2.Inflammatory bowel disease

1. Inflammatory Bowel Disease Professor mohammed Ahmed Bamashmos

2. Inflammatory bowel disease is an idiopathic and chronic intestinal inflammation • Types : • Ulcerative colitis : limited to the colon and rectum • Crohn’s disease : affects any portion of the GI tract from oesophagus to anus • Both exhibit extra intestinal inflammatory manifestations

3. Epidemiology • Ulcerative colitis – most common IBD • Peak age of onset of UC & CD is 15- 30 years – and 60 & 80 • M:F = 1:1 for UC and F>M for CD • Crohn’s diseases is more common in smokers, oral contraceptive users.

4. Etiology and pathogenesis : • Etiology and pathogenesis have not been defined • Current etiologic theories concerning IBD focus on environmental triggers, genetic factors, and immunoregulatory defects and microbial exposure • Two key points : • Strong immune responses against normal flora • Defects in epithelial barrier functions • Though idiopathic, it is postulated that IBD results from unregulated and exaggerated local immune response to commensals in gut, in genetically susceptible individuals

5. Genitical susceptibility : • Familial predisposition with no clear mendelian inheritance • Associated with HLA- DR1 , HLA- DR2, HLA-DR27 • Role of intestinal flora: • Exacerbate immune response by providing Ag and inducing constimulator and cytokines 🡪 t-cell activation 🡪 defects in barrier function • Infection: Chlamydia, atypical bacteria, measeals virus, helicobacter • Psychosocial factors: sensitive, reserved persons, death in family, divorce, conflict – STRESS. etc • Environmental factors : diets and smoking (Crohns’s)

6. PATHOPHYSIOLOGY: • The common end pathway is inflammation of the mucosal lining of the intestinal tract, causing ulceration, edema, bleeding, and fluid and electrolyte loss. • Both UC and CD , activated CD4+ T-cells in the lamina propria and pheripheral blood secrete inflammatory cytokines

7.  various antigenic stimuli🡪Cytokines, released by macrophages 🡪bind to different receptors and produce autocrine, paracrine, and endocrine effects🡪 leads to intestinal damage and increased permiability • T cells, type 1 (Th-1)= Crohn disease, • whereas, Th-2 cells = Ulcerative colitis

9. IBD: • Both UC and CD have waxing and waning in intensity and severity • In most cases, symptoms correspond with degree of inflammation • When patient is actively symptomatic, significant inflammation = flare-up of IBD • When asymptomatic, inflammation absent (or less) = in remission

10. Ulcerative colitis (UC): Pathophysiology – • Affects only the large intestine (very rarely terminal ileum may be inflamed superficially) • Always starts in rectum and is continuous until some proximal part of the colon ; and no "skip areas" • Involves the mucosa and submucosa with deeper layer unaffected ( except in fulminant disease).

11. Mucosa is: - Erythematous, has a granular surface that looks like a sand paper • In more severe diseases: - Hemorrhagic, edematous and ulcerated; formation of crypt abscesses • In fulminant disease : A toxic colitis or a toxic megacolon may develop ( wall become very thin and mucosa is severly ulcerated) • As UC becomes chronic, colon becomes rigid and loses its haustral (pouch-like) markings • Confined to rectum in 25% of cases; pancolitis in 10% of cases • when whole colon involved – 1-2 cm ileum involved = Backwash ielitis

12. Ulcerative colitis – clinical presentation The major symptoms of UC are: - Diarrhea - Rectal bleeding - Tenesmus - Passage of mucus - Crampy abdominal pain - Loss of weight - Psychological disturbances

13. Patients with proctitis usually pass fresh blood or blood-stained mucuseither mixed with stool or streaked onto the surface of normal or hard stool • When the disease extends beyond the rectum, blood is usually mixed with stool or grossly bloody diarrhea may be noted • When the disease is severe, patients pass a liquid stool containing blood, pus, fecal matter • Other symptoms in moderate to severe disease include: anorexia, nausea, vomitting, fever, weight loss

14. Investigation : • Active phase: rise in CRP, platelet counts, ESR , decrease in Hb. • Severe form : serum albumin will fall • Dig.:- history, clinical symptoms , negative stool examination for micro organisms; sigmoidoscopic appearance ;histology

15. Radiologic change of UC • The plain abd radiograph can show a dilated colon& small-bowel obstruction • Contrast barium enema: • Fine mucosal granularity • Mucosa become thickenned and superficial ulcers are seen (collar-button ulcers)– mucosa penetration • Loss of haustration • Shortened and narrowed colon . • Ileitis in UC (without the skip pattern)

16. CT & U/S best for demonstrating mesenteric inflammation, intra-abdominal abscesses and fistulas • Colonoscopy recommended for making diagnosis and determining severity of disease

17. Ulcerative colitis - complication • Hemorrhage • Perforation • Stricture • Toxic megacolon (transverse colon with a diameter of more than 5 cm to 6 cm with loss of haustration) • Malabsorbtion • Obstruction • Possibility of malignant transformation?

19. Colonic pseudopolyps

21. Ulcerative colitis:the left side of the colon is affected The image shows confluent superficial ulceration and loss of mucosal architecture.

26. lead pipe appearance

27. A 22-year-old man presented with abdominal pain, passage of blood and mucus per rectum, abdominal distention, fever, and disorientation. Findings from sigmoidoscopy confirmed ulcerative colitis. Abdominal radiographs obtained 2 days apart show mucosal edema and worsening of the distention in the transverse colon.

28. Diagnosis of UC • H&P • CT • Stool exam • Sigmoidscopy • Colonoscopy • Barium enema • Lab studies

29. Crohn’s disease (CD) • Crohn's disease differs from ulcerative colitis in the areas of the bowel it involves - it most commonly affects the last part of the small intestine and parts of the large intestine. • In 75% of patients with small intestinal disease the terminal ileum in involved in 90% • Crohn's disease isn't limited to these areas and can attack any part of the digestive tract • Crohn's disease generally tends to involve the entire bowel wall • Can have non-continuous pattern-”skip lesions”, with areas of severe inflammation with intervening normal mucosa • May be complicated by strictures, fistulas and abscesses

30. Distribution of gastrointestinal Crohn's disease. Based on data from American Gastroenterological Association.

31. Pathophysiology : • CD is a transmural process • CD is segmental with skip areas in the midst of diseased intestine • In one –third of patients with CD perirectal fistulas, fissures, abscesses, anal stenosis are present

32. mild disease is characterized by: apthous or small superficial ulcerations • In more active disease: stellate ulcerations fuse longitudinally and transversely to demarcate island of mucosa that are histologically normal • Cobblestone appearance is characteristic of CD (both endoscopically and by barium radiography)

33. Active CD is characterized by focal inflammation and formation of fistula tracts. • The bowel wall thickens and becomes narrowed and fibrotic, leading to chronic, recurrent bowel obstruction. • Aphtoid ulceration and focal crypt abscesses with loose aggregation of macrophages which form granulomas is formed in all the layers. • Transmural inflammation that is accompanied by fissures that penetrate deeply into the bowel wall

34. serpiginous ulcer, a classic finding in Crohn's disease

35. Crohn’s disease – sign and symptoms • Ileocolitis - right lower quadrant pain and diarhhea - palpable mass, fever and leucocytosis - pain is colickly and relieved by defecation - fistula formation leading to adjecent organs and bowel causing recurrent bladder infections , dyspareunia or foul smelling vaginal discharges. • Jejunoileitis - inflammatory disease is associated with loss of digestive and absorptive surface 🡪 malabroption and steatorrhoea

36. Crohn’s disease – sign and symptoms Colitis and perianal disease - low grade fever, malaise, diarrhea, crampy abdominal pain, sometimes hematochezia - pain is caused by passage of fecal material through narrowed and inflamed segments of large bowel Gastroduodenal disease - nusea, vomiting, epigastric pain - second portion of duodenum is more commonly involved than the bulb

38. The normal colon shows regular haustra and a transparent intact mucosa. The colon from the patient with Crohn's disease shows numerous deep ulcerations and areas of more normal appearing mucosa.

39. Endoscopic image of Crohn's colitis showing deep ulceration.

47. Crohn disease involving the terminal ileum. Note the "string sign" in the right lower quadrant

49. Crohn’s disease Diagnostic tests are the same except: 1- With Crohn’s will find string sign (segments of stricture separated by normal bowel) 2- With colonoscopy will find patchy areas of inflammations 🡪Skip areas & rectal sparing in CD 3- Need biopsy for definitive diagnosis • Complications: • Fistula formation • Peritonitis due to rupture of intraabdominal absecess • Intestinal obstructions • Massive hemorrhage • Malabsorption • Severe preianal diseases

50. The fistulae become symptomatic with drainage of fecal material around the anus (perianal fistulae), seepage of bowel contents through the skin (enterocutaneous fistulae), passage of feces through the vagina (rectovaginal fistulae)& pneumaturia or recurrent urinary tract infections (enterovesical fistulae).