IBD Flashcards

1
Q

Idiopathic IBD categories

A

Ulcerative colitis

Crohn’s disease

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2
Q

Ulcerative colitis

A

Mucosal inflammatory condition affecting the rectum and colon

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3
Q

Crohn’s disease

A

Transmural inflammation of any part of the GI tract, mouth to anus

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4
Q

Clinical findings for UC

A
Continuous inflammation (very common)
Toxic megacolon
Pseudopolyps
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5
Q

UC histology

A

Nontransmural

Crypt abscesses

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6
Q

Depth of UC ucleration

A

Superficial

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7
Q

Is UC a risk factor for colorectal cancer?

A

Yes

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8
Q

Clinical findings for CD

A

Patchy cobblestone appearance
Perianal involvement
Fistula, perforation, or strictures
Malabsorption/malnutrition - vitamin deficiencies; possible growth retardation

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9
Q

Depth of CD ulceration

A

May extend to submucosa or deeper

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10
Q

Histology of CD

A

Transmural lesions

Granuloma

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11
Q

Extraintestinal complications (more common in CD)

A
Spondylarthritis
Peripheral arthritis
Ocular
Primary sclerosing cholangitis
Anemia
C diff
Hypercoagulability
Malabsorption
Thromboembolic disease 
Osteoporosis
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12
Q

Thromboembolic disease in CD

A

Risk for VTE is three-fold higher than in general population

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13
Q

How is osteoporosis caused by IBD?

A

D/t systemic inflammation effects on bone, malabsorption of Vit D, and glucocorticoid use; bisphosphonates are the preferred drug of treatment

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14
Q

Smoking in UC

A

Nicotine offers a protective mechanism
The likelihood of a smoker developing UC is less than half that of a non-smoker
Patients with UC who stop smoking often relapse

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15
Q

Transdermal nicotine patches and UC

A

Shown improvement in disease remission rates but are not recommended as a standard of care

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16
Q

Smoking and CD

A

Ppl who smoke are 2x as likely to have CD

Patients who stop smoking will see reduction in severity of their condition

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17
Q

Assumed etiologies for IBD

A
Infectious
Genetic
Environmental
Psychologic
Immunologic
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18
Q

Genetics and IBD

A

CD is common among relatives
1st degree relatives are 13x more likely to suffer from IBD
Genes have been identified for UC and CD

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19
Q

Environment and IBD

A

No clear connection to diet

NSAID use - PG inhibition appears to impair the protective mechanism of the mucosal barrier in the GI tract

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20
Q

Psychology and IBD

A

Clear association between mental health and remissions/flares

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21
Q

Immunology and IBD

A

Cytokines - inappropriate T cell response to intestinal flora
TNF-alpha - activates coagulation and promotes granuloma formation (production enhanced in patients with CD)

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22
Q

Mild IBD

A

+/- blood in stool
No systemic sx
Normal ESR

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23
Q

Moderate IBD

A

+/- blood in stool
Minimal systemic sx
Normal ESR

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24
Q

Severe

A

+ blood in stool
+ systemic sx
Increased ESR (> 30)

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25
Q

CDAI

A

Chrone’s disease Activity Index
Mostly done in trials
Measures CD

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26
Q

IBDQ score

A

QOL

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27
Q

Genetics tests for IBD

A

Prometheus Labs

May indicate how severe a patient’s dz will be

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28
Q

Diagnosis of IBD

A

Pt sx
PE
Labs
Radiographic/endoscopic findings

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29
Q

Labs for IBD diagonsis

A

Compares carious IgG and IgM in patient with a database of IBD patients
Not extremely accurate

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30
Q

Non-pharm treatment of IBD

A

Nutrition (avoid exacerbating foods, use parenteral nutrition if needed)
Surgery (indications include uncontrolled disease despite max therapy, presence of complications or presence of premalignant changes)

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31
Q

Pharm treatment of IBD

A
Aminosalicylates
Corticosteroids
immunosuppressants
Cipro/flagyl
TNF-alpha
Humanized monoclonal antibody to alpha-4 integrin
Tofacitinib
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32
Q

Aminosalicylates

A

Balsalazide
Osalazine
Sulfasalazine
Mesalamine

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33
Q

Aminosalicylates MOA

A

Modulates leukotrienes to inhibit inflammatory response

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34
Q

Aminosalicylates time to effectiveness

A

2-4 weeks, treat for 6-8 weeks at full treatment dose

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35
Q

Aminosalicylates MD

A

50% treatment dose

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36
Q

Aminosalicylates and monitoring

A

SCr prior to starting therapy and periodically thereafter d/t risk for nephrotoxicity

37
Q

Balsalazide site of action

A

Colon

38
Q

Osalazine site of action

A

Colon

39
Q

Osalazine ADR

A

Dose-related diarrhea

40
Q

Sulfasalazine ADR

A

N/V
Ab pain
CI: sulfa allergy

41
Q

Mesalamine general

A

Easier to tolerate than sulfasalazine

42
Q

Mesalamine brands and site of action

A
Rowasa: rectum; terminal colon
Delzicol/Asacol HD: distal ileum; colon
Canasa: rectum
Pentasa: small bowel; colon
Lialda: colon
Apriso: colon
43
Q

Mesalamine monitoring

A

folic acid level

44
Q

Mesalamine DDI

A
Antacids
H2RAs
PPIs
**May cause premature relase of delayed release products
Preg risk cat D
45
Q

Corticosteroids MOA

A

Inhibit inflammatory mediator release (cytokines)

46
Q

Corticosteroids

A

Prednisone
Methylprednisolone IV
Budesonide

47
Q

Budesonide bioavailability

A

Poorly absorbed w/limited bioavailability d/t an extensive 1st pass metabolism by the liver allowing it to produce therapeutic benefit with reduced systemic toxicity

48
Q

Budesonide

A

Enterocort EC - for CD in the terminal ileum or right colon (12 week treatment then taper)
Uceris - UC (8 week treatment then taper)

49
Q

Budesonide monitoring

A

BMD yearly, receive vit D and calcium if long term use required

50
Q

Immunosuppresants

A

Azathioprine, 6-MP
CsA
MTX

51
Q

Azathioprine, 6-MP MOA

A

Antagonizes purine metabolism causing immunosuppresion

52
Q

how long until a patient on AZA, 6-MP sees a benefit

A

3 months (use something quicker in the meantime)

53
Q

AZA, 6-MP monitoring

A
Hg
WBC
Plts
LFTs
Amylase
TPMT testing may help prevent toxicity
54
Q

CSA MOA

A

Inhibits production and release of IL-2 causing immunosuppression

55
Q

CsA IV use

A

Severe UC and CD unresponsive to IV steroids

56
Q

MTX use

A

CD only

57
Q

MTX MOA

A

Anti-inflammatory and immunosuppression through irreversible dihydrofolate reductase inhibition

58
Q

MTX monitoring

A

CBC
LFTs
SCr

59
Q

MTX DDIs

A

PPIs - appears to only impact high dose MTX used in chemo regimens

60
Q

Cipro/flagyl use

A

CD only

  • Fistulizing Crohn’s: abx x 3 months
  • Potential role in post-op CD pt (pouchitis)
61
Q

Cipro/flagyl MOA

A

Benefit is thought to be through inhibiting bacterial stimulation of the inflammatory process

62
Q

TNF-alpha antagonists MOA

A

Monoclonal ab that bind to human TNF-alpha thereby interfering with endogenous TNG alpha activity

63
Q

TNF-alpha antagonists BBW

A
  • Serious infx (including tuberculosis, invasive fungal and other opportunistic infxns), some with fatalities, have been reprted in patients receiving TNF-blocking agents
  • Pts should be evaluated for TB risk factors and latent TB infxn (w/ a tuberculin skin test) prior to therapy. Tx of latent TB should be initiated before use. Pts with initial neg TB skin tests should receive continued monitoring for TB throughout treatment
64
Q

TNF-alpha antagonists

A

Infliximab
Adalimumab
Certolizumab

65
Q

Infliximab uses

A

Adults/pediatrics: CD or UC

Adults: fistulizing CD

66
Q

Infliximab ADR

A

Infusion rxn treated with benadryl and APAP (pre-med for future doses)

67
Q

Adalimumab uses

A

Adults/peds: CD/UC

68
Q

Certolizumab uses

A

CD in adults only

69
Q

TNF-alpha antagonists monitoring

A
CRP
Fecal calprotectin
Lactoferrin
Albumin
Antidrug ab
Anti-TNF drug level (if pt loses response to drug)
70
Q

TNF-alpha antagonists: if pt loses response with subtherapeutic drug levels AND low or no abs?

A

Increase anti-TNF and/or decrease interval

Consider adding thiopurine/MTX if not already on

71
Q

TNF-alpha antagonists: if patient loses response with subtherapeutic drug levels and high ab levels

A

Switch to different TNF-alpha antagonists

72
Q

TNF-alpha antagonists: if patient loses response with therapeutic drug levels

A

switch to vedolizumab w/ or w/o immunosuppressant (if CD; if UC, DC drug)

73
Q

Humanized monoclonal ab to alpha-4 integrin MOA

A

Inhibit leukocyte adhesion and migration (vedolizumab in GI tract only)

74
Q

Humanized monoclonal ab to alpha-4 integrin uses

A

Inducing and maintaining clinical response and remission in adult patients with mod-severe active CD (natalizumab and vedulizumab) or UC (vedolizumab) with an inadequate response to, or are unable to tolerate conventional CD/UC therapies and TNF-alpha antagonists

75
Q

What must be up-to-date before starting Humanized monoclonal ab to alpha-4 integrins

A

Immunizations

76
Q

Humanized monoclonal ab to alpha-4 integrins

A

Natalizumab

Vedolizumab

77
Q

Natalizumab ADR

A

Progressive multifocal leukoencepholopathy in MS

Severe cholestatic injury

78
Q

Natalizumab monitoring

A

LFTs (esp during first week of therapy)

79
Q

Vedolizumab ADR

A

HA
Arthralgia
Nasopharyngitis

80
Q

Tofacitinib (Xeljanz)

A

Janus Associated Kinase inhibitor approved for RA

Currently being studied in UC patients with mod-severe disease non-responsive to other treatment

81
Q

Vaccines for IBD

A
Flu
PCV13 or PPSV23
Zoster
Varicella
Yellow fever
Hep B
Meningococcal
82
Q

Flu vaccine and IBD

A

Annually

If on immunosuppressant: non-live trivalent

83
Q

PCV13 or PPSV23 vaccine and IBD

A

If on immunosuppressant

Should have PPSY23 booster 5 years after 1st dose

84
Q

Zoster vaccine and IBD

A

Not on immunosuppressants or on low dose MTX, AZA, or 6-MP

Not recommended if on anti-TNF therapy

85
Q

Varicella vaccine and IBD

A

Assess for prior exposure and vaccinate if naive PRIOR to initiating immunosuppressant therapy

86
Q

Yellow fever vaccine and IBD

A

Vaccinated prior to travel
Assessed before travel
-If highly immunosuppressed - should not travel
-To stop immunosuppressants in order to get vaccine - wait 3 months before vaccination; then wait at least 4 weeks to restart immunosuppressant

87
Q

Hep B vaccine and IBD

A

HBV can be re-activated in an immunocompromised patient
Test for HBV infection prior to starting treatment
Check for immunity to HBV and vaccinate if not immune prior to starting treatment
1-3 months after vaccination, check a titer to be sure patient is immune
Check a titer every 1-2 yr thereafter; give a single booster shot if necessary

88
Q

Health screenings in IBD

A

Cervical cancer - annual
Depression/anxiety screening
Melanoma
Non-melanoma squamous cell cancer screening - > 50 yo on immunosuppressants
Osteoporosis - those with conventional risk factors should be screened at the time of diagnosis and periodically after diagnosis