L14 inflammatory bowel disease sr f


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L14 inflammatory bowel disease sr f

  1. 1. Inflammatory Bowel diseaseSR-fContLECTURE 14
  2. 2. • Crohn disease and ulcerative colitis arechronic relapsing inflammatory disorders ofunknown orgin, collectively known asidiopathic inflammatory bowel disease (IBD),which share many common features.
  3. 3. IBD• Inflammatory• Chronic• Relapsing• Autoimmune ?• Idiopathic
  4. 4. They result from an abnormal local immune response against thenormal flora of the gut, and probably against some self antigens, ingenetically susceptible individuals.The pathogenesis of IBD involves genetic susceptibility, failure ofimmune regulation, and triggering by microbial flora.
  5. 5. Crohn Disease“terminal ileitis” or“regional enteritis
  6. 6. •A systemic inflammatorydisease withpredominant intestinalinvolvement.
  7. 7. • When fully developed , Crohn disease ischaracterized by:• Sharply limited transmural involvement ofthe bowel by an inflammatory process withmucosal damage• Presence of noncaseating granulomas• Fistula formation
  8. 8. Common symptoms of Crohns disease:•abdominal pain•diarrhoea•weight loss
  9. 9. Less common symptoms include:• poor appetite• fever,• night sweats• rectal pain/rectal bleeding
  10. 10. ExtraintEstinalsymptomsSome patients with Crohns disease also developsymptoms outside of thegastrointestinal tract;thesesymptoms include:• arthritis• skin rash• inflammation of the iris of the eye.
  11. 11. UlcerativeColitis
  12. 12. • Ulcerative Colitis is an ulceroinflammatorydisease affecting the colon, which islimited to the mucosa andsubmucosa, except in the most severecases.
  13. 13. • It begins in the rectum and extendsproximally in a continuous fashionsometimes involving the entire colon.
  14. 14. Epidemiology• More common in USA & Western countries.The incidence has risen in recent decades.More common among whites. No sexpredilection. A peak incidence between ages20-25 years. Has a familial association.
  15. 15. Morphology• Gross:• Rectum & Sigmoid --may involve entire colon.• The lesions are continuous.• inflammatory destruction of the mucosa withmacroscopic appearance of :• Hyperemia, edema, and granularity withfriability and easy bleeding.
  16. 16. • With severe active disease:• Extensive and broad based ulceration in thedistal colon.• Pseudopolyps• Toxic megacolon
  17. 17. • A diffuse, predominantly mononuclearinflammatory infiltrate in the lamina propriaand Crypt abscesses.
  18. 18. Complications:Perforation, peritonitis, abscess• Toxic megacolon• Venous thrombosis• Carcinoma
  19. 19. Clinical features• Bloody mucoid diarrhea• Cramps• Tenesmus• Colicky lower abdominal pain• Fever• Weight loss
  20. 20. Extra-intestinal symptoms• Migratory polyarthritis,• sacroilitis,• ankylosing spondilitis,• uveitis,• erythema nodosum and• hepatic involvement (pericholangitis andprimary sclerosing cholangitis).
  21. 21. Diagnosis•Endoscopy•Biopsy
  22. 22. Comparison of CD &UC• Crohn disease and ulcerative colitis differ inmany respects, including the natural history ofthe disease, pathological aspects, and in thetypes of therapies and responses totreatment.
  23. 23. Comparisons of various factors in Crohns disease and ulcerativecolitisCrohns DiseaseCrohns Disease Ulcerative ColitisUlcerative ColitisInvolves terminal ileumInvolves terminal ileum CommonlyCommonly SeldomSeldomInvolves colon?Involves colon?Involves rectum?Involves rectum?UsuallyUsuallySeldomSeldomAlwaysAlwaysUsuallyUsuallyBile duct involvement?Bile duct involvement? Not associatedNot associated Higher rate of PrimaryHigher rate of Primarysclerosing cholangitissclerosing cholangitisDistribution of DiseaseDistribution of Disease Patchy areas ofPatchy areas ofinflammationinflammationContinuous area ofContinuous area ofinflammationinflammationEndoscopyEndoscopy Linear and serpiginousLinear and serpiginous(snake-like) ulcers(snake-like) ulcersContinuous ulcerContinuous ulcerDepth of inflammationDepth of inflammation May be transmural, deepMay be transmural, deepinto tissuesinto tissuesShallow, mucosalShallow, mucosal
  24. 24. FistulaeFistulae,, abnormalabnormalpassageways betweenpassageways betweenorgansorgansCommonlyCommonly SeldomSeldomBiopsyBiopsy Can haveCan have granulomagranulomatata Crypt abscesses andCrypt abscesses andcryptitiscryptitisSurgical cure ?Surgical cure ?SmokingSmokingOften returnsOften returnsfollowing removal offollowing removal ofaffected partaffected partHigher risk for smokersHigher risk for smokersUsually cured byUsually cured byremoval of colon,removal of colon,Lower risk for smokersLower risk for smokersAutoimmune diseaseAutoimmune disease Generally regarded asGenerally regarded asan autoimmunean autoimmunediseasediseaseNo consensusNo consensusCancer risk?Cancer risk? Lower than ulcerativeLower than ulcerativecolitiscolitisHigherHigher than Crohnsthan CrohnsComparisons of various factors in Crohns disease andUC (Cont.)
  25. 25. Features UC CDMorphologicDistribution Diffuse,mucosal&submucosal,left sidedFocal, trans-mural, rightsidedMucosal atrophy Marked MinimalCytoplasmic mucin ↓ PreservedLymphoid aggregate Rare CommonEdema Minimal marked
  26. 26. Features UC CDMorphologicHyperemia Extreme MinimalGranuloma Absent 60% presentFissuring Absent PresentCrypt abscess Common RareLymph nodes Reactive Granulomas
  27. 27. Acute AppendicitisThe appendix is a normal true diverticulum ofthe cecum that is prone to acute and chronicinflammation. Acute appendicitis is mostcommon in adolescents and young adults, butmay occur in any age group. The lifetime risk forappendicitis is 7%;males are affected slightly more often thanfemales.
  28. 28. • Despite the prevalence of acute appendicitis,the diagnosis can be difficult to confirmpreoperatively and may be confused withmesenteric lymphadenitis, acute salpingitis,ectopic pregnancy, mittelschmerz (paincaused by minor pelvic bleeding at the timeof ovulation), and Meckel diverticulitis.
  29. 29. PathogenesisAcute appendicitis is thought to be initiated byprogressive increases in intraluminal pressurethat compromise venous outflow. In 50% to80% of cases, acute appendicitis is associatedwith overt luminal obstruction,usually caused by a small stone-like mass ofstool, or fecalith, or, less commonly, agallstone, tumor, or mass of worms (oxyuriasisvermicularis).
  30. 30. • Ischemic injury and stasis of luminalcontents, which favor bacterial proliferation,trigger inflammatory responsesincluding tissue edema and neutrophilicinfiltration of the lumen, muscular wall, andperiappendiceal soft tissues.
  31. 31. MorphologyIn early acute appendicitis subserosal vessels arecongested and there is a modest perivascularneutrophilic infiltrate within all layers of thewall.The inflammatory reaction transforms the normalglistening serosa into a dull, granular,erythematous surface.
  32. 32. • Diagnosis of acute appendicitis requiresneutrophilic infiltration of the muscularispropria.
  33. 33. • In more severe cases a prominentneutrophilic exudate generates a serosalfibrinopurulent reaction. As the processcontinues, focal abscesses may form withinthe wall (acute suppurative appendicitis).
  34. 34. • Further appendiceal compromise leads tolarge areas of hemorrhagic ulceration andgangrenous necrosis that extends to theserosa creating acute gangrenousappendicitis, which is often followed byrupture and suppurative peritonitis.
  35. 35. Clinical Features• Typically, early acute appendicitis producesperiumbilical pain that ultimately localizes tothe right lower quadrant, followed bynausea, vomiting, low-grade fever, and amildly elevated peripheral white cell count
  36. 36. Charles Heber Mc BurneyAmericansurgeon
  37. 37. • Regrettably, these signs and symptoms areoften absent, creating difficulty in clinicaldiagnosis. In some cases, a retrocecalappendix may generate right flank or pelvicpain, while a malrotated colon may give riseto appendicitis in the left upper quadrant. Inother cases the peripheral leukocytosis maybe minimal or, alternatively, so great thatother causes are considered.
  38. 38. • The diagnosis of acute appendicitis in youngchildren and the very elderly is particularlyproblematic, since other causes of abdominalemergencies are prevalent in thesepopulations, and the very young and old arealso more likely to have atypicalclinical presentations.
  39. 39. • Given these diagnostic challenges, it shouldbe no surprise that even highly skilledsurgeons remove normal appendices. This ispreferred to delayed resection of a diseasedappendix, given the significant morbidity andmortality associated with appendicealperforation. Other complications ofappendicitis include pyelophlebitis, portalvenous thrombosis, liver abscess, andbacteremia.