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Inflammatory bowel disease,


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Inflammatory bowel disease,

  1. 1. Inflammatory Bowel Disease Dr. Shivshankar Swamy M S
  2. 2.  Definitions  History  Epidemiology  Pathophysiology  Clinical features  Diagnosis with differentials  Complications  Management of disease  Ongoing research
  3. 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. 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. 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. 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. 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. 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. 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. 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. 11. Recent series on Crohn’s disease from India
  12. 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. 13. Etiopathogenisis Genetic susceptibility Environmental factors Host immunity
  14. 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. 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. 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. 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. 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. 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. 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. 21. Crohn’s Disease
  22. 22. Crohn’s Disease
  23. 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. 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. 25. Granuloma
  26. 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. 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
  28. 28. 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.
  29. 29. Clinical features
  30. 30. 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
  31. 31. 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)
  32. 32. 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
  33. 33.  Systemic symptoms  Weight loss  Fever  Sweats  Malaise  Arthralgias  A low-grade fever may be the first warning sign of a flare.
  34. 34. 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
  35. 35. 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.
  36. 36. 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 -
  37. 37. 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
  38. 38. 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
  39. 39. 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
  40. 40. CDAI  In remission <150  Mild-moderate 150-220  Moderate-severe 220-450  Fulminant >450
  41. 41. 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
  43. 43. 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.
  44. 44. Mucocutaneous  Pyoderma gangrenosum  Erythema nodosum  Granulomatous inflammation of the skin  Aphthous ulcers of the mouth  Angular cheilitis
  45. 45. Pyoderma Gangrenosum
  46. 46. Erythema Nodosum
  47. 47. Ocular  Occur in 6% of patients .  Episcleritis  Scleritis  Uveitis - the posterior segment  Keratopathy and night blindness
  48. 48. Hepatobiliary  Gallstones  Asymptomatic and mild elevations of liver biochemical tests  PSC more often is associated with UC  autoimmune hepatitis. Vascular  venous thromboembolism  arterial thrombosis.
  49. 49. Renal and Genitourinary  Inflammatory entrapment of the ureter  Uric acid and oxalate stones.  Membranous nephropathy &Glomerulonephritis  Renal amyloidosis.  . Penile and vulvar edema
  50. 50. 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
  51. 51. Abdominal pain, gastrointestinal bleeding, and/or intestinal ulceration  Ischemic colitis  Intestinal tuberculosis  Radiation-induced colitis  Arteriovenous malformations  NSAID enteropathy  Behcet disease  Colorectal malignancy
  52. 52. Diarrhea  AIDS  Celiac disease  Microscopic colitis  Irritable bowel syndrome  Lactose intolerance  Functional diarrhea  Gastrointestinal infections  Behcet disease  Colorectal malignancy
  53. 53. Investigations
  54. 54. 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
  55. 55. 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
  56. 56. 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.
  57. 57. Toxic megacolon
  58. 58. 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
  59. 59. Crohn’s colitis
  60. 60. String sign
  61. 61. lead-pipe or stove-pipe appearance
  62. 62. CT Enterography The sensitivity - 82% specificity - 89% accuracy - 85%.  Mural enhancement  Mesenteric fat stranding  The comb sign  Pseudosacculations
  63. 63. Comb sign
  64. 64. 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%.
  65. 65. 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
  66. 66. 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.
  67. 67. Ulcerative Colitis
  68. 68. Uses of colonoscopy  Determine the extent and severity of colitis  Provide tissue to assist in the diagnosis.  Therapeutic use is stricture dilation
  69. 69. 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
  70. 70. Complications of CD  Perforation  Abscess formation  Stricture & small bowel obstruction  Nutritional deficiencies  Cancer: small bowel adenocarinoma  Cancer: colon???
  71. 71. 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
  72. 72. 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
  73. 73. IBD - Treatment  Medications used in treatment  5- ASA  Antibiotics  Glucocorticoids  Immune modulators  Biologics
  74. 74. 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
  75. 75. 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)
  76. 76. 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
  77. 77. 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.
  78. 78. 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.
  79. 79.  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)
  80. 80. 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
  81. 81. 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.
  82. 82. 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.`
  83. 83. Side effects  Abnormal liver biochemical test results- LFT  Bone marrow suppression- CBC  Hypersensitivity reactions (fever, rash, arthralgia)  Infections  Lymphoma  Nausea, abdominal pain, diarrhea  Pancreatitis
  84. 84. 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
  85. 85. 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
  87. 87. 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.
  88. 88. 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.
  89. 89.  Risk factors for relapse include  male sex  leukocyte count > 6.0 109/L  CRP > 5.0 mg/L  Fecal calprotectin > 300 µg/g.
  90. 90. 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
  91. 91. Novel therapies CD  T-cell marker therapies  mesenchymal stem cells  Thalidomide  Interleukin (IL)-11  UC -  Anti-inflammatory proteins  Nicotine patch  butyrate enema  Heparin
  92. 92. 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
  93. 93.  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)
  94. 94. 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
  95. 95. 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
  96. 96. 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
  97. 97. 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;
  98. 98. 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)
  99. 99. 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.
  100. 100. Thank you
  101. 101. PG Quiz  Extraintestinal manifestation of IBD are all except? 1. Uveitis 2. Sclerosing cholangitis 3. Osteoarthritis 4. Skin nodules
  102. 102.  Drugs effective in CD are all except 1. 5 ASA 2. Cyclosporine 3. Steroids 4. Antibiotics
  103. 103.  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
  104. 104.  Following gene mutations predispose to CD except, 1. NOD2/ CARD !% 2. Autophagy related protein 3. MDR- 1 4. IL- 23 R
  105. 105.  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
  106. 106.  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
  107. 107.  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