:

Maintain serum ciclosporin levels 100-200ng/ml.

BP, Mg, K, lipids, FBC, Ur and Cr, LFTs before and during therapy.

Blood pressure.

28
Q

What biologic or targeted cell therapy could be used for treatment?

A

Anti-tumour necrosis factor α (anti-TNF-α) antagonists:
Infliximab
Adalimumab
Golimumab

α4β7 integrin antagonist:
Vedolizumab

IL-12, IL-23 antagonist:
Ustekinumab

Tyrosine kinase (JAK1 and JAK3) antagonist:
Tofacitinib
29
Q

Why is infliximab used for treatment?

A

Given concurrently with immunosuppressants to reduce antibody formation vs. infliximab (more common in carriers of HLA-DQA1*05) plus synergistic effects.

Two formulations:

IV infusion.
Subcutaneous (used after 2 initial iv loading doses).

Used to induce remission in:

Subacute UC.
Acute severe UC unresponsive to steroids and thiopurines.
Severe active UC when ciclosporin is contra-indicated.

30
Q

What counselling points should be given with infliximab?

A

Monitor infliximab trough levels (target: 3-7mg/ml) to determine whether dose can be increased.

Side effects:

Headache, rash, dizziness, dry skin, predisposition to infections (TB), hepatoxicity, infusion related reactions (acute or delayed).

Contraindicated in heart failure and active infection.

Given for 12 months or until treatment failure.

Only continued if evidence of active disease.

31
Q

Why is adalimumab used for treatment?

A

It’s a disease-modifying antirheumatic drug and monoclonal antibody that works by inactivating tumor necrosis factor-alpha.

Taken by subcutaneous injection.

32
Q

What anti-integrin therapies can be used for treatment?

A 
Vedolizumab
Interleukin inhibitors
Ustekinumab
Janus kinase inhibitors
Tofacitinib

Only used if anti-TNF-α agents cannot be tolerated, disease has responded inadequately or lost response to treatment.

Essential monitoring requirements for each therapy to promptly identify potentially significant side effects.

33
Q

What are the main treatment options for UC and CD: inducing remission

A

UC:

Aminosalicylates.
Thiopurines (azathioprine, mercaptopurine).

CD:
Aminosalicylates.
Thiopurines (azathioprine, mercaptopurine).
Metronidazole.
Methotrexate.
Anti TNF therapy (adalimumab, infliximab).

34
Q

Why are thiopurines used for treatment?

A

Azathioprine and 6-mercaptopurine.

Used to maintain remission in UC and CD
Steroid sparing properties
Used in patients having 2 or more exacerbations/year requiring steroids
Or: started after 1 episode of acute severe UC
Response in 2-3 months
 not suitable alone for acute exacerbations
Not all patients respond optimally- depends on TPMT activity and genotype
TPMT levels must be checked before commencing treatment

35
Q

What counselling points should be given with thiopurines?

A

Side effects:

Nausea & vomiting (6-mercaptopurine may be better tolerated).
Increased risk of infections.
Flu like symptoms, leucopenia, hepatoxicity and pancreatitis.

Counselling: Report any signs of infection or bruising.

Monitoring: FBC and LFTs weekly for first 2 months then monthly.

Significant interactions:

Allopurinol and azathioprine.
Trimethoprim and azathioprine.

36
Q

Why is methotrexate used for treatment?

A

Used to maintain remission in chronically active Crohn’s Disease.

Steroid sparing properties.

Not first line.

Used when thiopurines fail or are not tolerated.

Given orally or s/c or i/m once a week.

37
Q

What counselling points should be given with methotrexate?

A

Side effects:

Pneumonitis.
Hepatotoxicty.
Bone marrow suppression.

Monitoring:

FBC.
CrCl.
LFTs 1-2 weekly initially then every 2-3 months.
CXR.

38
Q

Why is metronidazole used for treatment?

A

Used to maintain remission in ileocolonic Crohn’s disease after complete resection of inflamed bowel.

3 months post-operative treatment with azathioprine.

3702 (34 decks)

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