ibd
DESCRIPTION
IBDTRANSCRIPT
Inflammatory Bowel Disease (IBD)
Presented by:
M. Sufian
student of Nutrition Sciences(B/Sc)
Science & Research Branch of Islamic Azad University(SRBIAU)
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Contents:• Introduction• Occurrence & Commonness• Pathophysiology• Diagnosis
Symptoms Signs
• Complications• Treatments
Medical Surgical
• Q & A• References
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• IBD:Chronic inflammatory diseases of GI tract of unknown etiology
• Commonly refers to 1) ulcerative colitis Ulcerative colitis (UC) affects only the large intestine (*)
2) Crohn’s disease Crohn’s disease (CD) can affect any part of the gastrointestinal tract but most frequently attacks the distal third of the small intestine & the colon
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Introduction:
Introduction (continued)
• Diagnosed using clinical, endoscopic, and histologic criteria
• No single finding is absolutely diagnostic for one disease or the other
• Approx. 20% of patients have clinical picture that falls between ulcerative colitis and Crohn’s disease (indeterminate colitis)
• Many of the treatments available are effective for both diseases
• Extraintestinal manifestations may be present in both
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Occurrence & Commoness
• Approx. 1 million people in U.S. have ulcerative colitis (UC) or Crohn’s disease (CD)
• Most commonly observed in industrialized nations; lowest in developing regions (also higher rate in urban areas vs. rural areas)
• Incidence higher in Ashkenazi Jews • Incidence is slightly higher in females than males• Vast majority diagnosed between ages 15-40
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Pathophysiology
• Still under investigation• ? Defect in function of the intestinal immune
system (breakdown in defense barrier)• Exposure of mucosa to microorganisms results in
inflammatory process causing ulceration, bleeding and loss of fluids and electrolytes
• ? Genetic predisposition (esp. when ileal disease involved)
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Pathophysiology(Cont’d)
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Pathophysiology in Crohn's disease vs. ulcerative colitis
Crohn's disease Ulcerative colitisAutoimmune disease
Widely regarded asan autoimmune disease
No consensus
Cyypkineresponse
Associated with Th
17Vaguely associated with Th2
Pathophysiology(Cont’d)
Diagnostic:Symptoms
Symptoms in Crohn's disease vs. ulcerative colitis
Crohn's disease Ulcerative colitis
Defecation Often porridge-like[6],sometimes steatorrhea
Often mucus-likeand with blood[6]
Tenesmus Less common[6] More common[6]
Fever Common[6] Indicates severe disease[6]
Fistulae Common[7] Seldom
Weight loss Often More seldom
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Diagnostic:Signs
Findings in diagnostic workup in Crohn's disease vs. ulcerative colitis
Sign Crohn's disease Ulcerative colitis
Terminal ileum involvement Commonly Seldom
Colon involvement Usually Always
Rectum involvement Seldom Usually[8]
Involvement aroundthe anus Common[7] Seldom
Bile duct involvement No increase in rate of primary sclerosing cholangitis Higher rate[9]
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Diagnostic:SignsFindings in diagnostic workup in Crohn's disease vs. ulcerative colitis
Sign Crohn's disease Ulcerative colitis
Distribution of Disease Patchy areas of inflammation (Skip lesions)
Continuous area of inflammation[8]
Endoscopy Deep geographic and serpiginous (snake-like) ulcers Continuous ulcer
Depth of inflammation May be transmural, deep into tissues[2][7] Shallow, mucosal
Stenosis Common Seldom
Granulomas on biopsyMay have non- necrotizing non-peri- intestinal crypt granulomas[7][10][11]
Non-peri-intestinal crypt granulomas not seen[8]
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Ulcerative colitis vs. Crohn’s
• Rectal bleeding common• Abdominal pain uncommon• Rectal involvement almost 100%• Fistula formation rare• Stricture & obstruction rare• Perirectal, perianal abscesses
uncommon• Continuous involvement• Mucosa & submucosa involved• Small bowel not involved (*)• Risk of malignancy greatly
increased
• Occasional rectal bleeding• Abdominal pain common• Rectal involvement 50%• Fistula formation common• Stricture and obstruction common• Perirectal, perianal abscesses
common• Discontinuous involvement• Transmural• Small bowel often involved• Risk of malignancy increased
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Treatment
Management in Crohn's disease vs. ulcerative colitis
Crohn’s disease Ulcerative colitis
Mesalazine less useful[12] More useful[12]
Antibiotics Effective in long-term[13] Generally not useful[14]
Surgery Often returns followingremoval of affected part
Usually cured byremoval of colon
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Treatment (Medical)
1. Anti-inflammatory agents(aminosalicylates,corticosteroids)
2. Immunosuppressant
3. Antibiotics
4. TNF (Tumor Necrosis Factor) inhibitors
5. Anti-diarrheal agents
6. Antispasmodic agents
7. Supportive therapy
** 75% of ulcerative colitis patients respond well to medical management
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1-Anti-inflammatories (aminosalicylates)
• Sulfasalazine (Azulfidine)-combination of sulfapyradine (anti-bacterial) + 5-aminosalicylic acid (5-ASA)– Greatest effect on IBD; mainstay of outpatient medical
treatment for mild-mod. active UC & CD– Originally used to treat rheumatoid arthritis– Possesses both anti-inflammatory & antibacterial properties– Partially absorbed in jejunum but remainder passes to colon– Therapeutic action of 5-ASA compounds: inhibition of
prostaglandin & leukotriene synthesis, free radical scavenging, impairment of white cell adhesion and function, inhibition of cytokine synthesis
– Watch for folate deficiency, abdominal discomfort & allergies to sulfa compounds
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1-Anti-inflammatories (aminosalicylates)
• Mesalamine group- Asacol, Pentasa, Rowasa– Coating 5-ASA with acrylic resins- permits drug delivery to distal
bowel & colon– Effective for ileal & colon involvement– Rapid absorption– Enemas and suppositories– Fewer side effects than sulfasalazine– Olsalazine-delayed absorption;useful in colonic disease
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1-Anti-inflammatories (corticosteroids)
• Treatment of choice for acute attack IBD (including IV treatment; enemas for acute proctitis)
• Generally used for moderate-severe IBD• Not to be used for maintaining remission due to multiple & severe
side effects *• Prednisone-synthetic glucocorticoid;powerful anti-inflammatory
action– Usually tapered doses– IV use- methylprednisolone, dexamethasone
• Budesonide (Entocort EC)- newer type– Synthetic steroid coated with ethylmethylcellulose which delays its
release until ileum & descending colon• **Side effects often outweigh benefits if used for prolonged period
of time
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2-Immunosuppressants
• Reduce inflammation by suppressing immune system’s response (which might damage digestive tissue) to invading virus or bacterium
• Azathioprine (Imuran) & mercaptopurine (6-MP, Purinethol) – help reduce signs and sx of IBD and heal fistulas from CD– inhibits mitosis– Increases risk of neoplasia– Serious hepatic, renal, & hematological side effects
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2-Immunosuppressants
• Methotrexate (Rheumatrex)- used for patients who do not respond to other medications
• Cyclosporine (Neoral, Sandimmune)- administered IV for CD with fistulas
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3-Antibiotics
• IBD is associated with frequent bacterial infections especially with toxic megacolon, fistulas and fulminant disease
• Most effective antibiotics: metronidazole (Flagyl), ampicillin, cephalosporins, amonioglycosides, ciprofloxacin (Cipro)
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4-TNF (tumor necrosis factor) inhibitors
• TNF is a protein produced by immune system; chemical messenger that can cause inflammation & tissue damage
• Etanercept (Enbrel) – TNF receptor blocker; binds to alpha & beta TNF– Used to treat RA; not yet FDA approved for treating
Crohn’s
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4-TNF Inhibitors
• Infliximab (Remicade)- neutralizes cytokine TNF alpha– Increased risk infections (reactivation of TB or
granulomatous disease)– Usually for moderate-severe disease– May be used for long-term therapy
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5-Antidiarrheal agents
• Decrease peristalsis & therefore intestinal motility
• Improves diarrhea& prevents loss of fluid & electrolytes
• Loperamide (Imodium), Atropine (Lomotil)• Cholestyramine (Questran)- inhibits
enterohepatic reuptake of bile salts
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5-Antispasmodic agents
• Treat functional disturbances of GI motility• Dicyclomine (Bentyl)- anticholinergic; blocks
action of acetylcholine at parasympathetic sites in secretory glands, smooth muscle & CNS
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6-Supportive therapy
• (In addition to adequate nutritional support)– Vitamin B12– Iron– Folic acid
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Surgical Treatment
• **Surgical removal of large bowel (colectomy) will result in cure for ulcerative colitis
• Not the case for Crohn’s; surgical removal of the affected bowel segment in CD will not prevent the later appearance of disease at an adjacent or distant site
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Surgical Treatment (Ulcerative Colitis)
• Main indications: failure of medical treatment, complications (toxic megacolon, perforation) and risk of malignancy
• Resection of colon & rectum (panproctocolectomy) is curative– Fecal diversion via ileostomy or ileo-anal anastomosis
in form of ileal pouch• Pouch may cause mechanical problems (40% develop
inflammation resembling UC, 15% may need further surgery)
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Surgical Treatment (Ulcerative Colitis)
• 10% will have colectomy during 1st year of dx– 4% will have surgery during 2nd year– 1 % annually in subsequent years– Extent of colitis at diagnosis affects need for
subsequent surgery (colectomy rate for patients with pancolitis is 32%)
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Surgical Treatment (Crohn’s Disease)
• Limited to dealing with complications such as stricture formation, perforation and fistulae
• 30% need surgery within 1st year• For the remainder, surgery rate is 5% per year• Following resection, 30% will require further
surgery within 5 years, & 50% within 10 years• Complications are frequent; least invasive
procedures desirable
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Underwriting IBD: Mild Ulcerative Colitis
Distal or rectal involvement only• 5 or fewer stools/day• Tx with retention enemas or oral anti-
inflammatory meds• No systemic or extracolonic manifestations
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Moderate Ulcerative Colitis
• No currently active pancolitis• No serious complications• No worse than mild anemia• Treatment may require intermittent use of oral
steroids or other cytotoxic drugs
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Severe Ulcerative Colitis
• Active pancolitis with frequent diarrhea, abdominal pain
• Severe & typical systemic findings• Weight loss > 10% of body weight• Lab results reveal moderate-severe anemia
and/or hypoalbuminemia• Recent (w/in 5 yrs) toxic megacolon or multiple
surgeries• Treatment requires high doses of steroids or
multiple cytotoxic medications
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Other considerations (UC)
• Cirrhosis or sclerosing cholangitis (documented or suspected)
• Alkaline phosphatase or LFT elevations w/out liver biopsy or work-up
• Fatty liver or pericholangitis confirmed by liver biopsy + significant LFT elevations
• (Postpone?) Recent diagnosis • (Postpone?) 0-6 months following surgery
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Underwriting IBD (Mild Crohn’s Disease)
• Use of anti-diarrheal meds, no antibiotic or immunosuppressive therapy
• Near normal bowel habits• Infrequent attacks• No anemia, normal sed rate
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Moderate Crohn’s Disease
• Medications needed to control symptoms (ie, Flagyl, Asacol, Azulfidine)
• Limited disease• No more than 2 surgeries• Sed rate up to 2x normal
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Severe Crohn’s Disease
• Multiple (3 or more) surgeries• Multiple medications including oral steroids,
immunosuppressants, TNF inhibitors• Extensive disease• Anemia, elevated sed rate• Weight loss (> 10% body weight)
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Crohn’s Disease- Favorable factors
• Normal CBC• Ileal involvement only• Stable weight• Non-steroidal meds only• Colonoscopies every 12-24 months• Older age
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Crohn’s Disease- Unfavorable Factors
• Low blood counts on CBC• Multiple sites in GI tract• Low and/or fluctuating weight• Steroid use• Surgical intervention (multiple)• Poor follow-up/compliance
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Crohn’s Disease – other consideratons
• Cirrhosis or sclerosing cholangitis (documented or suspected)
• Alkaline phosphatase or LFT elevations w/out liver biopsy or work-up
• Fatty liver or pericholangitis confirmed by liver biopsy + significant LFT elevations
• Consider postponing if recent diagnosis (0-1 year since dx)
• (Postpone?) If CD diagnosed > 10 yrs ago (w/colonic involvement) and there is no recent colonoscopy
• (Postpone?) Colonoscopy/biopsy shows any degree of dysplasia
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Questions?
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References
1. ^ Baumgart DC, Carding SR (2007). "Inflammatory bowel disease: cause and immunobiology.". The Lancet 369 (9573): 1627–40. doi:10.1016/S0140-6736(07)60750-8. PMID 17499605.
2. ^ a b Baumgart DC, Sandborn WJ (2007). "Inflammatory bowel disease: clinical aspects and established and evolving therapies.". The Lancet 369 (9573): 1641–57. doi:10.1016/S0140-6736(07)60751-X. PMID 17499606.
3. ^ Xavier RJ, Podolsky DK (2007). "Unravelling the pathogenesis of inflammatory bowel disease.". Nature 448 (7152): 427–34. doi:10.1038/nature06005. PMID 17653185.
4. ^ "Crohn's & Colitis Foundation of America".5. ^ Elson, CO; Cong, Y; Weaver, CT; Schoeb, TR; Mcclanahan, TK; Fick, RB; Kastelein, RA (2007). "Monoclonal Anti–Interleukin
23 Reverses Active Colitis in a T Cell–Mediated Model in Mice". Gastroenterology 132 (7): 2359. doi:10.1053/j.gastro.2007.03.104. PMID 17570211.
6. ^ a b c d e f internetmedicin.se > Inflammatorisk tarmsjukdom, kronisk, IBD By Robert Löfberg. Retrieved Oct 2010 Translate.7. ^ a b c d Hanauer, Stephen B.; William Sandborn (2001-03-01). "Management of Crohn's disease in adults" (PDF). American
Journal of Gastroenterology 96 (3): 635–43. doi:10.1111/j.1572-0241.2001.03671.x. PMID 11280528. Retrieved 2009-11-07.
8. ^ a b c Kornbluth, Asher; David B. Sachar (July 2004). "Ulcerative colitis practice guidelines in adults (update): American College of Gastroenterology, Practice Parameters Committee" (PDF). American Journal of Gastroenterology 99 (7): 1371–85. doi:10.1111/j.1572-0241.2004.40036.x. PMID 15233681. Archived from the original on April 6, 2008. Retrieved 2009-11-07.
9. ^ Broomé, Ulrika; Annika Bergquist (February 2006). "Primary sclerosing cholangitis, inflammatory bowel disease, and colon cancer". Seminars in Liver Disease 26 (1): 31–41. doi:10.1055/s-2006-933561. PMID 16496231.
10. ^ Shepherd, NA. (August 2002). "Granulomas in the diagnosis of intestinal Crohn's disease: a myth exploded?". Histopathology 41 (2): 166–8. doi:10.1046/j.1365-2559.2002.01441.x. PMID 12147095.
11. ^ Mahadeva, U.; Martin, JP.; Patel, NK.; Price, AB. (July 2002). "Granulomatous ulcerative colitis: a re-appraisal of the mucosal granuloma in the distinction of Crohn's disease from ulcerative colitis.". Histopathology 41 (1): 50–5. doi:10.1046/j.1365-2559.2002.01416.x. PMID 12121237.
12. ^ a b c Pages 152-156 (Section: Inflammatory bowel disease(IBD)) in:Elizabeth D Agabegi; Agabegi, Steven S. (2008). Step-Up to Medicine (Step-Up Series). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-7153-6.
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