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Year 3 - Clinical (Winter) > 17 - IBD > Flashcards

17 - IBD Flashcards

1
Q

What are the types of inflammatory bowel disease?

A
  • Crohn’s and ulcerative colitis -> based on pathophysiology

- Indeterminate colitis: features of both CD and UC; make up 15% of IBD

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2
Q

Describe the pathophysiology of IBD

A
  • Genetic predisposition w/ infectious and immunological responses involved
  • Keys in CD include:
    • NOD 2 gene on chromosome 16 (carriers of 2 copy of risk alleles have CD risk 20-40x normal population)
    • NF KB
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3
Q

Ulcerative colitis

A
  • Disease confined to bowel wall
  • Rectum almost always affected then progresses proximally
    • Initial sx can include urgency or pain when passing bowel movement
  • GI tract involvement confined to terminal ileum, colon and rectum
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4
Q

Crohn’s disease

A
  • Extensive destruction of bowel wall; invasion of adjacent tissues
  • Any part of GI tract may be involved (mouth to rectum); most common in colon + another site
  • Can occur in patchy segments; have sections of healthy bowel in between affected areas
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5
Q

Extra-intestinal manifestations of CD

A
  • Many organs involved; may or may not be related to disease activity
  • Eye -> iritis, uveitis
  • Skin and joints -> arthritis
  • Liver -> increased LFTs in 40%; rarely severe
  • Psychological -> depression, anxiety
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6
Q

Classic features of IBD

A
  • Crohn’s -> RLQ tenderness, painful w/ masses, diarrhea w/ low grade fever
  • Ulcerative colitis -> rectal bleeding and diarrhea, no masses or specific tenderness
    • Bloody diarrhea is almost always either an infectious cause (from recent travel) or UC
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7
Q

Prognosis of IBD

A
  • Crohn’s -> some px only have one attack; more common for px to have combination of years in relapse or remission in first 8 years after diagnosis
  • UC -> relapses frequent (50-70% in 1 year w/o therapy); higher risk for rectal cancer (over decades)
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8
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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9
Q

Non-drug therapy for IBD

A
  • Avoid precipitants, such as:
    • NSAIDs – increase risk of CD ulcers, colitis (may still be used, but if causes a flare then stop taking)
    • Constipating drugs in severe UC
    • Smoking -> helps UC, worsens CD
  • Nutrition
    • Malnutrition common in moderate to severe disease (especially Crohn’s)
    • Some foods may trigger abdominal pain
    • Lactase deficiency due to active inflammation (CD)
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10
Q

Surgery for IBD

A
  • Crohn’s -> MB data suggests 20% need resection at 5 years, 40% at 20 years
    • 1/3 of those need another surgery in the next 10 years
    • Generally reserved for strictures and obstructions as there is an increased risk of CD recurrence at surgical site
  • UC = “cured” w/ a colectomy; some post-op issues (ex: pouchitis)
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11
Q

Drug therapy options for IBD

A
  • Aminosalicylates
  • Corticosteroids
  • Immunomodulators (ex: azathioprine)
  • Cytokines (ex: infliximab)
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12
Q

Aminosalicylates – types and MOA

A
  • Sulfasalazine and 5-ASA (mesalamine)
  • May act in a few ways:
    • Prostaglandins
    • Decrease cytokines
    • Free radical scavenging
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13
Q

Sulfasalazine – MOA, SE, and AE

A
  • Diazo bond cleaved by bacteria
  • Sulfapyridine rapidly absorbed into circulation from colon
  • SE = fever, fatigue, headache, N/V, diarrhea, dyspepsia; many are dose related; occur in about 30% of px
  • Adverse effects:
    • Allergic reactions – rashes (SJS)
    • Hematologic – hemolysis, agranulocytosis, thrombocytopenia
    • Drug interactions
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14
Q

Mesalamine (5 ASA)

A
  • *Backbone of mild to moderate UC
  • About 25% absorbed from colon; rest passes through colon unchanged
  • Products to target different sites:
    • Asacol -> released in terminal ileum
    • Pentasa -> 40% released in small intestine; increases diarrhea
  • Don’t really worry which one is used
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15
Q

Use of aminosalicylates (formulation, indication, and SE)

A
  • Oral, enemas, suppositories (all act topically)
  • Enema or suppository preferred 1st line agents w/ distal UC
  • Other than enemas, no clear signs that it has additive effects to steroids
  • For mild to moderate UC -> combo of oral and rectal used as an alternative 1st line induction
  • For CD or severe UC, common to use 2-4-fold higher doses
  • SE -> less w/ 5 ASA (mesalamine) than w/ sulfasalazine; most common = flatulence, abdominal pain, nausea, diarrhea, headache
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16
Q

Aminosalicylates – clinical pearls

A
  • Can give any of the QID 5-ASA or capsules as a single daily dose despite what product monographs say
  • Can give 5-ASA (non-acetylated salicylate) in a pt w/ ASA allergy and in px w/ sulfa allergy (as opposed to sulfasalazine)
  • 4-8 weeks should be enough time to assess their clinical response (and need to modify tx)
  • With oral, can try to decrease dose to 2 g/day if doing well; lower doses not recommended
  • If fail 4.8 g of one agent, not recommended to try a different 5-ASA product -> pick a different agent
  • Always look closely at adherence
17
Q

Aminosalicylates – efficacy in IBD

A
  • UC -> induce remission in about 20%; decrease relapse rate in ½ px; most effective in more distal disease
  • CD -> benefit in the colon; w/ ileal disease, data supporting use is soft (perhaps 10% better than placebo)
18
Q

Topical corticosteroids for IBD

A
  • Suppositories for proctitis
  • Enemas for left sided (sigmoid/rectum) disease
    • Mostly for UC mild to moderate left sided disease not controlled w/ 5-ASA (enema or suppository); faster onset but inferior
  • In CD, decent data w/ budesonide MMX in mild to moderate right side colonic and ileal disease; often used 1st line for induction in ileal/ colonic CD
    • Problem = maintaining remission w/ it alone
    • In UC, MMX is an alternative 1st line induction tx
19
Q

Systemic corticosteroids for IBD

A
  • Backbone of initial induction tx for moderate to severe UC and CD (of 5-ASA failures in UC)
  • Better for flares, up to 60-90% response in UC
  • Prednisone almost exclusively used
  • Severe (hospitalized) cases = IV (hydrocortisone, methylprednisolone)
  • Quick onset -> see effect w/in few days to 1 week; in outpatient setting, re-evaluate pt w/in 2 weeks
  • Don’t taper too fast once you get a response
  • In severe disease, if fail 1 week of steroids look to other agents
  • Not good long-term to prevent relapse though many CD px can’t get off them
20
Q

Azathioprine & 6-mercaptopurine – MOA, onset, interaction

A
  • Induce T-cell apoptosis, might be important mechanism of how it works
  • Helps induce and maintain remission in up to 2/3 of px w/ CD or UC; also heals fistulas
  • Allow 25-55% elimination of steroids
  • Slow onset, need at least 3-month trial (1 month to start working and 3 months to see full effect, therefore need something to bridge them until it kicks in if pt has active disease; commonly use prednisone for this)
  • Risk of relapse when discontinued
  • Azathioprine broken down into 6-mercaptopurine
  • *Big interaction w/ azathioprine is allopurinol
21
Q

Thiopurine methyltransferase (TPMT)

A
  • Major regulator of 6-TG concentration
  • Low TPMT activity leads to preferential metabolism to 6-TG (ie: increased efficacy and toxicity)
  • Enzyme activity is genetically determined (polymorphism)
  • *Some people can be poor metabolizers of azathioprine
22
Q

TPMT testing issues

A
  • Testing becoming a standard of care in GI guidelines
  • Genotyping done by most labs is only for 3 most common alleles; other 14 are considered “rare”
  • Especially important in Inuit and other populations
  • Problem = px w/ recent blood transfusion
  • Can’t rely on TPMT testing alone to predict who will have severe myelosuppression (still have to follow CBCs)
23
Q

AZA and 6-MP – SE and monitoring

A
  • Major SE = neutropenia, atypical infections, pancreatitis, skin rash
    • Small increase in malignancies (lymphomas) in CD
  • CBCs – weekly for 1st month then q2weeks for month 2-3 then monthly
  • Atypical infections occur later; generally, no PJP prophylaxis unless also on high dose steroids
  • Pancreatitis -> mostly in first 6 weeks; watch for new abdominal or back pain, vomiting
24
Q

Immunomodulators – methotrexate for IBD

A
  • Primarily for CD
  • Similar results to AZA (except for combo w/ TNF)
  • Not recommended yet for UC; consider if intolerant or refractory to AZA
  • Somewhat faster onset than AZA, but still need at least a 1-month trial
  • No set standard dosing regimen
  • Major SE = neutropenia, atypical infections, liver dysfunction, pneumonitis
25
Q

Anti-TNFs for IBD

A
  • Adalimumab, golimumab, infliximab
  • Ab binds to tumour necrosis factor; also act by inducing T cell apoptosis
  • For moderate to severe UC and CD and fistulizing CD
  • Recommended regimen = induction regimen followed by assessment of response before going on to maintenance tx
  • Usually see response at end of 1st week
26
Q

Pivotal anti-TNF trials

A
  • SONIC -> established safety and efficacy endpoints of anti-TNF or AZA alone or in combination therapy
  • STORI -> provided guidance on long-term outcome of px who were d/c’ed anti-TNF after in “deep remission” for at least 1 year
27
Q

Anti-TNFs – clinical pearl

A
  • If not responding to induction doses, no benefit in continuing into maintenance therapy w/ the same agent
  • If not responding to first agent, there is evidence of benefit in trying another one though response is lower than in the anti-TNF naive
28
Q

Infliximab SE

A
  • Nausea, URT infections, GI pain
  • Infections
    • Impairment of immune system (TB reactivation)
    • Too rapid closure of fistulas
29
Q

Hepatosplenic T-cell lymphomas

A
  • Reports showed occurred in very young people (12-31 y/o) & 6 of the 8 cases were fatal
  • All cases w/ infliximab; all px also taking AZA, 6-MP
30
Q

Infliximab – Ab formation

A
  • Develop to murine component, yet still see Ab formation in non-murine anti-TNF agents (ex: adalimumab)
  • Impact on effectiveness of infliximab important -> loss of response or need to increase dose/ frequency
  • Intermittent infliximab use also increases risk of Ab
  • B/c of this, usually won’t start infliximab unless pt also agrees to go on AZA/6-MP; also pre-treat w/ steroids if just starting tx
31
Q

Supportive therapies – antidiarrheals for IBD

A
  • Loperamide, codeine (ex: prior to playing sports to decrease ileostomy drainage) -> should always stop temporarily when CD deteriorates quickly
    • In UC -> ok in mild to moderate disease but never in severe disease as increases risk of toxic megacolon
  • Cholestyramine for bile salt related diarrhea -> ok for terminal ileum disease/ resection in CD
32
Q

Which agents induce remission in UC?

A
  • Aminosalicylates (w/ mild to moderate disease)
  • Corticosteroids
  • Cyclosporine
  • Anti-TNF (all 3)
  • Vedolizumab
33
Q

Which agents maintain remission in UC?

A
  • Aminosalicylates (w/ mild to moderate disease)
  • AZA, 6-MP, maybe MTX
  • Anti-TNF (all 3)
  • Vedolizumab
34
Q

Monitoring UC

A
  • Scoring systems of disease activity available and usually recommended
  • Rectal bleeding and diarrhea, frequency of stools/day
  • Anemia, low albumin, increased ESR, fever, abdominal pain -> more serious findings
  • Fever, new abdominal pain -> refer to MD
  • Adherence very important (especially w/ 5-ASA)
35
Q

Which agents induce remission in CD?

A
  • Corticosteroids

- Anti-TNFs

36
Q

Which agents maintain remission in CD?

A
  • Aminosalicylates?
  • Budesonide?
  • AZA, 6-MP, MTX
  • Anti-TNFs
  • Metronidazole, cipro (sometimes in ileal or colonic CD)
37
Q

Monitoring CD

A
  • Heterogeneous features
  • Heal fistula, decrease diarrhea and abdominal pain frequency and severity
  • Weight, Hgb, endoscopic features
  • Frequency of needing supportive therapy (ex: # loperamide tabs/week)
  • Frequency of missing work or school

Year 3 - Clinical (Winter) (30 decks)

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