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PHAR255 > Inflammatory Bowel Disease > Flashcards

Inflammatory Bowel Disease Flashcards

1
Q

Differentiate the proximal and distal colon.

A

proximal: ascending and transverse colon
distal: descending and sigmoid colon

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2
Q

What is inflammatory bowel disease?

A

idiopathic disease caused by immune response to intestinal flora
-comprised of ulcerative colitis and Crohns

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3
Q

What is ulcerative colitis?

A

chronic inflammatory condition characterized by episodes of inflammation limited to the mucosal layer of the colon
-follows the pattern of relapse-remission
-typically starts in rectum and moves proximally
-no skip lesions

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4
Q

What is Crohns disease?

A

chronic transmural inflammation with skip lesions, affecting mouth to perianal area
-most commonly starts in proximal colon/ileum and then spreads unpredictably

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5
Q

Differentiate CD and UC.

A

skip areas:
-CD: common
-UC: never
transmural involvement:
-CD: common
-UC: occasional
rectal sparing:
-CD: common
-UC: never
perianal involvement:
-CD: rare
-UC: never
fistulas:
-CD: common
-UC: never
strictures:
-CD: common
-UC: occasional
granulomas:
-CD: common
-UC: occasional

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6
Q

When is the peak onset of IBD seen?

A

15-40 years old

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7
Q

Describe the pathophysiology of IBD.

A

initial trigger unknown
genetic influence plays a role
immune system creates antibodies to intestinal normal flora and food antigens; inflammatory mediators also involved

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8
Q

Differentiate the starting location for UC and CD.

A

UC: begins in rectum and spreads proximally
CD: begins anywhere then spreads unpredictably

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9
Q

What are the risk factors for IBD?

A

age and gender (15-40, male = female)
race and ethnicity (no direct link)
genetic influence
smoking
poor diet
sedentary lifestyle
obesity
stress
medications

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10
Q

Which medications are risk factors for IBD?

A

antibiotics (frequent use, esp if broad spectrum)
NSAIDs
oral contraceptives (only if genetic link and estrogen)
isotretinoin - likely not

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11
Q

Describe the prognosis for IBD.

A

mortality rates: 1.4-5x higher for CD (baseline for UC)
-primary disease is most common cause of death
-secondary infection is other leading cause
malignancy rates: 7.6% at 30yrs after diagnosis
frequent relapse (UC > CD)
lower QoL (CD > UC)

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12
Q

What are some complications of IBD?

A

colectomy
osteoporosis
hypercoagulability –> VTE
anemia
gallstones
kidney stones
ulcers
uveitis
arthritis
malnutrition and electrolyte imbalance

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13
Q

What are the symptoms of IBD?

A

abdominal pain
diarrhea
constipation
mucousy stool
bloody stool
weight loss
fever
sweats
malaise
arthralgia

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14
Q

Differentiate the classifications of UC.

A

mild:
-+1-2 stools/day over baseline
-may be streaks of blood in stool (~50% of time)
-no systemic involvement
moderate:
-+3-4 stools/day over baseline
-blood in stool most of the time
-minimal systemic involvement
severe:
-+5 stools/day over baseline
-blood in stool most of the time
-systemic toxicity begins
fulminant:
- > 6 stools/day
-systemic toxicity
-blood transfusion needed

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15
Q

Differentiate the classifications of CD.

A

mild:
-can tolerate oral intake
-no dehydration
-some abdominal pain/tenderness
- < 10% weight loss
moderate:
-unresponsive to treatment
-continuous fever, NVD, > 10% weight loss, anemia, dehydration
severe:
-sx persist despite steroid use
-obstruction, persistent vomiting, high fever

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16
Q

How is IBD diagnosed?

A

physical exam
lab exam
-stool testing
-blood tests
imaging and endoscopy (gold standard)

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17
Q

What are some monitoring parameters for IBD?

A

hemoglobin
iron indices
nutritional status
growth
BMD if increased osteoporosis risk
colonoscopy
-within 8yrs of onset, screen q1-3yrs if 2 negative results

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18
Q

What are the goals of treatment for IBD?

A

recognize disease early
induce and sustain remission with least toxic therapy
avoid complications
maintain current daily life
provide secondary care of symptoms

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19
Q

Which classes of medications are used for IBD?

A

corticosteroids
aminosalicylates
immune modifiers
-azathioprine/mercaptopurine
-biologics

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20
Q

What are the non-pharm treatments for IBD?

A

dietary
probiotics
smoking cessation
exercise

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21
Q

Explain the role of diet in IBD management.

A

bulk fiber to reduce diarrhea (25-30g/day)
reduce fat intake (except omega-3)
consider trigger foods, elimination diet
prevent malnutrition
-calcium, ADEK, zinc, magnesium, iron, B12, folic acid

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22
Q

What is the role of multivitamins in IBD?

A

useful and recommended
-monitoring and additional supplementation may be needed

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23
Q

Explain the role of probiotics in IBD management.

A

evidence lacking/conflicting (most data for UC)
looks promising; very safe
lactobacilli, bifidobacteria, saccharomyces most studied
possible benefit:
-induce remission, maintain remission, reduce diarrhea

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24
Q

Explain the role of smoking cessation in IBD management.

A

definite improvement in Crohns and relapse rates
possible risk increase in UC

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25
Q

Explain the role of exercise in IBD management.

A

50% RRR in reduction of flares
likely reduces incidence as well

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26
Q

What are the principles of therapy for IBD?

A

induce remission of acute episode
maintain remission
minimize use of steroids

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27
Q

What is remission in the context of IBD?

A

symptom free and
no inflammatory consequences and
not steroid dependent

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28
Q

True or false: treatment of choice are the same for UC and CD

A

false

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29
Q

What is the benefit of corticosteroids for IBD?

A

highly effective agents for inducing remission

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30
Q

Which route of administration are corticosteroids delivered in IBD?

A

orally for UC/CD
topical foams and enemas in UC (important option)

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31
Q

What are the indications for corticosteroids in UC?

A

topical: mild-mod UC induction
oral: mod-severe UC induction

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32
Q

What are the indications for corticosteroids in CD?

A

oral: mild-severe CD induction
budesonide: short term maintenance ( < 3 months)

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33
Q

What is the dosing of corticosteroids for IBD?

A

prednisone 40-60mg daily
budesonide:
-entocort capsules: ileal/ascending colon CD only-9mg daily
-entocort enema: distal UC only-2mg qhs
-cortiment tablets: UC only-9mg daily
hydrocortisone 10% enema/foams: UC only-qhs

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34
Q

How should corticosteroids be administered for IBD?

A

prednisone with food
topicals: lie on left side, retain contents as long as possible

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35
Q

What is the onset of corticosteroids for IBD?

A

symptom improvement as early as 2-3 days
average 2-4 weeks to see remission

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36
Q

What is the duration of therapy of corticosteroids for IBD induction?

A

use until remission:
-prednisone: ~ 4 weeks max recommended
-budesonide oral or topical: ~ 8 weeks max
taper recommended mainly due to relapse with abrupt dc
-taper budesonide as well (9-6-3-0 over 4 weeks)
-likely no need to taper budesonide enema
entocort (CD) budesonide capsules can be continued after induction for up to 3 months at 6mg/d (then taper, 6-3-0 over 2 weeks)

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37
Q

What is the role of switching from prednisone to budesonide in IBD?

A

done to reduce ADRs, HPA-axis suppression or reduce disease recurrence
max dose of 6mg budesonide
prednisone stills needs to be tapered
strongly consider also tapering budesonide when therapy complete

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38
Q

What are the common side effects of corticosteroids?

A

GI intolerance
appetite increase
nervousness/anxiety
insomnia
tremors/heart palpitations

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39
Q

What are the serious side effects of corticosteroids?

A

Cushingoid features
blood glucose increase
psychiatric side effects
GI bleeds
cataracts
osteoporosis
electrolyte imbalance

40
Q

What are the monitoring parameters for corticosteroids if used long-term?

A

annual eye exam
blood glucose
CBC
electrolytes
BMD

41
Q

What should be done if drug interactions or systemic toxicity are a concern with corticosteroids in IBD?

A

consider budesonide or topicals if possible

42
Q

How are corticosteroids best used at the first presentation of disease for IBD?

A

monotherapy to induce remission
60-80% of patients respond within 10-14 days

43
Q

What are examples of aminosalicylates?

A

5-ASA (mesalamine-many forms)
sulfasalazine
olasalazine

44
Q

What are the most commonly used agents in UC?

A

aminosalicylates
-topical and oral agents available

45
Q

What is the role of aminosalicylates in CD?

A

questionable efficacy in acute CD
ineffective for maintenance

46
Q

What are the indications for induction of IBD for aminosalicylates?

A

5-ASA (oral +/- topical) therapy for mild UC
5-ASA + prednisone for mod-severe UC
SSZ for induction of mild-mod CD

47
Q

What are the indications for maintenance of IBD for aminosalicylates?

A

5-ASA (oral +/- topical) for maintenance of remission for mild-mod UC

48
Q

What are the contraindications to aminosalicylates?

A

hypersensitivity to salicylates
hypersensitivity to sulfonamides (SSZ only)
severe renal impairment ( < 30)
severe hepatic impairment
existing gastric or duodenal ulcer

49
Q

What is the MOA of aminosalicylates?

A

5-ASA controls inflammation by inhibiting COX pathways and blocks PG/leukotriene production in the colon
SSZ is converted into 5-ASA in the colon

50
Q

What is the difference in dosing for aminosalicylates in regard to induction and maintenance of UC?

A

topical induction: higher dose
topical maintenance: lower dose
oral induction: higher dose
oral maintenance: lower dose

51
Q

Which aminosalicylate is dosed once daily?

A

Mezavant (others are TID-QID)

52
Q

Describe administration of suppository/enema aminosalicylates.

A

suppositories reach rectum only
enemas extend into distal colon
must be able to retain enema contents for > 30 min

53
Q

What is the benefit of suppository/enema aminosalicylates for UC?

A

equal or more effective than oral agents
better tolerated
less dosing frequency, lower cost

54
Q

What is the onset of aminosalicylates?

A

2-4 weeks to achieve remission

55
Q

What are the common side effects of aminosalicylates?

A

GI (NVD, pain)
headache
rash
arthralgia
urine discolouration
SSZ only: higher rates of above, reversible oligospermia

56
Q

How can the adverse effects of aminosalicylates be managed?

A

change from SSZ to 5-ASA
take with food
consider an EC product
restart at lower dose and slowly titrate
divide dose BID-QID instead of OD
switch to topical product
olsalazine has more diarrhea than other agents
in general, GI effects lessen over time

57
Q

What are the serious side effects of aminosalicylates?

A

hematologic abnormalities
hepatoxicity
photosensitivity
bone marrow toxicity

58
Q

What are the monitoring parameters for aminosalicylates?

A

CBC
renal function
liver function

59
Q

What are the drug interactions of aminosalicylates?

A

5-ASA
-antacids, PPIs, H2RAs
-digoxin decreased
-azathioprine/mercaptopurine toxicity increased
SSZ same as above plus phenytoin

60
Q

Which 5-ASA formulations are pH dependent? Which are time dependent?

A

pH dependent: Asacol, Salofalk, Mesavant
time based: Pentasa

61
Q

Describe the clinical evidence of aminosalicylates for UC.

A

induction achieved in 50% of patients
maintains remission in 59% vs 24% placebo
SSZ slightly more effective in induction and maintenance
all different formulations of oral 5-ASA are equal
combining both oral and topical 5-ASA is superior to either agent alone

62
Q

Describe the clinical evidence of aminosalicylates for CD.

A

sulfasalazine inferior to corticosteroids for induction
sulfasalazine superior to placebo for induction
other 5-ASA preps: not superior to placebo for induction or maintenance

63
Q

What are examples of immune modifiers?

A

immunosuppressants:
-azathioprine, mercaptopurine, methotrexate
biologics:
-TNF inhibitors: infliximab, adalimumab, certolizumab, golimumab
-integrin receptor blockers: vedolizumab
-IL 12 and 23 inhibitors: ustekinumab

64
Q

When are immune modifiers used for IBD?

A

severe or unresponsive disease

65
Q

What is the key benefit of immune modifiers for IBD?

A

steroid sparing

66
Q

When are immune modifiers used for maintenance of UC and CD?

A

2 or more courses of steroids used in 12 months; or > 12 wks of use per year
relapse during steroid taper
relapse within 6 months of stopping steroids
non-response to steroids or 5-ASA
frequent flares

67
Q

True or false: immune modifiers are used earlier in the course of UC vs CD

A

false
used earlier in course of CD vs UC

68
Q

What are the indications for immune modifiers for induction of IBD?

A

biologics indicated for induction in mod-severe UC or CD
azathioprine/mercaptopurine indicated as part of an induction regimen in CD, but not as monotherapy

69
Q

What is the MOA of the immune modifiers?

A

general: all reduce immune response
azathioprine/mercaptopurine:
-purine antagonists–>immune suppression
TNF-inhibitors
vedolizumab: integrin receptor blocker
ustekinumab: inhibits Il-12 and Il-23, disrupts T-lymphocytes

70
Q

How are immune modifiers dosed?

A

start low and titrate slowly
doses differ from induction compared to maintenance

71
Q

How are immune modifiers administered?

A

mercaptopurine/azathioprine: OD
biologics:
-IV: infliximab, vedolizumab
-SC: adalimumab, certolizumab, golimumab, ustekinumab

72
Q

What is the onset of immune modifiers?

A

mercaptopurine/azathioprine: 3-6 months
most biologics: 2-8 weeks
vedolizumab: 18-20 weeks

73
Q

What is the duration of therapy of immune modifiers for IBD?

A

generally life-long
de-escalation therapy poorly understood
-likely not possible for the majority of patients
-very mild UC/CD may attempt, but relapses common

74
Q

What are the common side effects of immune modifiers?

A

mercaptopurine/azathioprine:
-flu like sx
-GI sx
biologics:
-infection rate increase
-infusion reactions
-nausea
-headache
-malaise

75
Q

What are the serious side effects of mercaptopurine and azathioprine?

A

myelosuppression
hepatotoxicity
infection increase

76
Q

What are the serious side effects of TNF inhibitors?

A

reactivation of serious infections
neutropenia
malignancy increase (skin cancer, lymphoma)
antibody development
hepatotoxicity
heart failure
autoimmune disease activation
seizure risk

77
Q

What are the serious side effects of vedolizumab and ustekinumab?

A

antibody development
serious infection rates increase
-less risk with vedolizumab
latent infection concern

78
Q

Which immune modifier used for IBD has the lowest infection risk?

A

vedolizumab (gut selective)

79
Q

What are the monitoring parameters for mercaptopurine and azathioprine?

A

CBC baseline, every other week while titrating, q3m
LFTs baseline
renal function

80
Q

What are the monitoring parameters for TNF inhibitors?

A

baseline TB test and sx of bacterial or fungal inf
Hep B/C screening
baseline and q8-12 wks: CrCl/urinalysis, CBCs, LFTs
signs of infection

81
Q

What are the monitoring parameters for vedolizumab and ustekinumab?

A

same as TNF inhibitors

82
Q

What are the drug interactions of mercaptopurine and azathioprine?

A

allopurinol and febuxostat: increased toxicity of mer/aza
aminosalicylates: increased levels of mer/aza
live vaccines

83
Q

What are the drug interactions of biologics?

A

live vaccines
other immunosuppressants

84
Q

Describe the clinical evidence of azathioprine and mercaptopurine for IBD.

A

superior to 5-ASA for UC
well tolerated, steroid sparing

85
Q

Describe the clinical evidence of biologics for IBD.

A

considered superior to other agents

86
Q

Which biologics are generally first line for IBD?

A

TNF inhibitors
-no response after induction doses, switch therapy

87
Q

Is maintenance therapy always indicated for IBD?

A

UC: always provide maintenance
CD:
-for mild disease, may not need
-consider if 2 or more exacerbations per year

88
Q

What are some combo therapy options for UC?

A

steroid (topical or oral) + SSZ + 5-ASA has high induction rates
5-ASA oral + 5-ASA enemas improve induction rates
biologics + AZA = improved induction/maintenance
notably: limited evidence for 5-ASA + immune modifiers

89
Q

What are some combo therapy options for CD?

A

prednisone + SSZ possibly better for induction vs mono
prednisone + AZA to speed time to induction
biologics + AZA or 6MP = improved induction/maintenance rates, steroid sparing, less Ab formation, but more toxicity

90
Q

Describe fistula management.

A

metronidazole +/- ciprofloxacin used to prevent septic complications of CD
-often used if perianal fistulas or abscesses develop
-limited benefit during active disease
-combo used for 2 weeks

91
Q

What are some new treatments for IBD?

A

mirikizumab or risankizumab (IL-23 inhibitors)
JAK inhibitors
considered last line options to consider

92
Q

What are some “secondary” medications for IBD?

A

anti-diarrheals
pain medications
immunization
antidepressants/anxiety
nutrition

93
Q

Explain the role of anti-diarrheals in IBD.

A

may be used if mild diarrhea without systemic toxicity
loperamide preferred
frequent use indicates uncontrolled disease
psyllium or methylcellulose useful

94
Q

Explain the role of pain medications in IBD.

A

may treat if no signs of systemic toxicity
anticholinergics may be used
hyoscine (Buscopan) and pinaverium commonly used

95
Q

Which pain medications should be avoided in IBD?

A

NSAIDs and opiates

96
Q

What is a common comorbidity of IBD?

A

depression/anxiety

97
Q

Which antidepressants are preferred for IBD?

A

TCAs
-seem to lower relapse rates, improve QoL, and reduce steroid use

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