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Chapter 28 Irritable Bowel Disease IBD

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IBD Chronic, idiopathic, relapsing inflammatory disorder of gastrointestinal tract (GIT) Mainly ulcerative colitis (UC) and Crohn s disease (CD) ... – PowerPoint PPT presentation

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Title: Chapter 28 Irritable Bowel Disease IBD


1
Chapter 28 Irritable Bowel Disease IBD
  • John Noviasky

2
IBD
  • Chronic, idiopathic, relapsing inflammatory
    disorder of gastrointestinal tract (GIT)
  • Mainly ulcerative colitis (UC) and Crohns
    disease (CD)
  • gt600,000 in U.S. have IBD
  • Table 28-1

3
Etiology
  • True cause unclear
  • may be genetic, infectious, environmental,
    autoimmunity
  • generally recognized as dysregulation of mucosal
    immune system
  • smoking decreases risk for UC, smoking increases
    risk for CD
  • NSAID -exacerbation of IBD

4
Etiology continued
  • Breast-fed infants decreased risk for IBD
  • some feel emotional stress plays a part but
    objective evidence limited
  • Increased in pro inflammatory cytokines,
    chemokines, prostaglandins, and reactive oxygen
    leads to increased inflammation and tissue
    destruction

5
UC (ulcerative colitis)
  • Shallow inflammation of the colon ranging from
    proctitis (rectal involvement only) to disease
    involving the entire colon, symptom worse in
    later
  • no fistulas, no fissures, no abscesses, no small
    bowel involvement
  • chronic, loose bloods stools (most common
    symptom)

6
UC continued
  • Tenesmus - (urge to defecate)
  • abdominal pain
  • mild UC - lt 4 stools/day, no systemic signs of
    toxicity and normal ESR
  • severe UC - gt 6 bloody stools/day, fever,
    tachycardia, anemia, ESRgt30
  • Relapse and remission common

7
CD (Crohns Disease)
  • Chronic, transmural, patchy, granulomatous,
    inflammatory disease that can involve entire GIT
    (mouth to anus)
  • discontinuous ulceration (skip lesions)
  • fistula formation, peri-anal involvement
  • severity of disease does not correlate directly
    with extent of bowel involvement

8
CD continued
  • Three main patterns of disease (predominantly
    inflammatory, stricturing, or fissuring)
  • patients often present with abdominal pain and
    chronic, often nocturnal diarrhea
  • weight loss, low grade fever and fatigue also
    common
  • mild to moderate CD - ambulatory pts who are able
    to tolerate oral feeding without systemic toxicity

9
CD continued
  • Moderate to severe CD - fever, weight loss,
    abdominal pain, nausea and vomiting and/or
    significant anemia
  • surgery often cures UC
  • disease often recurs after surgery in CD
  • Table 28-2
  • Extra intestinal complications of CD and UC
    (table 28-3)

10
Treatment
  • Specific therapy depends on disease location
  • Goals
  • relief of symptoms
  • improve QOL
  • maintain nutrition
  • relieve inflammation
  • maintain remission

11
Aminosalicylates
  • First class to show benefit
  • sulfasalzine (Azulfidine) - composed of 5-ASA
    attached to sulfapyridine. This allows for 5-ASA
    transport past upper intestine so can work in
    colon. Sulfapyridine - no benefit but can cause
    adverse effect.
  • 80 of dose reaches distal small intestine and
    colon where the diazo bond is broken.
    Sulfapyridine liberated in colon is poorly
    absorbed.

12
Aminosalicylates continued
  • 15 of pts discontinue d/t adverse effects (eg.
    Nausea, vomiting, headache, alopecia, anorexia)
    Table 28-4
  • Newer agents contain 5-ASA and are sulfa-free,
    Also pH-dependent (delays absorption until lower
    bowel) eg. Aminosalicylate, mesalamine
  • 90 of sulfasalazine intolerant pts can tolerate
    the new agents

13
Aminosalicylates continued
  • Mesalamine formulations
  • 1)Asacol - pH sensitive -releases in distal ileum
    and colon
  • 2)Pentasa- contains acid-resistant microgranules
    that release 5-ASA in duodenum, jejenum, ileum,
    and colon
  • 3) Rowasa- topical enema or suppository works at
    rectum and distal colon

14
Corticosteroids
  • Common treatment for moderate to severe
    flares/Not for maintenance
  • 40-60 mg prednisone
  • 30 may not respond
  • topical steroids (enemas, foams and supp.) can
    work for distal colitis in those that fail 5-ASA
    (can have adrenal suppression w/long term use)

15
Immunomodulators
  • Useful in steroid-dependent IBD
  • Azathioprine converts to 6-mercaptopurine
    metabolized to thioinosinic acid which inhibits
    purine ribonucleotide synthesis and cell
    proliferation
  • also, suppresses T-cell function

16
Immunomodulators continued
  • Some clinicians use steroids/inflixinnals to
    induce remission then maintain of Azathioprine
  • adverse effects-rash, nausea and diarrhea,
    myelosuppression can occur (monitor CBC q month x
    3 months then q 3 months) need to d/c drug d/t
    neutropenia 10 of the time

17
Immunomodulators continued
  • Methotrexate-folate antagonist-impairs DNA
    synthesis
  • inflammatory mediators
  • decrease IL-1
  • decrease T cells - decrease cytokines (IL-2) and
    interferon)
  • Not for UC
  • useful for CD in pts intolerant to azathioprine

18
Immunomodulators continued
  • Takes weeks to months to work
  • adverse effects- stomatitis, neutropenia, nausea,
    pneumonitis, alopecia, hepatotxicity
  • folic acid 1 mg daily
  • can decrease nausea/ stomatitis

19
Cyclosporine (CSA)
  • Selective to T-cell
  • quicker effect than Azathioprine, methotrexate
  • can manage severe UC refractory to steroids
  • 60 of pts with steroid-resistant or fistulizing
    CD respond to CSA

20
Infliximab
  • Binds and neutrolizes tumor necrosis factor (TNF)
    alpha
  • used to induce and maintain remission of moderate
    to severe CD (and fistulizing CD) in those with
    inadequate response to usual therapy
  • Dose-5mg/kg IV over 2 hours at O,2, and 6 weeks
    and then q 8 weeks
  • rapid response-with in days, 60 efficacy

21
Infliximab
  • Adverse effects -
  • immediate
  • fever, chills, pruritis, urticaria and
    cardiovascular problems
  • Delayed- serum sickness, pulmonary symptoms
  • Infections- pneumonia, cellulitis, sepsis,
    cholecystitis, endophthalmitis, furunculosis,
    reactivate TB, reactivate histoplasmosis

22
Infliximab continued
  • Avoid infliximab- pts with active infection,
    history of chronic infection, neural
    demyelinating disorder (exacerbate MS), heart
    failure (exacerbate heart failure)

23
Antibiotics
  • Used in CD not UC
  • flagyl and cipro have been used

24
Nutrition
  • CD - responds to bowel rest, TPN, or enteral
    nutrition
  • Bowel rest and TPN as effective as steroids for
    CD
  • not used for maintenance
  • fish oil - inhibits inflammatory cytokines,
    modest efficacy for UC and CD

25
Supportive Therapy
  • Pain relief and diarrhea control
  • loperamide/lomotil- used when obstruction or
    toxicity is not evident (watch for toxic
    megacolon-severe worsening of symptoms and
    abdominal distention

26
Surgery
  • Page 28-6

27
Irritable Bowel Syndrome (IBS)
  • Most common chronic disorder causing pts to seek
    medical treatment
  • functional bowel disorder in which abdominal pain
    is associated with defecation or a change in
    bowel habit (diarrhea-predominant/constipation
    predominant)
  • incidence 15-20

28
IBS continued
  • FM 31
  • cost about 33 billion/year

29
Pathophysiology
  • Psychological stress may exacerbate disease
  • hypersensitive colon
  • serotonin may play a role- gt95 of 5HT is in GIT,
    when released, 5HT triggers GI smooth muscle
    contraction and relaxation and mediates GI
    sensory function
  • IBS pts may have more 5HT than normal

30
Diagnosis
  • No good biochemical or physical markers
  • diagnosis is by symptoms Table 28-7
  • extensive testing not needed unless alarm
    symptoms (table 28-6)
  • treatment (fig. 28-4)

31
Question 1
  • How has drug-induced and parasitic cause of CMs
    diarrhea been ruled out?
  • What is classic triad of UC?
  • What is diarrhea in UC secondary to ?
  • What is range of diarrhea frequency?
  • What is the usual consistency of stools?
  • Besides diarrhea, what are other secondary
    results of UC?

32
Question 1 continued
  • What does bright-red blood mixed in stools
    indicate? Blood streaked stool?
  • What can happen to Hb, HCT, and Alb in UC?

33
Question 3
  • What is most effective agent to induce remission
    of acute, severe UC exacerbation?
  • How often does clinical improvement occur in pts
    taking prednisone 15-60 mg/day?
  • When and how should prednisone taper be handled?

34
Question 4
  • When should a patient receive parenteral
    nutrition?
  • What is definition of adequate response?
  • When is diarrhea considered resolved?
  • When might surgery be considered?

35
Question 5
  • What should initial dose of oral prednisone for
    CM be?

36
Question 6
  • When prednisone is given in equivalent doses
    orally and rectally, the incidence of side
    effects and therapeutic effects are_______?
  • Which are preferred for distal UC, 5 ASA supp or
    topical corticosteroids and why?

37
Question 7
  • What adverse effects are seen when steroids are
    used?
  • Which therapies should be considered in patients
    on more than 3 months of steroids?

38
Question 8
  • What is usual response rate of mild to moderate
    UC with use of 1.5 to 4.8 g/day of 5-ASA?
  • Which therapy is first-line for mild to moderate
    UC 5-ASA or steroids?
  • When should steroids be considered?
  • Which is preferred 5-ASA, sulfasalazine or
    mesalamine? Fig. 28-2

39
Question 14
  • When is a patient considered toxic (as in toxic
    megacolon)?
  • What are major complications of toxic megacolon?

40
Question 19
  • What is classic symptom triad of crohns disease
    (CD)
  • How do the usual stools of CD differ from UC?

41
Question 20
  • What is the most widely used agent for treatment
    of active symptomatic CD?
  • What is usual response rate of CD to steroids?
  • For what degree of severity of CD is
    sulfasalazine used?
  • How long does improvement take with use of
    sulfasalazine?

42
Question 20 continued
  • With what section of affected GI is sulfasalazine
    useful? Not useful?
  • Figure 28-3

43
Question 24
  • What is yearly cost of infliximab?
  • What premedications are sometimes used with
    infliximab?
  • What adverse reactions can occur with infliximab?
  • Which skin test should be given to patients
    considering infliximab and why?

44
Quesiton 26
  • Name some strategies that can help patients with
    IBS?

45
Quesiton 27
  • With which type of IBS is dietary fiber a
    reasonable first-line treatment?

46
Question 28
  • After fiber, what is usual therapy for
    Constipation Predominant (CP)-IBS
  • Why should stimulant laxatives generally be
    avoided for CP-IBS?

47
Question 29
  • How does tegaserod work?
  • What was the efficacy of tegaserod in clinical
    studies?
  • What was most common adverse effect reported?

48
Question 29 continued
  • What type of surgeries were increased in pts on
    tegaserod compared to control?
  • Why cant tegaserod be recommended for use in
    men?
  • In which pts is tegaserod contraindicated?

49
Question 30
  • Which antispasmodics are options for pain
    predominant IBS (PP-IBS)
  • should antispasmodics be used prn or RTC?
  • In what type of PP-IBS pts are antidepressants a
    reasonable option?
  • What dose of amitriptyline should be tried first,
    what is target dose, what is reasonable trial
    period?

50
Question 31
  • Which is preferred agent for diarrhea-predominent
    IBS (DP-IBS)
  • is RTC or prn antidiarrheal use preferred for
    DP-IBS?
  • When is prophylactic dosing a reasonable option?
  • Why is lomotil a second-line agent?
  • When is cholestyramine used for DP-IBS?

51
Question 31 continued
  • How does alosetron work?
  • What is most frequent adverse effect of
    alosetron?
  • what are severe adverse effects of alosetron?
  • What is new dosing regimen for alosetron?

52
Question 31 continued
  • Who should not use alosetron?
  • Who should d/c alosetron?
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