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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
Explain the role of exercise in IBD management.
50% RRR in reduction of flares likely reduces incidence as well
26
What are the principles of therapy for IBD?
induce remission of acute episode maintain remission minimize use of steroids
27
What is remission in the context of IBD?
symptom free and no inflammatory consequences and not steroid dependent
28
True or false: treatment of choice are the same for UC and CD
false
29
What is the benefit of corticosteroids for IBD?
highly effective agents for inducing remission
30
Which route of administration are corticosteroids delivered in IBD?
orally for UC/CD topical foams and enemas in UC (important option)
31
What are the indications for corticosteroids in UC?
topical: mild-mod UC induction oral: mod-severe UC induction
32
What are the indications for corticosteroids in CD?
oral: mild-severe CD induction budesonide: short term maintenance ( < 3 months)
33
What is the dosing of corticosteroids for IBD?
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
34
How should corticosteroids be administered for IBD?
prednisone with food topicals: lie on left side, retain contents as long as possible
35
What is the onset of corticosteroids for IBD?
symptom improvement as early as 2-3 days average 2-4 weeks to see remission
36
What is the duration of therapy of corticosteroids for IBD induction?
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)
37
What is the role of switching from prednisone to budesonide in IBD?
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
38
What are the common side effects of corticosteroids?
GI intolerance appetite increase nervousness/anxiety insomnia tremors/heart palpitations
39
What are the serious side effects of corticosteroids?
Cushingoid features blood glucose increase psychiatric side effects GI bleeds cataracts osteoporosis electrolyte imbalance
40
What are the monitoring parameters for corticosteroids if used long-term?
annual eye exam blood glucose CBC electrolytes BMD
41
What should be done if drug interactions or systemic toxicity are a concern with corticosteroids in IBD?
consider budesonide or topicals if possible
42
How are corticosteroids best used at the first presentation of disease for IBD?
monotherapy to induce remission 60-80% of patients respond within 10-14 days
43
What are examples of aminosalicylates?
5-ASA (mesalamine-many forms) sulfasalazine olasalazine
44
What are the most commonly used agents in UC?
aminosalicylates -topical and oral agents available
45
What is the role of aminosalicylates in CD?
questionable efficacy in acute CD ineffective for maintenance
46
What are the indications for induction of IBD for aminosalicylates?
5-ASA (oral +/- topical) therapy for mild UC 5-ASA + prednisone for mod-severe UC SSZ for induction of mild-mod CD
47
What are the indications for maintenance of IBD for aminosalicylates?
5-ASA (oral +/- topical) for maintenance of remission for mild-mod UC
48
What are the contraindications to aminosalicylates?
hypersensitivity to salicylates hypersensitivity to sulfonamides (SSZ only) severe renal impairment ( < 30) severe hepatic impairment existing gastric or duodenal ulcer
49
What is the MOA of aminosalicylates?
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
What is the difference in dosing for aminosalicylates in regard to induction and maintenance of UC?
topical induction: higher dose topical maintenance: lower dose oral induction: higher dose oral maintenance: lower dose
51
Which aminosalicylate is dosed once daily?
Mezavant (others are TID-QID)
52
Describe administration of suppository/enema aminosalicylates.
suppositories reach rectum only enemas extend into distal colon must be able to retain enema contents for > 30 min
53
What is the benefit of suppository/enema aminosalicylates for UC?
equal or more effective than oral agents better tolerated less dosing frequency, lower cost
54
What is the onset of aminosalicylates?
2-4 weeks to achieve remission
55
What are the common side effects of aminosalicylates?
GI (NVD, pain) headache rash arthralgia urine discolouration SSZ only: higher rates of above, reversible oligospermia
56
How can the adverse effects of aminosalicylates be managed?
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
What are the serious side effects of aminosalicylates?
hematologic abnormalities hepatoxicity photosensitivity bone marrow toxicity
58
What are the monitoring parameters for aminosalicylates?
CBC renal function liver function
59
What are the drug interactions of aminosalicylates?
5-ASA -antacids, PPIs, H2RAs -digoxin decreased -azathioprine/mercaptopurine toxicity increased SSZ same as above plus phenytoin
60
Which 5-ASA formulations are pH dependent? Which are time dependent?
pH dependent: Asacol, Salofalk, Mesavant time based: Pentasa
61
Describe the clinical evidence of aminosalicylates for UC.
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
Describe the clinical evidence of aminosalicylates for CD.
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
What are examples of immune modifiers?
immunosuppressants: -azathioprine, mercaptopurine, methotrexate biologics: -TNF inhibitors: infliximab, adalimumab, certolizumab, golimumab -integrin receptor blockers: vedolizumab -IL 12 and 23 inhibitors: ustekinumab
64
When are immune modifiers used for IBD?
severe or unresponsive disease
65
What is the key benefit of immune modifiers for IBD?
steroid sparing
66
When are immune modifiers used for maintenance of UC and CD?
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
True or false: immune modifiers are used earlier in the course of UC vs CD
false used earlier in course of CD vs UC
68
What are the indications for immune modifiers for induction of IBD?
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
What is the MOA of the immune modifiers?
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
How are immune modifiers dosed?
start low and titrate slowly doses differ from induction compared to maintenance
71
How are immune modifiers administered?
mercaptopurine/azathioprine: OD biologics: -IV: infliximab, vedolizumab -SC: adalimumab, certolizumab, golimumab, ustekinumab
72
What is the onset of immune modifiers?
mercaptopurine/azathioprine: 3-6 months most biologics: 2-8 weeks vedolizumab: 18-20 weeks
73
What is the duration of therapy of immune modifiers for IBD?
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
What are the common side effects of immune modifiers?
mercaptopurine/azathioprine: -flu like sx -GI sx biologics: -infection rate increase -infusion reactions -nausea -headache -malaise
75
What are the serious side effects of mercaptopurine and azathioprine?
myelosuppression hepatotoxicity infection increase
76
What are the serious side effects of TNF inhibitors?
reactivation of serious infections neutropenia malignancy increase (skin cancer, lymphoma) antibody development hepatotoxicity heart failure autoimmune disease activation seizure risk
77
What are the serious side effects of vedolizumab and ustekinumab?
antibody development serious infection rates increase -less risk with vedolizumab latent infection concern
78
Which immune modifier used for IBD has the lowest infection risk?
vedolizumab (gut selective)
79
What are the monitoring parameters for mercaptopurine and azathioprine?
CBC baseline, every other week while titrating, q3m LFTs baseline renal function
80
What are the monitoring parameters for TNF inhibitors?
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
What are the monitoring parameters for vedolizumab and ustekinumab?
same as TNF inhibitors
82
What are the drug interactions of mercaptopurine and azathioprine?
allopurinol and febuxostat: increased toxicity of mer/aza aminosalicylates: increased levels of mer/aza live vaccines
83
What are the drug interactions of biologics?
live vaccines other immunosuppressants
84
Describe the clinical evidence of azathioprine and mercaptopurine for IBD.
superior to 5-ASA for UC well tolerated, steroid sparing
85
Describe the clinical evidence of biologics for IBD.
considered superior to other agents
86
Which biologics are generally first line for IBD?
TNF inhibitors -no response after induction doses, switch therapy
87
Is maintenance therapy always indicated for IBD?
UC: always provide maintenance CD: -for mild disease, may not need -consider if 2 or more exacerbations per year
88
What are some combo therapy options for UC?
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
What are some combo therapy options for CD?
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
Describe fistula management.
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
What are some new treatments for IBD?
mirikizumab or risankizumab (IL-23 inhibitors) JAK inhibitors *considered last line options to consider*
92
What are some "secondary" medications for IBD?
anti-diarrheals pain medications immunization antidepressants/anxiety nutrition
93
Explain the role of anti-diarrheals in IBD.
may be used if mild diarrhea without systemic toxicity loperamide preferred frequent use indicates uncontrolled disease psyllium or methylcellulose useful
94
Explain the role of pain medications in IBD.
may treat if no signs of systemic toxicity anticholinergics may be used hyoscine (Buscopan) and pinaverium commonly used
95
Which pain medications should be avoided in IBD?
NSAIDs and opiates
96
What is a common comorbidity of IBD?
depression/anxiety
97
Which antidepressants are preferred for IBD?
TCAs -seem to lower relapse rates, improve QoL, and reduce steroid use

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