1. Inflammatory Bowel Disease
Dr. Shivshankar Swamy M S

2.  Definitions
 History
 Epidemiology
 Pathophysiology
 Clinical features
 Diagnosis with differentials
 Complications
 Management of disease
 Ongoing research

3. IBD
Inflammatory bowel disease is an idiopathic inflammatory
intestinal disease resulting from an inappropriate immune
activation to host intestinal microflora.
Types of IBD are
 Ulcerative colitis
 Crohn’s disease
 Indeterminate colitis

4. History
 Morgagni provided a description of intestinal inflammation
characteristic of Crohn's disease in 1761.
 After the identification of the tubercle bacillus by Koch in
1882 it was possible to describe persons with ileocecal disease
similar to intestinal tuberculosis but lacking the organism.
 In 1932, the landmark publication of Crohn, Ginzburg, and
Oppenheimer called attention to “terminal ileitis” as a distinct
entity and chronic disease.

5. History
 The term “Regional enteritis” embraced the focal nature of the
process, but failed to incorporate knowledge of the possibility
of disparate sites of involvement within the GI tract and
multisystemic nature.
 The term “Granulomatous enterocolitis” lost acceptance when
it became clear that granulomas were not a sine qua non of the
diagnosis.

6. History
 The name “Crohn's disease” has been adopted to encompass
the many clinical presentations of this pathologic entity. But for
the alphabetic priority these authors chose Crohn's disease.
 IT might well have been Ginzburg's or Oppenheimer's disease.

7. Epidemiology
 The incidence of UC is 3 times higher than that of CD. But
recent data suggest that the incidence of CD is increasing.
 The highest rates of IBD are seen in developed countries, and
the lowest in the developing regions;

8. Racial, sexual, and age-related differences
 Highest rates are seen in the Jewish populations
 The M:F ratio is approximately 1:1 for UC and females having
a slightly greater incidence in CD
 The age distribution of newly diagnosed IBD cases has double
peak, the 1st peak in people aged 15-40 years. A 2nd smaller
peak in patients aged 55-65 years

9. Two major types of IBD
 Crohn’s disease
 Incidence – 5.8 per 100,000 persons
 Prevalence - 116 per 100,000 persons
 Ulcerative colitis
 Incidence – 7.8 per 100,000 persons
 Prevalence - 156 per 100,000 persons
 Minnesota study, 2009

10. Indian perspective
 Probert CS and colleagues found out that the minimum
incidence on CD is 0.14/1lakh persons-years,
 Hindus have a much lower incidence of CD than Europeans

11. Recent series on Crohn’s disease from India

12. Incidence and prevalence of ulcerative colitis in Punjab,
North India
A Sood, V Midha, N Sood, A S Bhatia, and G Avasthi
 Crude prevalence rate- 44.3/ 100,000 inhabitants
 Crude incidence rate- 6.02 cases/ 100,000 inhabitants

13. Etiopathogenisis
Genetic
susceptibility
Environmental
factors
Host immunity

14. Genetics
 Increased risk among first-degree relatives is 14 to 15 times
higher than that of the general population
 Jews are at a 2-4 fold higher risk of developing IBD than non-
Jews of the same geographic location
 Studies in twins suggest that genetics is a more powerful
determinant of disease for CD(67%) than for UC(13%).

15. Genetics
Crohn’s disease Ulcerative colitis
 anti-OmpC ab is more common
among healthy family
members of CD probands
 3 imp. pathways in
pathogenesis of CD
1. NOD2/CARD15
2. Autophagy-related
genes
3. Interleukin (IL)-23
1. MDR 1
2. HLA-DR1
3. HLA-DR3,DQ2

16. ENVIRONMENTAL FACTORS
 Rising incidence of Crohn's disease
 Associated with higher socioeconomic status
 Breast-feeding to be protective for IBD
 Increased risk among women who use OCPs
 Increased intake of refined sugars and a paucity of fresh fruits
and vegetables

17. ENVIRONMENTAL FACTORS
 UC is more common among nonsmokers than current
smokers, whereas CD is more prevalent among smokers
 UC is more common in current light smokers than in heavy
smokers
 Several infectious organisms, including mycobacteria and
viruses, have been implicated in the pathogenesis of IBD

18. Humoral Immunity
 A marked increase in the number of plasma cells
 Proportional increase occurs in immunoglobulin Ig G synthesis
 IgG synthesis in UC is in the IgG1 and IgG3 subclasses,
whereas in CD it is IgG2
 Autoantibody in UC patients is pANCA, whereas in CD, Anti-
CBir1, Anti-OmpC or Anti I2 antibodies are seen.

19. Cellular Immunity
 Bacteria prompt immune responses through PRRs
 Activation of the PRRs results in downstream activation of NF-
κB, which then stimulates the transcription of various
proinflammatory cytokines
 Based on the cytokines they produce, CD4+ T cells have been
divided into three major immune phenotypes:
 T helper 1 – CD (IL-12)
 T helper 2 - UC
 T helper 17 (IL-23)

20. Pathology of CD
 Focal intestinal inflammation is the pathologic hallmark of CD
 Characterised by presence of aphthae on a background
uninvolved bowel
 Minute superficial ulcers, ranging from barely visible to 3 mm,
and are surrounded by a halo of erythema
 Coalesce into Linear or serpiginous ulcers with a stellate
appearance.
 Cobblestoned appearance

21. Crohn’s Disease

22. Crohn’s Disease

23.  Intestinal inflammation in CD is a transmural process
 The location of disease,
 35 – 50 % - both ileum and colon.
 35 % - small intestine
 15- 30% - isolated colonic disease
 Large ulcers, sinus tracts, and strictures, adhesion of bowel
loops are late features of CD
 fat wrapping - creeping of mesenteric fat onto the serosal
surface of the bowel.

24. Microscopic findings
 Granulomas are highly characteristic of CD
 Prevalence of granulomas in CD
 15% in endoscopic series
 70% in surgical series
 Pyloric metaplasia
 The presence of lymphoid aggregates in the submucosa and
external to the muscularis propria is a reliable sign of CD even
when granulomas are not seen
 TNF is the key cytokine in the formation of granulomas.

25. Granuloma

26. Ulcerative colitis
 At the time of initial presentation, approximately
 45% -limited to the rectosigmoid,
 35% - extending beyond the sigmoid
 20% of patients have pancolitis
 Continuous and symmetrical involvement
 Mucosa appears hyperemic, edematous, and granular in mild
disease becomes hemorrhagic, with visible punctate ulcers as it
progresses.

27.  In long-standing UC.
 Epithelial regeneration with recurrent attacks results in the
formation of pseudopolyps
 Atrophic and featureless colonic mucosa, associated with
shortening and narrowing of the colon

30. Microscopy
 Inflammation in UC characteristically is confined to the
mucosa
 Neutrophilic infiltration of colonic crypts leads to cryptitis &
crypt abscesses
 Cryptitis is associated with discharge of mucus from goblet
cells. Results in the characteristic histopathology of goblet cell
mucin depletion, formation of exudates, and epithelial cell
necrosis.
 Crypt architectural distortion or dropout of glands.

32. Clinical features

33. Manifestations of inflammatory bowel disease
 Recurrent abdominal pain and diarrhoea.
 Cramping
 Irregular bowel habits, passage of mucus without blood or pus
 Grossly bloody stools, occasionally with tenesmus: Typical of
UC, less common in CD
 Growth retardation and delayed or failed sexual maturation in
children
 Perianal disease in 50% of patients with CD

34. Patients with UC
 Rectal bleeding
 Frequent stools- Mucous discharge from the rectum
 Tenesmus (occasionally)
 Lower abdominal pain and severe dehydration from purulent
rectal discharge (in severe cases, especially in the elderly)

35. WHO- symptoms suggestive of inflamed GIT
 Diarrhea: mucus or blood may be present in the stool; can
occur at night; incontinence may occur.
 Constipation: this may be the primary symptom in UC
limited to the rectum; obstipation may occur and may
proceed to bowel obstruction
 Bowel movement abnormalities: pain or rectal bleeding
may be present, as well as severe urgency and tenesmus
 Abdominal cramping and pain: commonly present in the
right lower quadrant in CD; occur periumbilically or in the
left lower quadrant in moderate to severe UC
 Nausea and vomiting: occurs more often in CD than in UC

36.  Systemic symptoms
 Weight loss
 Fever
 Sweats
 Malaise
 Arthralgias
 A low-grade fever may be the first warning sign of a flare.

37. Signs
 Fever
 Tachycardia
 Dehydration
 Toxicity
 Pallor, anemia
 Toxic megacolon: patients appear septic, high fever with chills
tachycardia & increasing abdominal tenderness & distention
 Mass in the right lower abdominal quadrant: May be present in
CD

38. Perianal disease of CD
1. Skin lesions- include maceration, superficial ulcers,
abscesses, and skin tags
 type 1 (elephant ears) are typically soft and painless and
large
 type 2 are typically edematous, hard, and tender.
2. Anal canal lesions - fissures, ulcers, and stenosis
3. Perianal fistulas.

39. Unusual Presentations of CD
 Gastroduodenal - H-pylori-negative peptic ulcer disease,
dyspepsia or epigastric pain as the primary symptoms
 Esophageal - < 2% of patients.
 Dysphagia, odynophagia, substernal chest pain, and
heartburn
 Mouth ulcers
 Esophageal stricture and esophagobronchial fistula
 acute granulommatous appendicitis -

40. DISEASE BEHAVIOR IN CD
 Aggressive fistulizing disease
 anti-OMPC
 pANCA
 25% of pts present with an intra-abdominal abscess
 Indolent cicatrizing disease
 NOD2 variants
 anti-CBir1
 Anti I2

41. Aggressive fistulizing disease
 Fistulas are manifestations of the transmural nature of CD
 Perianal fistulas are common and occur in 15% to 35% of
patients.
 Enterovaginal fistulas occur in women
 Enterovesicular - recurrent polymicrobial UTI or as frank
pneumaturia and fecaluria.
 Enterocutaneous fistula after appendectomy
 Other types- enteroenteric, enterocolonic, and colocolonic
fistulas

43. Stricture
 Stricture is another characteristic complication of long-standing
inflammation
 Symptoms can include colicky, postprandial abdominal pain
and bloating, punctuated by more-severe episodes, and often
culminating in complete obstruction.
 String sign - markedly narrowed bowel segment amid widely
spaced bowel loops

44. CDAI
 In remission <150
 Mild-moderate 150-220
 Moderate-severe 220-450
 Fulminant >450

45. Ulcerative Colitis: Disease
Presentation
Mild Moderate Severe
Bowel movements <4/day 4-6/day >6/day
Blood in stools Small Moderate Severe
Tachycardia None <90/min >90/min
Fever None <99.5F >99.5F
Anemia Mild Moderate Severe
ESR <30 >30
Endoscopy Erythema,
decreased vascular
pattern, fine
granularity
Marked erythema,
coarse granularity,
absent vascular
markings, contact
bleeding, no
ulcerations
Spontaneous
bleeding,
ulcerations

46. EXTRAINTESTINAL MANIFESTATIONS

47. Musculoskeletal
 Clubbing
 Arthritic manifestations
 Peripheral arthropathy - 16% to 20%
 Pauciarticular arthropathy (type I, affecting four or fewer joints)
 Polyarticular arthropathy (type II, with five or more joints
affected)
 Axial arthropathies - 3% to 10%
 Metabolic bone disease
 Granulomatous vasculitis, periostitis and amyloidosis.

48. Mucocutaneous
 Pyoderma gangrenosum
 Erythema nodosum
 Granulomatous inflammation of the skin
 Aphthous ulcers of the mouth
 Angular cheilitis

49. Pyoderma Gangrenosum

50. Erythema
Nodosum

51. Ocular
 Occur in 6% of patients .
 Episcleritis
 Scleritis
 Uveitis - the posterior segment
 Keratopathy and night blindness

52. Hepatobiliary
 Gallstones
 Asymptomatic and mild elevations of liver biochemical tests
 PSC more often is associated with UC
 autoimmune hepatitis.
Vascular
 venous thromboembolism
 arterial thrombosis.

53. Renal and Genitourinary
 Inflammatory entrapment of the ureter
 Uric acid and oxalate stones.
 Membranous nephropathy &Glomerulonephritis
 Renal amyloidosis.
 . Penile and vulvar edema

54. DIFFERENTIAL DIAGNOSIS
 Intestinal tuberculosis
 Irritable bowel syndrome
 Anorexia Nervosa &Bulimia
 Ischemic bowel disease
 Neoplasia, including carcinoma and lymphoma
 Infectious diarrheas & Clostridium Difficile Colitis
 Celiac Sprue
 Collagenous and Lymphocytic Colitis

55. Abdominal pain, gastrointestinal bleeding, and/or intestinal
ulceration
 Ischemic colitis
 Intestinal tuberculosis
 Radiation-induced colitis
 Arteriovenous malformations
 NSAID enteropathy
 Behcet disease
 Colorectal malignancy

56. Diarrhea
 AIDS
 Celiac disease
 Microscopic colitis
 Irritable bowel syndrome
 Lactose intolerance
 Functional diarrhea
 Gastrointestinal infections
 Behcet disease
 Colorectal malignancy

57. Investigations

58. Investigations
 CBC
 Nutritional evaluation: Vitamin B12 , iron studies, folate &
other nutritional markers
 ESR and CRP levels
 Fecal calprotectin level
 Serologic studies: pANCA, ASCA, anti-CBir1
 Stool studies: Stool R/M, C/S, evaluation for Clostridium
difficile toxin

59. Imaging studies
 Upright chest and abdominal radiography
 Barium double-contrast enema radiographic studies
 Abdominal ultrasonography
 Abdominal/pelvic computed tomography scanning/magnetic
resonance imaging with enterography
 Colonoscopy, with biopsies of tissue/lesions
 Upper gastrointestinal endoscopy
 Capsule enteroscopy/double balloon enteroscopy

60. Plain radiograph
 In severe disease, the luminal margin of the colon becomes
edematous and irregular.
 Thickening of the colonic wall often is apparent on a plain film
 Plain films also are useful for detecting the presence of fecal
material.
 The presence of marked colonic dilatation suggests fulminant
colitis or toxic megacolon.

62. Toxic megacolon

64. Barium studies
 Aphthous ulcers, a coarse villus mucosal pattern, and thickened
folds.
 Pseudo sacculation of the antimesenteric border
 Cobblestone appearance
 Fistulas, sinus tracts, and fixed strictures
 The earliest radiologic change of UC seen is fine mucosal
granularity

65. Crohn’s colitis

66. String sign

67. lead-pipe or stove-pipe appearance

68. CT Enterography
The sensitivity - 82%
specificity - 89%
accuracy - 85%.
 Mural enhancement
 Mesenteric fat stranding
 The comb sign
 Pseudosacculations

70. Comb sign

71. MR enterography
 Intestinal wall thickening, submucosal edema, vasa recta
engorgement, and lymphadenopathy are signs of active diseas
 FIESTA images can add information regarding the functional
status of fibrotic segment
 MRI images yield a diagnostic accuracy of 91%.

73. Enteroscopy
 Aphthous ulcers
 Mucosal edema
 Cobblestoning
 Luminal narrowing
 Rectal sparing is more specific before treatment has been
initiated.
 Skip lesions - Crohn’s does not affect the intestinal mucosa in
a continuous fashion

75. Colonoscopy
 The hallmark of UC is continuous inflammation that begins in
the rectum.
 The earliest endoscopic sign of UC is a mucosal erythema and
edema
 As disease progresses, the mucosa becomes granular and
friable.
 In severe inflammation, the mucosa may be covered by yellow-
brown mucopurulent exudates associated with mucosal
ulcerations.

76. Ulcerative Colitis

77. Uses of colonoscopy
 Determine the extent and severity of colitis
 Provide tissue to assist in the diagnosis.
 Therapeutic use is stricture dilation

78. Tablet Enteroscopy
 Swallows encapsulated video camera
 Transmits an image to a receiver outside the pt.
 It is most commonly used for finding obscure sources of GI
blood loss,
 The images can find ulcerations associated with CD if
endoscopy and colonoscopy are unrevealing
 The major risk is the potential to get lodged at the point of
a stricture

79. Complications of CD
 Perforation
 Abscess formation
 Stricture & small bowel obstruction
 Nutritional deficiencies
 Cancer: small bowel adenocarinoma
 Cancer: colon???

80. Complications of UC
Toxic Megacolon:
 Defined as a transverse or right colon with a diameter of
>6 cm, with loss of haustration in patients with severe
attacks of UC.
 It occurs in about 5% of attacks and
 It can be triggered by electrolyte abnormalities and
narcotics.
 About 50% of acute dilations will resolve with medical
therapy alone
 Urgent colectomy is required for those that do not improve

81. Complicatins of UC
 Colon adenocarcinoma
 After 8–10 years of colitis, annual or biannual surveillance
colonoscopy with multiple biopsies at regular intervals should be
performed
 extensive mucosal involvement (pancolitis)
 family history of carcinoma of the colon.
 Perforation
 Massive hemorrhage

82. IBD - Treatment
 Medications used in treatment
 5- ASA
 Antibiotics
 Glucocorticoids
 Immune modulators
 Biologics

84. 5- ASA
 Mainstay of therapy for mild to moderate UC and CD
 Effective at inducing remission in both UC and CD( ?)
 Maintains remission in UC
 No role in maintenance of CD

86. Side effects
Sulfasalazine Anorexia, dyspepsia, nausea and
vomiting
Hemolysis
Neutropenia-Agranulocytosis
Folate deficiency
Reversible male infertility
Neuropathy
Sulfa-free 5-ASAs (mesalamine,
olsalazine, balsalazide)
Headache; drug fever; rash; paradoxical
disease exacerbation; pancreatitis;
hepatitis; pericarditis; pneumonitis;
nephritis; secretory diarrhea (olsalazine)

87. Antibiotics
 To treat perianal disease, fistulas, and active luminal Crohn's
disease.
 Beneficial in healing perianal fistulas.
 Metronidazole demonstrated a prophylactic effect on
endoscopic and clinical recurrence at one year
 Ciprofloxacin 1 g/day to be equivalent to mesalamine 4 g/day
in achieving remission of mild to moderately active CD at
week 6
 Combination was comparable with glucocorticoids in
achieving remission over 12 weeks

88. Glucocorticoids
 Moderate-to-severe cases benefit from glucocorticoids.
 Oral prednisone is started at doses of 40–60 mg/d
 Parenteral glucocorticoids
 Hydrocortisone- 300mg/d
 Methylprednisolone - 40–60 mg/d
 Topically applied glucocorticoids are also beneficial for distal
colitis
 Budesonide is used for 2–3 months at a dose of 9 mg/d, then
tapered.(entocort)
 No role in maintenance therapy in either UC or CD.

89. Pearls of glucocorticoid use
 Use an effective dose
 Do not overdose.
 Do not treat for excessively short periods.
 Do not treat for excessively long periods.
 Anticipate side effects.

90.  Patients are candidates for immunomodulators or anti-TNF
agents
 If flares are frequent (>1-2 times),
 If the duration of steroid use is prolonged
 If reduction of the steroid dose causes recurrence
of symptoms(steroid dependent),
 If steroids do not appear to be working (steroid refractory)

91. AZATHIOPRINE AND 6-MERCAPTOPURINE
 Purine analogs that interfere with nucleic acid metabolism
 Azathioprine - 2.0 to 2.5 mg/kg/day
 6-MP -1.0 to 1.5 mg/kg/day
 Used in patients with IBD in whom remission is difficult to
maintain with the ASA alone
 Used as glucocorticoid- sparing agents in upto 2/3rds of pts
 Patients who failed with antibiotics for a fistula

92. Selection of Pt. for Azathioprine
 AGA recommends that Pts should undergo an assessment of
the thiopurine methyltransferase genotype before starting
therapy with AZA or 6-MP.
 Individuals who have low enzyme activity or are homozygous
deficient in the TPMT mutation are at risk of very severe
leukopenia, with potential septic complications, and are not be
good candidates for therapy with these drugs.

93. how long to continue?
A randomized, controlled trial demonstrated a clinical relapse
rate of 21%, 18 months after withdrawal of azathioprine in
patients who had been in remission for at least 3.5 years on the
drug, compared with a relapse rate of only 8% in the group
who continued azathioprine.`

94. Side effects
 Abnormal liver biochemical test results- LFT
 Bone marrow suppression- CBC
 Hypersensitivity reactions (fever, rash, arthralgia)
 Infections
 Lymphoma
 Nausea, abdominal pain, diarrhea
 Pancreatitis

95. Methotrexate
 Dihydrofolate reductase inhibitor
 IM or SC MTX (25 mg/week) is effective in inducing
remission and reducing glucocorticoid dosage;
 15 mg/week is effective in maintaining remission in active CD.
 Potential toxicities include leukopenia, hepatic fibrosis and
Hypersensitivity pneumonitis

96. CYCLOSPORINE
 Lipophilic peptide with an inhibitory effects on both the
cellular and humoral immune systems.
 Dose is 2–4 mg/kg per day IV, in severe UC that is refractory
to IV glucocorticoid
 Hypertension, gingival hyperplasia, hypertrichosis,
paresthesias, tremors, headaches, and electrolyte abnormalities
are common side effects.
 Renal function and seizures are dose limiting side effects

97. BIOLOGIC THERAPIES

98. Anti-TNF therapy
 Infliximab, Adalimumab & certolizumab pegol
 Treatment of moderate to severe active CD or UC.
 Effective in CD patients with refractory perianal and
enterocutaneous fistulas
 If a patient does not have an initial response , currently it is
considered futile to try another.

99. Infliximab
 INDUCTION- 3 separate infusions of 5 mg/kg for moderate to
severe IBD at weeks 0, 2, and 6
 MAINTENANCE- infusions every 8 weeks
 Before anti-TNF agents are administered, screening should be
done for coexistent infection with perianal and abdominal
abscess (includingMycobacterium tuberculosis), and caution is
advised if a patient is a carrier for the hepatitis B virus.

100.  Risk factors for relapse include
 male sex
 leukocyte count > 6.0 109/L
 CRP > 5.0 mg/L
 Fecal calprotectin > 300 µg/g.

101. Side effects
 The FDA reviewed 147 postmarketing reports of leukemia and
69 cases of new-onset psoriasis
 Other morbidities
 acute infusion reactions
 severe serum sickness.
 infections.
 optic neuritis,
 seizures,
 new-onset or exacerbation of MS

102. Novel therapies
CD
 T-cell marker therapies
 mesenchymal stem cells
 Thalidomide
 Interleukin (IL)-11
 UC -
 Anti-inflammatory
proteins
 Nicotine patch
 butyrate enema
 Heparin

103. Step up approach
 Step I – Aminosalicylates -For treating flares and maintaining
remission; more effective in UC than in CD
 Step IA – Antibiotics:
 Used sparingly in UC (limited efficacy, increased risk for
antibiotic-associated pseudomembranous colitis);
 In CD, most commonly used for perianal disease, fistulas,
intra-abdominal inflammatory masses

104.  Step II – Corticosteroids (intravenous, oral, topical, rectal): For
acute disease flares only
 Step III – Immunomodulators: Effective for steroid-sparing
action in refractory disease; primary treatment for fistulas and
maintenance of remission in patients intolerant of or not
responsive to aminosalicylates
 Step IV – : Tend to be disease-specific (ie, an agent works for
CD but not for UC, or vice versa)

105. Management of remission
 A general rule of thumb is that once remission is achieved, the
medications used to achieve remission should be continued,
except steroids, which should be tapered off, because they have
no role in maintaining remission

106. Adjunctive Therapies
 Antidiarrheal (diphenoxylate and atropine, loperamide,
cholestyramine)
 anticholinergic agents(eg, dicyclomine, hyoscyamine)
 Vitamin supplementation
 Iron supplementation
 Smoking cessation in CD pts
 Patients with active CD respond to bowel rest, along with TPN,
but does not reduce inflammation in UC.
 Probiotics, Prebiotics, and Synbiotics

107. Surgery
 Indications for urgent surgery
Toxic megacolon refractory to medical management
Fulminant attack refractory to medical management
Uncontrolled colonic bleeding
 Indications for elective surgery
Long-term steroid dependence
Dysplasia or adenocarcinoma found on screening
biopsy
Disease present 7-10 years

108. Surgical intervention in IBD includes the following:
 UC: Proctocolectomy with ileostomy, total proctocolectomy
with ileoanal anastomosis, UC is surgically curable
 Fulminant colitis: Surgical procedure of choice is subtotal
colectomy with end ileostomy and creation of a Hartmann
pouch
 CD: Surgery (not curative) most commonly performed in cases
of disease complications;

109. Pouchitis
 Patients who undergo the IPAA procedure may develop an
idiopathic inflammation termed “pouchitis,”
 which typically presents with variable symptoms of increased
stool frequency, rectal bleeding, abdominal cramping, rectal
urgency, tenesmus, incontinence & fevers.
 Patients who develop typical symptoms and signs of pouchitis
after the IPAA should be treated with a short course of
antibiotics (Evidence A)

110. Factors influencing disease relapse and remission
 The use of NSAIDs and antibiotics
 Bacterial and viral infections
 Smoking
 Psychosocial stress.
 Both the severity and extent of disease are important
prognostic factors after the first attack of UC.

113. Thank you

114. PG Quiz
 Extraintestinal manifestation of IBD are all except?
1. Uveitis
2. Sclerosing cholangitis
3. Osteoarthritis
4. Skin nodules

115.  Drugs effective in CD are all except
1. 5 ASA
2. Cyclosporine
3. Steroids
4. Antibiotics

116.  A 41 yr old male present wit recurrent episodes of bloddy
diarrhea for 3 yrs, despite adequate doses of sulfasalzine. He
had several exacerbations requiring steroids to control the
flares. Wat would be the next line of treatment
 Methotrexate
 Azathioprine
 Cyclosporine
 Cyclophosphomide

117.  Following gene mutations predispose to CD except,
1. NOD2/ CARD !%
2. Autophagy related protein
3. MDR- 1
4. IL- 23 R

118.  Which of the following features is more commonly associated
with ulcerative colitis than with Crohn’s disease?
 (A) Fistulas
 (B) Rectal bleeding
 (C) Segmental involvement
 (D) An abdominal mass
 (E) Mesenteric lymph node involvement

119.  A 40-year-old man has a history of ulcerative colitis. Features
of his illness that would contribute to an increased risk of
developing colon cancer include which of the following?
 (A) Disease duration of less than 10 years
 (B) History of toxic megacolon
 (D) Presence of pseudopolyps on colonoscopy
 (E) High steroid requirements

120.  A 20-year-old woman with a family history of IBD presents
with a history of intermittent right lower quadrant pain and
diarrhea. Colonoscopy shows no evidence of rectal
involvement but does show aphthous ulcerations in the
proximal colon. Of the following serologic markers, which has
a 50% likelihood to be elevated in this situation?
1. Anti-goblet cell autoantibody
2. Elevated titre against Entamoeba histolytica
3. Anti-Saccharomyces cerevisiae antibody
4. pANCA