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IBD lecture ppt FINAL.pptx
This document provides an overview of inflammatory bowel disease (IBD). It discusses the spectrum of IBD, which includes ulcerative colitis and Crohn's disease. The pathogenesis of IBD involves genetic, environmental, immune, and microbial factors that lead to chronic gut inflammation. Ulcerative colitis causes inflammation of the colon only, while Crohn's disease can impact any part of the gastrointestinal tract. The document outlines the clinical presentation, diagnosis, and management of both conditions, including medications like 5-aminosalicylic acid and biological therapies. It emphasizes achieving mucosal healing as the primary treatment goal for controlling symptoms and modifying the long-term course of IBD.
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IBD lecture ppt FINAL.pptx
- 1. Inflammatory Bowel Disease 30thmarch 2023 Dr DN SURYA
- 2. Spectrum of InflammatoryBowel Disorders Normal ? IBS Microscopic Colitis IBD Inflammation Drug induced colitis Diversion Colits
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- 4. Spectrum of IBD Ulcerativecolitis Crohn’s Disease Indeterminate colitis Term reserved for pathologists to describe a colectomy specimen which has overlapping features of ulcerative colitis and Crohn‘s IBD unclassified (IBDU) Minority of cases where a definitive distinction between UC, Crohn's disease, or other cause of colitis cannot be made Dignass A, et al;Definitions and diagnosis,Journal of Crohn's and Colitis(2012)
- 5. • Ulcerative Colitisis a chronic gastrointestinal condition which causes the inflammation of the digestive tract. • It is labelled as inflammatory bowel disease which occurs due to ulcerations on the inner walls of the intestine and rectum. • Ulcerative colitis is a painful long term condition which can cause severe distress, debilitating pain and other complications over time. It affects an estimated It is known to graduate and worsen over time, when left untreated. ULCERATIVE COLITIS
- 6. Ulcerative Colitis •Type ofIBD •Presentation: Bloody diarhea •Rectal involvement •Diffuse involvement •Colonic disease •Mucosal in most patients •Associated with complications •Medical & Surgical
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- 8. Genetic Factors •Risk intwins •CD> UC •Familial •Not simplistic Mendelian •7.5% of entire risk is genetic (cf 13% in CD) •Autophagy related genes: IRGM • IL-23R
- 9. Environmental •Antigenic stimulus •Ubiquitous antigen •Excessiveimmune response •Dysbiosis
- 12. Environmental/drugs Risk Factor CDUC Smoking ↑ ↓ Appendectom y ↑ ↓ NSAIDs ↑ ↑ Stress ↑ Antibiotics, Vitamin D, OCP ↓
- 13. Immune Dysregulation •Humoral: Antibodies •ASCA • CBir1 (Flagellin, Clostridium) • OmpC (E coli) • Anti-I2 (Pseudomonas) •Cellular • Innate : 1st line defence eg NLR, TLR • Adaptive : T cells and B cells
- 14. Pathology •Severity Distal> Proximal •Continuous •Symmetric •Sharptransition •Hyperemia, edematous, granular, friable, hemorrhagic, ulcers, •Pseudopoylps , mucosal bridging, featureless colon
- 16. Microscopy •Acute Colitis • Neutrophils •Cryptitis • Crypt abscess •Chronic Colitis • Crypt distortion • Branching • Widening • Crypt loss and mucodepletion
- 17. Differentiation of ulcerativecolitis from Crohn’s disease Ulcerative colitis Crohn’s disease Site of disease Distribution Colon only Diffuse Mucosal Any part of GI trat Focal (segmental)-skip areas Transmural Complications Fistulae/abscess or rarely Fistlae/abscess can occur occur Strictures appearance uncommon Cancer risk after long ++++ Standing disease Common ++
- 18. GROSS APPEARANCE OFUC AND CD
- 20. Extent at Presentation PROCTITIS LEFTSIDED DISEASE EXTENSIVE COLITIS
- 21. Clinical Presentation •Rectal Bleeding:Mixed or Streaked •Diarrhea with mucus •Tenesmus •Urgency •Abdominal pain? •Constipation? •Weight loss, Edema, Anemia?
- 22. Disease activity :Truelove and Witts Parameter Mild Moderate ‘in between mild and severe’ Severe Bloody stools/day <4 4 or more ≥6 Pulse <90 bpm ≤90 bpm > 90 bpm Temperature <37.5 °C ≤37.8 °C >37.8 °C Haemoglobin >11.5 g/dL ≥10.5 g/dL <10.5 g/dL ESR <20 mm/h ≤30 mm/h > 30mm/h CRP Normal ≤30 mg/L >30 mg/L Dignass A, et al; Definitions and diagnosis, Journal of Crohn's and Colitis(2012)
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- 24. Score Feature Stool Frequency Rectal Bleeding 0 1 23 Normal 1-2/day more than normal 3-4/day more than normal 5 or more than normal None Streaks of blood with stool less than half of the time Obvious blood with stool most of the time Blood alone passes Mucosal Appearance Normal Erythema, loss of vascular pattern, mild friablity Marked Erythema, loss of vascular pattern, friablity, erosion Spontaneous bleeding or ulceration Physicians global assessment Normal Mild Moderate Severe
- 25. Grade I: Loss ofvascular Pattern Erythema Grade III: Erosions Ulcers Spontaneous bleeding Grade II : Friability Petechiae
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- 27. Crohn’s disease •Intervening mucosa normal (skip lesions) •Longitudinal, deep Ulcers •Earliest lesion is Aphthoid ulcers • Rectal sparing •Terminal ileum involvement
- 28. Differential •Intestinal tuberculosis Ulcers, nodules Interveningmucosa normal Biopsy Differential of granulomatous Ileocolotis is a problem where both diseases are prevalent
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- 30. Crohn’s disease vsIntestinal TB Crohns Intestinal TB Age Sex (M:F) 20-50 yr any age 3:1 1:3 Malabsorbtion frequent infrequent Obstructive sx occasional Perianal dis/fistula frequent Ulcer/stricture long deep multiple frequent rare Transverse small <3 cm
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- 36. Treatment aims inIBD •Traditional treatment goals of IBD • Control of symptoms • ?Improvement in quality of life • Induction of remission • Improvement in quality of life • ? Reduction in complication related to inflammation •Treatment of goals in the era of biologicals & IM • Mucosal healing: Histological/Endoscopic • In addition to above, change in course of disease • Deep remission • Dream destination – achievable for some • Reduced risk of all complications • Change in course of disease – Concept of DMAIDs
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- 38. Treatment of UC •Inductionvs. Maintenance •Proctitis vrs Left-sided vs. Extensive disease •Severe disease •Steroid dependent/refractory disease
- 40. Serendipity in IBD a Sulfaslazine 5-Aminosalicylic acid Sulfapyridine
- 41. A bit ofHistory •1965: Placebo controlled trial of Sulfasalazine •Active component: 5-ASA (Mesalazine) •Azad Khan and Truelove: Retention enemas of 5-ASA •5-ASA unstable and absorbed in small bowel
- 42. Oral 5-ASAReleaseSites Stomach Small Intestine Large Intestine Azo bond AZO- COMPOUNDS Mesalaminein microgranules Pentasa® Mesalamine w/ eudragit-S Asacol®
- 43. Management of UlcerativeProctitis •Rectal ASA • Suppositories •Add oral ASA • Rectal steroids •Maintain with rectal ASA
- 44. Remission • Remission isdefined as complete resolution of symptoms and endoscopic mucosal healing • UCDAI <2 • Clinical practice: ‘Remission’ • Stool frequency ≤3/day with no bleeding and no urgency • Absence of visible blood and absent mucosal friability • 86% sensitivity • 76% specificity • Sigmoidoscopy to confirm mucosal healing is generally unnecessary in practice Dignass A, et al; Definitions and diagnosis, Journal of Crohn's and Colitis(2012)
- 46. Left -UC ManagementAlgorithm •5-ASA enema or foam •Hydrocortisone enema •Oral ASA (combination of oral and rectal) •Oral steroid if no response •Maintain with ASA enema ± oral ASA
- 48. Relapse • Relapse: Flareof symptoms in a patient with established UC who is in clinical remission • Spontaneously or after medical treatment • Pattern: • Infrequent (≤1/year) • Frequent (≥2 relapses/ year) • Continuous (persistent symptoms of active UC without a period of remission) Dignass A, et al; Definitions and diagnosis, Journal of Crohn's and Colitis(2012)
- 49. Steroid /Immunomodulator use •Steroid-dependent colitis: • Inability to reduce steroids below the equivalent of prednisolone 10 mg/day within 3 months of starting steroids, without recurrent active disease • Relapse within 3 months of stopping steroids • Steroid refractory: • Active disease despite prednisolone up to 0.75 mg/kg/day over a period of 4 weeks • Immunomodulator refractory: • Active disease or relapse in spite of thiopurines at an appropriate dose for at least 3 months (Azathioprine 2–2.5 mg/kg/day or mercaptopurine 1–1.5 mg/kg/day in the absence of leucopenia)
- 50. Steroids •Steroids introduced 1950s •Cornerstone •Response ❖30days: Oral steroids (40 mg prednisolone) ❖10 days: IV steroids
- 51. Azathioprine & 6-MP •Amajor limitation is the delay in the onset of action •Requires up to 3 months before becoming fully effective •Patients with severe disease often require colectomy before the azathioprine has had an opportunity to exert its full effects
- 52. Azathioprine & 6-MP •Sideeffects ❖Intolerance ❖Flu ❖Leucopenia ❖Hepatotoxicity ❖Pancreatitis GUT 2004
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- 54. Takeaways •ASUC: are mainstayof therapy •ASUC : Rescue medical therapy may prevent colectomy •ASUC: Infliximab is effective in ASUC •Moderate to Severe UC: Adalimumab and Golimumab are also effective
- 55. Biological agents fortreatment of IBD
- 56. Role of Surgery •Toxicmegacolon •Perforation •Dysplasia or malignancy Intolerable adverse effects of medical Rx •Refractory to medical Rx •Uncontrollable bleeding
- 57. Therapeutic Pyramid for ActiveUC Severe Moderate Mild Aminosalicylates Surgery Oral Steroids AZA/6-MP Systemic Corticosteroids Infliximab Cyclosporine
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- 59. Vienna and Montrealclassification for Crohn's disease Vienna Montreal Age at diagnosis disease A1 < 40 y < 16y A2 > 40 y 17 and 40 y A3 - > 40 y Location L1 ileal ileal L2 colonic colonic L3 ileocolonic ileocolonic L4 upper - isolated upper Behaviour B1 non-stricturing, non-penetrating non-stricturing, non-penetrating B2 stricturing stricturing B3 penetrating penetrating perianal disease - P modifier • L4 is a modifier that can be added to L1–L3 when concomitant upper gastrointestinal disease is present. • “p” is added to B1–B3 when concomitant perianal disease is present Gut. 2006
- 61. Phenotypes of CDpatients according to montreal Age at diagnosis (years) A1: ≤16 4 (15%) A2: 17-40 20 (74%) A3: >40 3 (11%) Disease location L1: ileal 3 (11%) L2: colonic 6 (22%) L3: ileocolonic 18 (67%) L4: isolated upper disease (0) Disease behaviour B1: non-stricturing, non-penetrating 17 (63%) B2: stricturing 4 (15%) B3: penetrating 6 (22%) p: peri-anal disease modifier 10 (37%) Hong Kong Med J 2007;13:436-41
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- 66. Treatment goals Historic goals •Inductionand maintenance of clinical response and remission Current evolution of Rx goals • Improvement in quality of life •Steroid free remission •Induction / maintenance of endoscopic healing •Reduction in hospitalization •Reduction in surgery
- 67. single goal Mucosal healing •Increasesteroid free remission •Reduce hospitalization •Reduce surgery need •Change the natural history of IBD by preventing bowel damage and disability •Reduce the risk of neoplasia
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- 69. Identifying the needfor biologics •Predictors for disabling disease • Age < 40 years • Extensive small bowel/ stricturing disease • Perianal disease • Smokers • Initial need for steroid therapy These patients may benefit from early biologics
- 70. SUTD (Step-Up/Top-Down): StudyDesign Conventional management (‘step-up’) (n=66) Early combined immunosuppression (‘top-down’) (n=67) Steroids + AZA/MTX Steroids + IFX Steroids + (episodic) IFX IFX + AZA SUTD
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- 72. Biologicals in IBD:Aims of therapy • Induction of remission • Maintenance of steroid-free remission • Closure of fistulizing disease • Minimization of complications and surgery • Prevention of disease-related mortality • Preservation of intestinal function • Improvement of the quality of life of patients • Minimization of the adverse effects of treatment
- 73. Conclusion •CD progressive disease •Mucosalhealing single desirable goal •Biologics preferred modality – Disease modifying drugs
- 74. Take home message •IBDis a common disorder with profound effect on morbidity •Despite advances, a substantial number of patients are not fully responsive to treatment or lose efficacy over time •Recent novel therapies are under development with the target for better disease remission
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