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Inflammatory Bowel Disease (UC + CD) Flashcards

1
Q

Define inflammatory bowel disease

A

mucosal inflammatory conditions with chronic or recurring immune response and inflammation of the gastrointestinal tract

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2
Q

What are the two types of IBD?

A

ulcerative colitis

crohn’s disease

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3
Q

Define UC

A

mucosal inflammation confined to rectum and colon

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4
Q

Define CD

A

transmural inflammation of GI tract that can affect any part from the mouth to the anus (deeper inflammation)

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5
Q

CD etiology

A

increased Th1 cytokine activity (interferon gamma, interleukin 12 [IL-12])

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6
Q

UC etiology

A

Increased Th2 cytokine activity (IL-13, IL-5)

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7
Q

smoking and UC

A

potentially protective

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8
Q

smoking and CD

A

increased frequency and severity of CD

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9
Q

NSAIDs and IBD

A

doesn’t really cause the disease but can make symptoms worse

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10
Q

Antibiotics and IBD

A

doesn’t really cause the disease but can mess with flora and exacerbate symptoms

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11
Q

UC pathophysiology

A

confined to the rectum and colon and affects mucosal and submucosal layers (its more superficial than CD)

abscess formation in mucosal crypts, coalescence results in ulceration

ulcers can surround normal tissue

mucosal damage –> substantial diarrhea and bleeding

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12
Q

UC complications

A

local, systemic, extraintestinal complications

local: hemorrhoids, anal fissures, perirectal abscesses

Major complications: colonic perforation, massive colonic hemorrhage, colonic structure

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13
Q

UC Toxic megacolon

A

severe and potentially fatal complications

segmental or total colonic distention (> 6cm) with acute colitis and signs of systemic toxicity

increased depth of ulceration

vasculitis and thrombosis

colonic dilation and potential perforation

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14
Q

UC Toxic megacolon symptoms

A

fever, tachycardia, abdominal distention, elevated WBCs, abdominal distention on radiograph

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15
Q

UC pathophysiology: colonic dysplasia/colorectal cancer (CRC)

A

risk of colonic dysplasia w/ transition to CRC is 5x greater in UC

cumulative risk of CRC is up to 20 - 30% at 30 years

Screening colonoscopy with biopsies recommended at 8 years after UC onset and every 1 - 2 years after that

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16
Q

CD pathophysiology

A

transmural inflammation

can occur anywhere in the GI tract

often discontinuous (normal bowel separating diseased bowel)

deep, elongated ulcers, cobblestone appearance

bowel wall injury may be extensive, associated with luminal narrowing

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17
Q

Where most common to see CD in GI tract?

A

terminal ileum

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18
Q

CD Pathophysiology Complications

A

small bowel stricture and obstruction possible

fistula common (20 - 40% lifetime risk)

less bleeding than UC (anemia is possible)

Risk of carcinoma is increased (not as high a risk as UC)

nutritional deficiencies: wt loss, growth failure in children deficiencies (iron deficiency anemia, vitamin B12, folate), hypoalbuminemia, hypokalemia, osteomalacia

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19
Q

Extraintestinal Manifestations of IBD: Bone and Joint

A

arthritis –> asymmetrical, migratory, typically involves one/few large joints

may be at increased risk for metabolic bone disease and osteoporosis (nutritional deficiencies: Ca and vitamin D, inflammation, hypogonadism, use of corticosteroids)

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20
Q

Extraintestinal Manifestations of IBD: Hematologic

A

anemia (prevalence up to 74%): iron deficiency, anemia of chronic disease, blood loss

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21
Q

Extraintestinal Manifestations of IBD: Coagulation***

A

1.5 - 3.6x increase risk of VTE

higher during flares, consider prophylaxis if admitted for flare

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22
Q

Extraintestinal Manifestations of IBD: Dermatologic and Mucocutaneous

A

variety of skin and mucosal lesions

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23
Q

Clinical Presentation of UC

A

highly variable

abdominal cramping

frequent BMs +/- blood +/- mucous

wt loss

paradoxical constipation possible

fever/tachycardia

extraintestinal: blurred vision/ocular signs

hemorrhoids, anal fissures

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24
Q

UC Laboratory Tests

A

decreased Hb/HCT

Increased ESR/CRP

leukocytosis, hypoalbuminemia (severe dz)

***fecal calprotectin (FC) and fecal lactoferrin (FC correlates with degree of inflammation, more sensitive and specific than serum markers)

diagnosis made on clinical suspicion and confirmed by endoscopy and biopsy

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25
UC: disease extent determined by ____________
endoscopy
26
4 ways to classify a UC patient
remission mild (< 4 stools, intermittent blood, normal hemoglobin) moderate-severe (> 6 stools, frequent blood in stools, Hgb < 75% normal) fulminant (> 10 stools, continuous bloody stool, required transfusion)
27
Clinical Presentation of CD
highly variable, characterized by periods of remission and exacerbation typically diarrhea and abdominal pain (hematochezia in ~50% of patients) Dx involves clinical evaluation in addition to endoscopic (upper and lower), laboratory, radiologic testing malaise, fever, abdominal pain, frequent BMs, wt loss
28
CD Laboratory Tests
Hb/HCT increased WBCs, ESR, CRP fecal calprotectin and fecal lactoferrin (+) anti-saccharomyces cervisiae antibodies (routine use not recommended)
29
CD Disease Classification
no global classification CDAI (Crohn's disease activity index): Used most frequently in research to gauge response to therapy and determine remission
30
How to classify CD***
Mild-moderate: ambulatory with minimal other Sx (dehydration, systemic toxicity), CDAI 150 - 220 Moderate-severe: patients who fail therapy for mild-moderate disease or those with fever, wt loss, abdominal pain/tenderness, vomiting, obstruction, anemia (here is where you really start to see Sx), CDAI 220 - 450 Severe-fulminant: persistent Sx or evidence of systemic toxicity despite corticosteroid or biologic tx or presence of cachexia (wasting disease), CDAI > 450
31
IBD Tx Overview
highly individualize. May include: - resolve acute inflammation/tx of disease flare - resolve and/or prevent complications - maintain remission - alleviate extraintestinal manifestations - avoid need for surgical palliation/cure Want to get patients off of steroids~! Inducing remission is an important aspect of therapy
32
IBD nutrition support
no specific diet shown to be beneficial address nutritional deficiencies (avoid parenteral nutrition unless absolutely necessary) some benefit with probiotic therapy
33
Nonpharmacologic therapy: Surgery
resecting areas of inflammation colectomy rates in UC ~ 5 - 30% (may be necessary if failed pharmacologic therapy) surgery indications for CD are less established
34
Certolizumab pegol (Cimzia)
only for CD SQ injection for mod-severe active CD we do see the development of antibodies against these drugs
35
Natalizumab (Tysabri)
anti-alpha-subunit of integrin's (prevents leukocyte adhesion/migration) CD: induces and maintains remission NOT used in combo w/ immunosuppressants ONLY for CD used in pts who fail TNF-alpha inhibitors d/c in pts w/ no benefits by 12 weeks --> associated w/ progressive leukoencephalopathy (PML) --> the activation of a latent virus --> can be rapidly debilitating or fatal. can test pts for JC antibodies drug is non specific
36
Vedolizumab (entyvio)
related to natalizumab inhibits alpha 4 beta 7 subunit which is gut specific targets lymphocytes active in the gut --> safer than natalizumab for UC and CD same ADRs as other biologics NOT associated w/ PML (still monitor neurological changes)
37
Ustekinumab (stelara)
for both UC and CD IL-12 and IL-23 specific dosed IV (wt based induction) and subQ ADRs similar as other biologics unique ADR: rapidly developing skin cancer, possible neurotoxicity (PRES, typically stops once d/c drug) TDM (therapeutic drug monitoring is possible)
38
For biologics...
...monitor tx response after start to see lack of response. Check [ ]
39
ADA
anti-drug antibodies
40
Tofacitinib (Xeljanz) - NOT A BIOLOGIC
Newer small molecule drug oral Janus kinase (JK) inhibitor UC only (for pts who had inadequate response/can't tolerate other therapies like TNF inhibitor) serious ADR, poorly tolerated, can be associated w/ neutropenia. Black box warning (2): increase mortality in RA pts 50 years and older w/ at least one CV risk factor AND thrombosis (PE, DVT, Arterial) in RA pts 50 years and older w/ at least one CV risk factor rapid onset do not use with other immunosuppressants or biologics if pt has renal impairment, maybe avoid this drug don't use with strong CYP3A4 inhibitor, but if you do, decrease dose by 50%
41
Ozanimod (Zeposia)
just approved in May of 2021! oral selective sphingosine-1-phosphate (S1P) receptor modulator. prevents lymphocyte mobilization to inflammatory sites moderate-severe UC only 7 day dose titration contraindicated in pts who had previous CV events, pts w/ sleep apnea, in pt's taking MAO inhibitor 21 hour half life metabolized by ALDH/____ ---> dont use in pts with hepatic impairment theoretical PML risk make sure pt is vaccinated we see increases in ALT 5 fold upper limit of normal. If LFTs have a > 5 fold increase, d/c drug associated with Hypertensive crisis has an active metabolite, avoid using with MAO inhibitors co-administration with CYP2C8 inducers + inhibitors --> can increase active metabolite --> coadministration not recommended
42
antimicrobials role
if pt has CD and they have fistulas and abscesses, use anti-microbials as adjunctive tx worry about Clostridium difficile because it mimics other Sxs
43
sulfasalazine (ASA Agent)
sulfapyridine (a sulfonamide) + 5-ASA (mesalamine) sulfapyridine is inactive but associated with ADRs 5-ASA is the active component (MOA = include anti-inflammatory effects, free radical scavenging)
44
Mesalamine (ASA Agent)
CAN administer mesalamine alone rapidly and completely absorbed in small intestine BUT NOT COLON generally topical is more effective than oral can use oral and topical together
45
Topical (enema) mesalamine for
left-sided disease
46
Suppository mesalamine for
proctitis (inflammation of the rectum lining)
47
Oral mesalamine for
delayed/controlled release examples - Apriso releases in colon and dissolves at >/= pH 6 - Lialda releases evenly throughout colon (terminal ileum) at pH >/= 6.8 - Pentasa releases in duodenum and ileum, up to 60% of dose reaches colon - Asacol HD and Delzicol dissolves at >/= pH 7. releases in terminal ileum - olsalazine (dipentum) released after colonic bacteria cleaves bond, release in colon - Balsalazide (colazal) released after colonic bacteria cleaves bond, releases in colon
48
Apriso releases in
colon
49
Lialda releases in
terminal ileum
50
Pentasa releases in
duodenum, ileum
51
Asacol HD, Delzicol releases in
terminal ileum
52
Osalazine releases in
colon
53
Balsalazide releases in
colon
54
sulfasalazine is associated with
ADRs (really NO reason to continue using this) >10%: N/V, HA, anorexia, rash <10%: anemia, hepatotoxicity, thrombocytopenia hypersensitivity rxns in sulfonamide allergy always titrate slowly
55
sulfasalazine monitoring parameters
CBC, LFTs, BUN/Scr
56
sulfasalazine drug interactions
antiplatelet/anticoagulants/NSAIDs --> may increase bleeding risk (ASA)
57
mesalamine _____________ than sulfasalazine
much better tolerated common SEs: N/V, HA up to 80% of pts intolerant to sulfasalazine will tolerate mesalamine
58
mesalamine drug interactions
antiplatelet/anticoagulants/NSAIDs --> may increase bleeding risk (ASA) agents affecting gastric pH (PPIs, H2RAs, antacids) --> could influence release of drug in pH dependent dosage forms
59
Corticosteroids used for ____________ but not for _____________
remission; maintenance corticosteroids = anti-inflammatory can be parenteral, oral or rectally rectal hydrocortisone: - suppositories, foam, enema - note that systemic absorption is possible with rectal formulations
60
Budesonide General Information
administered PO in CR formulation first pass metabolism --> minimal systemic exposure 6 - 8 g 8 weeks (16 weeks) Enterocort (brand) dosage form dissolves at PH > 5.5 Uceris (brand) dissolves at pH >/= 7. both PO and a foam
61
Budesonide drug interactions
CYP3A4 inhibitors --> may increase systemic exposure ADRs: similar to other glucocorticoids but it is generally well-tolerated
62
Systemic Corticosteroids
must taper parental typically for in-patients *may be used for disease flares/induction of remission give Ca and vitamin D while on steroids. may consider bisphosphonates in pts w/ osteoporosis monitoring: occasional bone mineral density scan (DEXA) in pts > 60
63
Oral Corticosteroids
Prednisone, Prednisolone
64
IV Corticosteroids
Methylprednisolone, hydrocortisone
65
Azathioprine (AZA) and Mercaptopurine (MP, 6-MP) facts
can be effective in long term tx of UC and CD Do not induce but can MAINTAIN remission generally reserved for pts who fail 5-ASA and/or patients who are refractory to/dependent on steroids b4 initiating, check genetics, check TPMT
66
Azathioprine (AZA) and Mercaptopurine (MP, 6-MP) not recommended for...
...MONOTHERAPY
67
AZA is a...
pro-drug that is rapidly converted to 6-MP
68
AZA and 6-MP ADRs
GI: N/V/D, anorexia, stomatitis hematologic: BONE MARROW SUPPRESSION hepatic: hepatotoxicity idiosyncratic: fever, rash, arthralgia, pancreatitis
69
AZA and 6-MP monitoring
TPMT (anything other than wild type = adverse effects) CBC LFTs
70
Cyclosporine facts
common in transplant patients effective inducing remission in pts w/ refractory IBD NOT recommended for CD Not for long term use NOT COMMON for IBD
71
Cyclosporine ADRs
nephrotoxicity (dose related) neurotoxicity metabolic (HTN, hyperlipidemia, hyperglycemia) other: GI upset, gingival hyperplasia, hirsutism
72
Cyclosporine monitoring
BP BUN/Scr LFTs Cya tr. conc
73
Cyclosporine drug interactions
substrate for CYP3A4 and P-glycoprotein drugs/foods that increase cyclosporine concentrations: azole anti-fungals, macrolide antibiotics, ca channel blockers, grapefruit and grapefruit juice drugs that decrease cyclosporine concentrations: phenytoin, rifampin
74
Tacrolimus and IBD...
used in refractory disease although role is less defined
75
Methotrexate (MTX) facts
can be used in CD. may have steroid sparing effects
76
MTX ADRs
hematologic: bone marrow suppression (add folic acid 1 mg/day) GI: N/V/D, stomatitis, mucositis (1mg folic acid) hepatic: cirrhosis, hepatitis, fibrosis pulm: hypersensitivity pneumonitis derm: rash, urticaria (hives), alopecia ALSO MTX IS TERATOGENIC
77
MTX contraindications
pregnancy pleural effusions chronic liver disease/EtOH abuse immunodeficiency preexisting blood dyscrasias leukopenia/t. cytopenia CrCl < 40 ml/min
78
MTX monitoring
CXR, CBC, Scr, LFTs
79
infliximab (Remicade)
anti-TNF alpha antibody CD and UC
80
adalimumab (Humira)
anti-TNF alpha antibody CD and UC
81
golimumab (Simponi)
human monoclonal anti-TNF-alpha antibody UC
82
certolizumab pegol (Cimzia)
human pegylaged anti-TNF alpha Fab fragment CD
83
natalizumab (Tysabri)
anti-alpha-subunit of integrin's (prevents leukocyte adhesion/migration) CD
84
vedolizumab (Entyvio)
anti-alpha-4-beta-7 integrin antibody (alpha-4-beta-7 integrin is expressed on subset of T-lymphocytes) UC and CD
85
ustekinumab (Stelara)
IL-12 and IL-23 antagonist CD and UC
86
Name the two small molecule drugs
ozanimod (Zeposia) tofacitinib (Xeljanz)
87
ozanimod (Zeposia)
oral sphingosine-1-phosphate (S1P) receptor modulator UC
88
tofacitinib (Xeljanz)
oral Janus kinase inhibitor (JK) inhibitor UC
89
Do NOT initiate TNF-alpha inhibitors during...
...active infections
90
TNF-alpha inhibitor ADRs
increase risk of serious infections (bacterial, viral, fungal) live vaccines contraindicated during tx and for 3 mo after risk of malignancy hepatosplenic T-cell lymphoma (HSTCL) risk risk of demyelinating disease may exacerbate CHF
91
Monitoring for TNF-alpha inhibitors
CXR, PPD, S/S infection, UA, CBC, Scr, lytes, LFTs, Hep B, Hep C
92
Infliximab (Remicade)
UC and CD (both moderate to severe) development of antibodies to infliximab --> decreased tx response combining with immunosuppressives may be of value hepatosplenic T-cell lymphoma (HSTCL) risk infusion related reactions
93
Adalimumab (Humira)
UC and CD (both moderate to severe) *can use for pts with poor response to infliximab can lead to the development of ADAs (human-derived, potentially less likely than infliximab)
94
Golimumab (Simponi)
UC (moderate to severe) can lead to the development of ADAs (human-derived, potentially less likely than infliximab) TDM possible: > 2.5 - 3.8 mcg/ml (week 6) and > 1.4 - 2.4 mcg/ml (maintenance)

Therapeutics IV (19 decks)

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