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The Patient 20300 > IBD > Flashcards

IBD Flashcards

1
Q

What are the two types of IBD and when is it most commonly diagnosed

A

ulcerative colitis and crohn’s disease

Known as “disease of young people”
as the peak age of diagnosis is age 10-25

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2
Q

What is crohns disease

A

Inflammation of the gastric mucosa
Relapsing and remitting

Crohn’s disease

Can affect anywhere in the whole of GI tract from mouth to anus

Transmural (all layers of intestinal wall) ulceration

Patchy

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3
Q

What is ulcerative colitis

A

Inflammation of the gastric mucosa
Relapsing and remitting

Ulcerative colitis

Affects the mucosa of colon and rectum
Diffuse, confluent mucosal inflammation and ulceration (doesnt affect all layers of the wall)

Mucosal and submucosal layers involved

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4
Q

What causes IBD

A

Precise mechanism unknown. Likely combination of factors.

Genetic (first degree relative with IBD – 10 times more likely to develop IBD)
Environmental
Immunological factors
Gut microbes
Smoking (but has protective effect in UC!)
?Infection
Diet
Medication
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5
Q

What are the Signs and Symptoms of IBD (intra intestinal)

A 
Abdominal pain
Diarrhoea (watery, bloody, mucus)
Tiredness and fatigue
Urgency
Weight loss
Anaemia
Fever
Nausea and vomiting 
Abdominal bloating and distension
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6
Q

What are the differences between the symptoms of ibd and uc

A

Symptoms of CD and UC similar but not identical

UC – more bleeding due to extensive erosion of blood vessels supplying lining of colon
CD – Symptoms of obstruction of bowel more common as entire bowel wall inflamed

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7
Q

What are the extra-Intestinal symptoms

A

Swollen joints – arthritis
Eye problems – episcleritis, iritis, uveitis
Erythema nodosum – swollen fat under skin causing redness, bumps and lumps
Pyoderma gangrenosum – skin ulceration
Primary sclerosing cholangitis

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8
Q

Define stricutres and fistulas as seen in crohns disease

A

Strictures

Narrowed segments of bowel
Lead to blockages, acute dilatation, perforation

Fistulas

Abnormal channels lined with granulation tissue
From between intestine and skin/other parts of intestine/organs e.g. bladder

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9
Q

Which body fluid/matter investigations do we use to diagnose ibd

A

Full history and detailed clinical examination

Blood tests including:
full blood count (FBC)
inflammatory markers
urea and electrolytes
thyroid function tests
liver function tests
bone profile

Stool culture - rule out other infective bacterial causes such as Clostridium difficile

Coeliac screen

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10
Q

What physical investigations can we carry out to diagnose ibd

A

Faecal calprotectin

Released into intestines in excess when inflammation present
Distinguish between IBD and non-inflammatory causes e.g. irritable bowel syndrome (IBS)

Abdominal imaging

Endoscopy including capsule endoscopy

Colonoscopy

Biopsies taken during above – differentiate between CD and UC

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11
Q

Which index is used to determine the severity of UC

A

Truelove and Witt’s Severity Index (Adults)

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12
Q

Which index isused to determine the severity of CD and which variables are assessed

A

Crohn’s Disease Activity Index

Number of variable are assessed to calculate Crohn’s Disease Activity Index (CDAI) including:

Number of liquid or soft stools
Severity of abdominal pain 
General well-being
Presence of complications 
Fever
Use of loperamide
Presence anaemia
Body weight
Abdominal mass absent or present

Score calculated which is used to classify disease activity
Number of online calculators available

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13
Q

Give the criteria used to categorise severe active crohns disease

A

Very poor general health and one or more symptoms including:

Weight loss
Fever
Severe abdominal pain
Frequent diarrhoeal stools daily (≥3 to 4)

May develop new fistulae or have extra-intestinal manifestations

Normally (but not exclusively) corresponds to a CDAI score of ≥300 or a Harvey-Bradshaw score of ≥8 to 9

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14
Q

Summary: which monitoring parameters are used to detect an acute relapse/flare (and to monitor treatment)

A

Faecal calprotectin
Stool frequency
Presence of blood and/or mucous in the stool
Temperature
C reactive protein (CRP)
U & Es
Heart rate (tachycardia) and blood pressure (hypotension)

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15
Q

What does the strategy for the management of ibd depend on

A

Treatment of IBD depends on:

Type of IBD (CD or UC)
Location and extent of disease
Severity

Treatment can involve:
Medicines
Nutritional “supplements”
Surgery
New and novel approaches e.g. faecal transplant
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16
Q

What are the primary and secondary aims of IBD

A

Primary aims:
Achieving remission
Maintaining remission
Improving quality of life

Secondary aims:
Avoiding surgery
Reducing long-term steroid use
Reducing risk of development of colorectal cancer
Reducing risk of development other complications

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17
Q

Why do we use different formulations when treating ibd

A

They will act in different areas

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18
Q

How do corticosteroids work (mechanism of action and rationale) in the treatment of ibd

A

Mechanism of action:
Reduce inflammation and modulates immune system
Prednisolone - binds to cellular glucocorticoid receptors, inhibiting inflammatory cells and suppressing expression of inflammatory mediators
Used in mild, moderate and severe disease
Choice of agent, route and dose depend on severity of disease

Rationale
Induce disease remission - “flares” usually treated with corticosteroids
Do not prevent progression of disease or development of complications

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19
Q

Which corticosteroids are used for the treatment of IBD

A

Prednisolone, Methylprednisolone, Hydrocortisone, Budesonide

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20
Q

Which steroid regimen do we use to treat mild-moderate flares

A

Prednisolone tablets 40mg daily commonly prescribed to treat mild-moderate flare. Dose then reduced by 5mg/week

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21
Q

Which steroid regimen do we use to treat acute-severe flares

A

Acute-severe disease – hospital admission and IV (as oral route may not be effective) Hydrocortisone 100mg four times a day

22
Q

What are the side effects of corticosteroids

A 
Number of side-effects including:
GI side-effects
Fluid and electrolyte imbalance
Increased appetite
Hypertension
Effect on blood sugar
Mood and behaviour changes

Infection risk - dampening down immune system

Risk development of osteoporosis (long term use)

Must not be stopped abruptly
(can lead to adrenal suppression)

Steroid Emergency Card

23
Q

How do aminosalicylateswork (rationale) in the treatment of ibd

A

Rationale
Induction and maintenance of remission – mild-moderate UC
Less frequently used in mild-moderate CD. Can be used post-surgery

24
Q

Which formulas are aminosalicylates available in

A

Variety of topical (rectal) and oral preparations available

Suppositories
Foams - often used for treatment acute attack (flare)
Enemas - “
Tablets – often used for maintenance of remission
Granules

Can give topical and oral together if required e.g. if acute flare

25
Q

What is the mechanism of action of aminosalicylates

A

Mechanism of action

MOA not fully understood and thought to be quite diverse
Anti-inflammatory action – reduces inflammation in GI tract through variety of anti-inflammatory processes
Decreases prostaglandin production in the colon and inhibits production of pro-inflammatory cytokines

26
Q

What was the first aminosalicylate widely used for IBD

A

Sulfasalazine was the first aminosalicylate to be widely used for IBD

There were some problematic side-effects such as headache, nausea, rashesso it is less commonly used now.

27
Q

Name 3 commonly used Aminosalicylates

A

Balsalazide – 5-ASA with another inert carrier molecule
Olsalazine – 5-ASA linked to itself
Mesalazine – 5-ASA in pH sensitive coating

28
Q

What is a key consideration that must be taken into account when dispensing mesalazine

A

Number of different brands and formulations available
Oral mesalazine products are not interchangeable
BNF – “There is no evidence to show that any one oral preparation of mesalazine is more effective than another; however, the delivery characteristics of oral mesalazine preparations may vary”

29
Q

What are the side effects of aminosalicylates and how do we counsel patients on them

A 
Side Effects
Arthralgia, abdominal pain, diarrhoea, dizziness
Blood dyscrasias (changes in blood cell counts - low platelets, low wbc count, low haemoglobin)

Counselling
Blood dyscrasias - report unexplained bleeding, bruising, purpura, sore throat, mouth ulcers, fever or malaise

Administration advice e.g. enema, tablets

Ideally maintain same brand - if brand switched then report any changes in symptoms

30
Q

How do we monitor patients using aminosalicylates

A 
Renal function (baseline, 3 months then annually – more frequent if impairment). Can rarely cause kidney disease and renal impairment
Blood dyscrasias – if suspicion – full blood count and immediate cessation
31
Q

When do we use thiopurines and what is their mechanism of action

A

Rationale

First-line immunomodulators for IBD used in UC and CD
Induce (add-on therapy) and maintain remission
Can take 3-6 months for full effects

Mechanism of action
Not fully understood – reduces inflammation in the GI tract

Immunomodulator – suppress immune response and inflammation

Metabolites have the capacity to impact on adaptive immune cells, innate immune cells and non-immune cells within the inflamed intestine

“Steroid-sparing”

Azathioprine (pro-drug) metabolised to => Mercaptopurine

(Weight-based dosing
Azathioprine – 2 - 2.5mg/kg/day
Mercaptopurine – 1 - 1.5mg/kg/day)

32
Q

Give two examples of thiopurines

A

Azathioprine and Mercaptopurine

33
Q

How is mercaptopurine metabolised

A

Mercaptopuruine is metabolised into thioguanine nucleotides (TGN) (the active metabolite).

These are further metabolised by the enzyme thiopurine methlytransferase (TMPT)

34
Q

What happens if there isnt enough TMPT to break down mercaptopurine

A

The drug will start accumulating in the body. This can cause side effects - there is a risk of developing myelosurpression.

35
Q

What happens if theres too much TMPT when administering mercaptopurine

A

If there is too much TMPT in the body the TGN will not be broken down properly and will instead be converted into mercaptopurine methylmercaptopurine (MeMP)

MeMP is not pharmacologically active and can cause hepatotoxicity

36
Q

How do we ensure patients have the right balance of TMTP

A

Patients must have TMPT levels measured prior to starting treatment

low TMPT levels – reduce dose (risk myelosuppression)
high TMPT levels – risk hepatotoxicity

Repeat after one month and also if not responding to treatment

37
Q

What are the side effects and councelling points of the thiopurines

A

Side Effects

Hypersensitivity reaction – the drug must be stopped immediately
Myelosuppression (bone marrow suppression)
Neutropenia and thrombocytopenia
GI – nausea, vomiting, diarrhoea
Liver disorders

Counselling
What the signs and symptoms of bone marrow suppression are e.g. report unexplained bleeding, bruising, purpura, sore throat, mouth ulcers, fever or malaise

38
Q

How do we monitor the use of thiopurines

A

Monitor

TMPT levels - pre-treatment and on therapy
Full blood count – pre-treatment, weekly for first 4 weeks then at least every 3 months

39
Q

What are the 3 less common immunomodulators which can be used to treat IBD

A

Methotrexate
Maintenance in CD (alternative to Azathioprine)
Given once weekly
Co-prescription of folic acid

Tacrolimus
Oral Tacrolimus can be used to induce remission in mild-moderate UC if not responsive to other treatments

Ciclosporin
IV Ciclosporin – induce remission in severe acute UC refractory to steroids

40
Q

What are the two biologic medicines used to treat IBD

A

Infliximab and Adalimumab

41
Q

How do Infliximab and Adalimumab work

A

They are monoclonal antibodies which bind to the cytokine - Tumour Necrosis Factor-α (TNF- α)
Inhibit inflammatory effects in gut

(TNF- α) has multiple actions

TNF:
Naturally occurring cytokine with multiple actions
Mediates inflammatory responses and modulates the immune system
TNF alpha – central role in Crohn’s

42
Q

When do we use biologics

A

In moderate-severe active IBD and if the patient has not responded to/intolerant of anti-inflammatory and immuno-modulating therapies

Therapeutic drug monitoring can be performed

If no response to one biologic options include:
Increasing dose
Decreasing time interval between administration
Switching to alternative agents

43
Q

What is infliximab and how does it work

A

First TNF blocker (biologic) approved for IBD
Given by intravenous (IV) infusion

Murine and human amino-acid sequences

44
Q

What precautions must be taken before administeing infliximab

A

Infusion related reaction can occur – flu-like symptoms so pre-medication is given

Pre-treatment screening to ensure the effects it has on the immune system wont cause damage. These include:
Tuberculosis (TB)
Hepatitis B
Hepatitis C
HIV
45
Q

What is adalimumab and what precautions must be taken when a patient is put on it

A

Fully humanised

Given by subcutaneous (SC) injection

Risk of reactivation of infections and malignancy as with Infliximab

Pre-treatment screening must be performed as per Infliximab

Biosimilar available

46
Q

Ustekinumab
and Vedolizumab
are also biologics. Give details on how they work and why we might use these instead of the first line biologics

A

Other monoclonal antibodies which can be used in refractory cases e.g. lost response or intolerant to TNF- α treatment

Ustekinumab
Anti-interleukin – blocks interleukin-12 (IL-12) and interleukin-23 (IL-23)
Inhibit inflammatory effects in gut
Initial IV infusion then SC injection
Risk of reactivation of infections and malignancy

Vedolizumab
Leucocyte adhesion inhibitor – inhibits leucocyte migration to parenchymal tissue in the gut and reduces inflammation
IV infusion
Risk of reactivation of infections and malignancy

47
Q

How do Faecal Microbiota Transplants (FMT) work

A

It is thought the composition of gut microbes in IBD is different and possibly abnormal

We can transfer healthy gut micro-organisms into the intestinal tract of recipient

Routes range from colonoscopy to enteric coated capsules

Clinical trials ongoing

48
Q

What other ‘future therapies’ are used in IBD

A

Probiotics

New biologics

Small molecule inhibitors of RNA and intracellular cytokine pathways

49
Q

Why might we resort to surgery to treat IBD

A 
Some IBD complications will require immediate surgery:
Intestinal blockage
Bleeding
Perforation
Fistula
Abscess 
Toxic megacolon
50
Q

Can surgery cure IBD

A

Yes, but only in UC (not in CD - surgery can only help treat certain areas of disease and manage symptoms and complications)

51
Q

What is the pharmacists general role in the treatment of IBD

A

Recommendations on choice of therapy and treatment options

Ensure appropriate formulations used

Practical administration advice to patient’s and other healthcare professionals

Safe and appropriate use of biologics

Plan how to stop medicines for patient’s in remission

“Rescue strategies” if relapse

Support adherence and health literacy

Therapeutic drug monitoring

Number of more specialist roles have developed with advent biologics – prescribing clinics

Input into IBD standards, NICE guidelines etc.

Use of biosimilars

52
Q

What must the pharmacist ensure they are aware of with particular reference to corticosteroids and aminosalicylates

A

Patients on corticosteroids:
Ensure appropriate dose and reduction regimen
Co-prescription of calcium and vitamin d to prevent osteoporosis
Adverse effect monitoring

Patients on aminosalicylates:
Adjustment dose during flares/remission
Side-effect counselling – blood dyscrasias

The Patient 20300 (24 decks)

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