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Clinical 2 (Part B) > 15 - Inflammatory Bowel Disease (IBD) > Flashcards

15 - Inflammatory Bowel Disease (IBD) Flashcards

1
Q

Define IBD

A

chronic inflammatory disorder of the GI tract

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2
Q

List two types of IBD

A

CD: Crohn’s disease

UC: Ulcerative colitis

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3
Q

What is indeterminate colitis ?

A

features of both CD and UC

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4
Q

Describe the pathophysiology of IBD

A

-genetic predisposition with infectious and immunological responses involved

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5
Q

Ulcerative Colitis:

Where is it confined to ?

A
  • bowel wall
  • GI tract involvement confined to terminal ileum, colon and rectum
  • will only go as far as the ileum
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6
Q

Ulcerative Colitis:

What is almost always affected?

A

rectum almost always affected (>95%) then progresses proximally

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7
Q

Crohn’s Disease:

Describe it.

A
  • extensive destruction of bowel wall
  • invasion of adjacent tissues
  • any part of the GI tract may be involved
  • colon + another site in 2/3 of patients
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8
Q

List some other organs involved in IBD

A

Many organs involved. May or may not be related to disease activity.

  • Eye
  • Skin & joints
  • Liver
  • Psychological (depression and anxiety)
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9
Q

Crohn’s:

Classic signs?

A
  • RLQ tenderness
  • painful with masses
  • diarrhea with low grade fever
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10
Q

UC:

Classic signs?

A
  • RECTAL BLEEDING
  • diarrhea
  • no masses or specific tenderness
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11
Q

Crohn’s:

Lifetime risk of a ___ is 30%

A

fistula

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12
Q

UC:

high risk of _____ _____

A

rectal cancer

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13
Q

Goals of therapy for IBD?

A
  • control acute flares
  • induce remission
  • maintain remission
  • avoid or manage complications
  • can be very individualized in Crohn’s
  • location, severity, previous response to therapy involved in the selection
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14
Q

Non-pharms for IBD

A

1) Avoid precipitants:
- NSAIDs: increase risk of CD ulcers and colitis (but may still be used)
- Constipating drugs in severe UC
- Smoking: helps UC, worsens CD

2) Nutrition:
- malnutrition is common
- some foods trigger abdominal pain
- lactase deficiency due to active inflammation (CD)

3) Surgery

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15
Q

How does smoking affect UC

A

helps it

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16
Q

How does smoking affect CD

A

worsens it

*stopping smoking is as good as any drug therapy for CD

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17
Q

How does constipating drugs affect IBD?

A

*constipating drugs can cause colon to expand 4-5 times it’s size and you lose ability to regulate balance and if it perforates, it has a very high mortality rate

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18
Q

How does inflammation cause lactase deficiency ?

A

Inflammation can shed lactase enzyme and produce temporary lactose intolerance

*easy way to tell is just to see if you tolerate dairy

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19
Q

Describe surgery for Crohns

A

-generally reserved for strictures and obstructions as there is an increased risk of CD recurrence at surgical site

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20
Q

Describe surgery for UC

A
  • “cured” with a colectomy

- some post op issues (ex. pouchitis)

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21
Q

List the options for drug therapy

A
  • Aminosalicylates
  • Corticosteroids
  • Immunomodulators (ex. Azathoprine)
  • Cytokines (ex. Infliximab)
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22
Q

Aminosalicylates:

List 2 examples

A
  • sulfasalazine

- 5-ASA (mesalamine)

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23
Q

Aminosalicylates:

MOA

A

May be a few ways they act:

  • PGs
  • decrease cytokines
  • free radical scavenging
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24
Q

Aminosalicylates:

How much sulfasalazine is equivalent to 5-ASA ?

A

1g sulfasalazine = 400 mg 5-ASA

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25
Q

Aminosalicylates:

Describe the metabolism of sulfasalazine

A
  • diazo bond cleaved by bacteria
  • turned into sulfapyridine which is rapidly absorbed into circulation from colon
  • sulfapyridine is responsible for adverse effects
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26
Q

Aminosalicylates:

SE of sulfasalazine

A

Many dose and phenotypic related:

  • fever, fatigue, headache, n/v/d, dyspepsia
  • allergic reactions (SJS rash)
  • hematologic: hemolysis, agranulocytosis, thrombocytopenia
  • drug interactions
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27
Q

Aminosalicylates:

Describe the absorption of Melamine (5 ASA)

A
  • 25% absorbed from colon

- rest passes through colon unchanged

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28
Q

Aminosalicylates:

List 2 examples of 5-ASA products and where they target

A

1) Asacol: released in terminal ileum

2) Pentasa: 40% released in small bowel. Increased diarrhea

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29
Q

Aminosalicylates:

What is good about Pentasa (5 ASA) ?

A

can open capsules which is good if you’re putting it into a feeding tube

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30
Q

Aminosalicylates:

Is Asacol or Pentasa better than the other?

A

Doesn’t seem to matter which 5-ASA product you use, they all seem to work

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31
Q

Aminosalicylates:

Are NOT _____ inhibitors

A

cox 2

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32
Q

Aminosalicylates:

What forms do they come in?

A

oral, enemas, suppositories

*all act topically

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33
Q

Aminosalicylates:

Other than enemas, no clear signs has additive effects to _____

A

steroids

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34
Q

Aminosalicylates:

Common to use higher doses for ?

A

CD or bad UC

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35
Q

Aminosalicylates:

Most common SE

A

Less than with sulfasalazine

Most common SE: flatulence, ab pain, nausea, diarrhea, headache

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36
Q

Aminosalicylates:

List 2 clinical pearls

A

1) Can give any of the QID 5-ASA tabs or caps as a single daily dose (ex. asacol as 800mg QID or 3200mg once daily) despite what the product monographs say
2) Can give 5-ASA (non-acetylated salicylate) in a patient with an ASA (aspirin) allergy

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37
Q

Aminosalicylates:

____ weeks should be enough time to assess their clinical response (and need to modify tx)

A

4-8

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38
Q

Aminosalicylates:

With oral formulation, can try to decrease dose to ___ g/day if doing well. Lower doses not recommended.

A

2

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39
Q

Aminosalicylates:

If they fail _____ g of one agent, it is not recommended to try a different 5-ASA product.

After ensuring adherence, pick a different agent

A

4.8

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40
Q

Aminosalicylates:

Why do we ensure adherence?

A

Bc once you move past the 5-ASA products, they are associated with big time toxicities and you don’t want to use these agents unless absolutely necessary

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41
Q

Aminosalicylates:

How effective are they for UC?

A
  • induce remission in 20%
  • decrease relapse rate in 1/2 patients from 60% to 20%
  • most effective in a more DISTAL disease
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42
Q

Aminosalicylates:

How effective are they for CD?

A
  • benefit is in the colon (>3 years)

- with ideal disease data supporting use is soft-perhaps 10% better than placebo

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43
Q

Topical Corticosteroids:

Suppositories for _____

A

proctitis (inflammation of rectum and anus)

44
Q

Topical Corticosteroids:

Enemas for ?

A

-left sided (sigmoid/rectum) disease

  • lie on left side then on right side for 20 min HS
  • mostly for UC not controlled with 5-ASA
  • faster onset
45
Q

Topical Corticosteroids:

When are they used in UC ?

A

mostly mild-mod left sided disease not controlled with 5-ASA - recommend an enema or suppository

46
Q

Topical Corticosteroids:

When are they used in CD ?

A
  • decent data with budesonide MMX in mild-mod right side colonic and ideal disease
  • many are using it first line for induction in ideal-colonic CD
  • problem is maintaining remission with it alone
  • in UC, the MMX is an alternate 1st line induction Tx
47
Q

Systemic Corticosteroids:

Role in IBD ?

A
  • backbone of initial induction Tx for mod-severe UC & CD (or 5-ASA failures in UC)
  • better for flares, up to 60-90% response in UC
48
Q

Systemic Corticosteroids:

most common one?

A

prednisone

49
Q

Systemic Corticosteroids:

What IV corticosteroids are used for severe/hospitalized cases?

A
  • hydrocortisone

- methylprednisolone

50
Q

Systemic Corticosteroids:

onset of action

A

Quick: see within a few days to 1 week

In outpatient setting, re-evaluate patient within 2 weeks

51
Q

Systemic Corticosteroids:

Once you get a response, _____ the dose

A

taper (ex. 5mg/week)

52
Q

Systemic Corticosteroids:

In severe disease, if fail 1 ____ of steroids, look to use the big guns

A

week

53
Q

Systemic Corticosteroids:

Are they good long term?

A

Not good long term to prevent relapse though many CD patients can’t get off of them

54
Q

Systemic Corticosteroids:

What is affected with long term use?

A

bones, eyes, muscles

55
Q

Azathioprine & 6-MP:

MOA

A

Inducing T cell apoptosis may be important mechanism of how it works

56
Q

Azathioprine & 6-MP:

Role in IBD ?

A
  • helps induce & maintain remission in up to 2/3 of patients with CD or UC
  • also heals fistulas
57
Q

Azathioprine & 6-MP:

onset ?

A

slow onset, need > 3 month trial

58
Q

Azathioprine & 6-MP:

Risk of _____ when discontinued

A

relapse

59
Q

Thiopurine Methyltransferase (TPMT):

What is it?

A
  • major regulator of 6 TG concentration
  • low TPMT activity leads to preferential metabolism to 6 TG (i.e. increase efficacy and toxicity)
  • enzyme activity is genetically determined (polymorphism)
  • homozygous low TPMT < 1%
  • heterozygous low TPMT 10%
  • high TPMT 90%
60
Q

TMPT Testing Issues

A
  • TPMT testing becoming a standard of care in GI guidelines
  • There are 17 mutant alleles
  • Genotyping done by most labs is only for the 3 most common ones. Other ones are considered “rare”
  • Esp. important in Inuit and other populations
  • Functional Assay available in WPG ($70/test). Problem with it is in pt with recent blood transfusion
  • If they had a blood transfusion, they will have other ppl’s RBC’s and may have normal TPMT when in fact their own RBCs have low TPMT
  • Have to wait 3 months til RBC dies
61
Q

Side effect of AZA/6-MP (azathioprine) ?

A

-Severe myleosuppression

62
Q

How do we test for severe myleosuppression that can be caused by AZA/6-MP ?

A
  • genetic testing for TPMT activity in 41 CD patients with severe myleosuppression on AZA/6-MP
  • can’t rely on on TPMT testing alone to predict who will have severe myleosuppression
  • Still need to check RBC and WBC regularly
63
Q

What is a severe interaction ?

A

-Azathioprine & Allopurinol

64
Q

Azathioprine & 6-MP:

Major SE ?

A
  • neutropenia, atypical infections, pancreatitis, skin rash

- small increase in malignancies (lymphomas) in CD

65
Q

Azathioprine & 6-MP:

Monitoring?

A
  • CBCs weekly for 1st month then q2w for months 2-3, then monthly
  • monitor for infections
  • generally no PJP prophylaxis unless also on high dose steroids
  • monitor for pancreatitis (mostly in first 6 weeks, watch for new abdominal or back pain and vomiting)
66
Q

Methotrexate is an ______

A

immunomodulator

67
Q

MTX is primarily for ___

A

CD

68
Q

MTX has similar results to ____

A

AZA (except for combo with TNF where trial not positive for extra efficacy combo)

69
Q

Is MTX recommended for UC ?

A

not recommended yet

*consider if intolerant or refractory to AZA

70
Q

MTX has a ____ onset compared to AZA

A

faster

*still need at least 1 month trial

71
Q

Do you give MTX to pregnant patients?

A

nope

72
Q

MTX Dosing regimen

A

no set standard dosing regimen

we start with 25mg IM x 16 weeks then switched to oral

73
Q

SE of MTX ?

A
  • neutropenia
  • atypical infections
  • liver dysfunction
  • pneumonitis
74
Q

Cyclosporine:

Role in IBD ?

A
  • for severe active UC refusing surgery or are bad surgical risks
  • also used to bridge patients to AZA/6-MP
75
Q

Cyclosporine:

___% of patients on cyclosporine need a colectomy

A

50

76
Q

Cyclosporine:

Dose

A

Given 2mg/kg/day IV for 7-14 days then orally for 3-6 months

77
Q

Cyclosporine:

Serious long term SE ?

A

renal, lipids, BP

78
Q

Cyclosporine:

Limit use in UC to __ months

A

6

79
Q

Bc prednisone doesn’t work we recommend surgery, if they refuse, try an ?

A

anti-TNF

80
Q

What are some anti-TNFs ?

A
  • Adalimumab
  • Certolizumab
  • Golimumab
  • Infliximab
  • Ustekinumab
  • Vedolizumab
81
Q

Infliximab:

MOA

A
  • Antibody that binds to tumor necrosis factor

- Also induces T cell apoptosis

82
Q

Infliximab:

Used in ?

A

IBD and rheumatoid arthritis

83
Q

Infliximab:

Role in IBD ?

A

used in severe active or fistulizing CD disease or active UC

84
Q

Infliximab:

Best data for ?

A

inducing remission in fistulizing Crohn’s perianal closure rate

85
Q

Infliximab:

Dosing regimen ?

A

3 doses of 5mg/kg at 0, 2 and 6 weeks

*usually see response at end of 1st week

Maintenance:
-dosed 5mg/kg q8 weeks (range of 4-12 weeks)

86
Q

Infliximab:

If not responding to induction doses, what do you do?

A

no benefit in continuing into maintenance therapy with the same agent

87
Q

Infliximab:

If not responding to first agent, can you try another agent?

A

there is evidence of benefit in trying another one though response is lower than in the anti-TNF naive

88
Q

Infliximab:

SE?

A

-nausea, URT infections, GI pain

  • infections (impairment of immune system - TB reactivation)
  • too rapid closure of fistulas

*sometimes will put a string through the fistula to keep it a little bit open and allow drainage ?

89
Q

Infliximab:

Long term issues ?

A
  • infections - Tb
  • malignancies
  • lupus like syndromes
  • demyelinating: optic neuritis, MS
  • hematologic - WBC, PLT, pancytopenia
  • hepatic
  • lymphomas in kids & young adults
  • leukemias in adults, adolescents and children
  • new onset psoriasis
90
Q

Describe allergic rxns of Infliximab ?

A

Allergic reactions - acute and delayed hypersensitivity

Infusion-related reactions - most commonly include:

  • headache
  • dizziness
  • flushing
  • pruritus
  • dyspnea
91
Q

Infliximab antibodies develop to _____ component

A

murine

*yet you will still see antibody formation in non-murine anti-TNF agents (ex. adalimumab)

92
Q

____ infliximab increases risk of antibodies

A

intermittent

93
Q

How does antibody formation affect infliximab?

A
  • impact on effectiveness of infliximab is important

- loss of response or need to increase dose/frequency

94
Q

For the reason of antibody formation, usually won’t start Infliximab unless patient also aggress to go on ______. Also pretreat with _____ if just starting tx.

A

AZA/6MP

steroids

95
Q

Some questions for the pharmacist about anti-TNFs?

A
  • Has pt previously been exposed to anti TNF ?
  • Is pretreatment steroids required ?
  • Has a Mantoux Test (or CXR), baseline, LFTs and hepatitis viral studies been performed recently ?

CXR = chest x ray

96
Q

List some supportive therapies

A

Antidiarrheals:

  • Loperamide, Codeine: prior to playing sports to decrease ileostomy drainage
  • Should always stop temporarily when CD deteriorates quickly
  • In UC, ok in mild - moderate disease but never in severe disease as increased risk of toxic megacolon

-Cholestyramine: For bile salt related diarrhea - terminal ileum disease/resection in CD

97
Q

What drugs induce remission in UC ?

A
  • Aminosalicylates (with mild-mod disease)
  • Corticosteroids (backbone therapy for inducing remission)
  • Cyclosporine
  • Anti TNF
  • vedolizumab
98
Q

What drugs maintain remission in UC ?

A
  • Aminosalicylates (with mild-mod disease)
  • Azathioprine, 6-MP, maybe MTX
  • Anti TNF
  • vedolizumab
99
Q

look at algorithms on page 11

A

ok

100
Q

Monitoring for UC ?

A
  • scoring systems of disease activity available and usually recommended (ex. Mayo score)
  • rectal bleeding and diarrhea, frequency of stools/day, can they make it to the bathroom in time ?
  • anemia, low albumin, increased ESR, fever, ab pain
  • adherence important
101
Q

What drugs induce remission in Crohn’s ?

A
  • corticosteroids

- anti TNFs

102
Q

What drugs maintain remission in Crohn’s?

A
  • aminosalicylates?
  • budesonide ?
  • azathioprine, 6 MP, methotrexate
  • anti TNF
  • metronidazole, ciprofloxacin
103
Q

Monitoring for Crohn’s ?

A
  • Heterogenous features
  • Heal fistula, decrease diarrhea and abdominal pain - frequency & severity
  • weight, hemoglobin, endoscopic features
  • frequency of needing supportive therapy (ex. number of loperamide tabs per week)
  • frequency of missing work or school
104
Q

IBD (UC and Crohn’s) are common ______ diseases.

A

autoimmune

105
Q

____ is the backbone of mild-mod UC

A

5-ASA

106
Q

Many patients with advanced IBD need ______ and/or _______

A

immunosuppressives and/or cytokines

Clinical 2 (Part B) (30 decks)

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