Inflammatory bowel disease (IBD) includes ulcerative colitis and Crohn's disease. IBD is common in Western countries and peaks between ages 20-40, affecting men and women equally. IBD involves periods of remission and relapse. The etiology involves genetic and environmental factors. Diagnosis involves blood tests, stool cultures, imaging tests like CT scans and endoscopy to assess severity and distinguish between UC and CD. Treatment includes medications, diet, surgery, and management of complications.

1. Inflammatory Bowel Disease By Dr. Osman Bukhari

2. -Includes ulcerative colitis (UC) & Crohns disease( CD). -There is overlap between or they are spectrum of the same disease. -In 10% of colitis it is difficult to differentiate between them. -Common in the west. Peak age is20-40 y. M=F. -Remission & relapses. Aetiology -Genetic & enviromental factors. -Familial:10% with high concordance in id. twins

3. -Genetics: HLAB27. Association with autoimmune diseases. -High sugar & low residue diet and smoking are associated with CD. -Transmissible agent in CD( measles & T.b.) -Multiangiitis leading to infarction. -Bact. Endotoxins release NO causing damage. -Immune response to luminal Ag.( bacterial product or diet) leading to inflammation through cytokins & free O2 radicals with activation & attraction of polymorphs, plasma cells & lymphocytes causing inflmm.& ulcers .

4. Pathology -In CD whole GIT is involved. Terminal ileum & ascending colon being commonly affected. Rectal disease is rare. In UC proctitis is invariable & back wash ileitis is rare. -Macroscopically : In CD small bowel is thickened & narrowed. The lesions are skipped deep ulcers with enlarged L.nodes, abscesses, fissures & fistulae. Toxic colonic dilatation can follow fulminant colitis. -In UC colitis is continuous with ulceration & is more distally. Pseudopolyps are common.

5. toxic dilatation can follow fulminant colitis. -Microscopically: In CD there is transmural non casiating granuloma with normal goblet cells & infrequent crypt abscesses. In UC inflamm. is superficial with chronic inflamm. infiltrates, loss of goblet cells, frequent crypt abscesses. Displasia & Ca are more common. Clinical features of CD - presentation is variable depending on the severity & extent of the disease. Mild cases lead normal life with repeated admission in severe cases.

6. -Major symptoms of abd. Pain, diarrhoea (80%) & weight loss. Abd. Pain is due to peritoneal involvement or obstruction. 10% present wuth acute pain in RIF. Diarrhoea is bloody in colitis & steatorrhoeic in small bowel disease -Constitutional symptoms of anorexia, N, V, general illhealth & fatigue ( Anemia due to malabsorption of Fe, FA,& B12). -Abdominal ex.=normal or tender or masses in the RIF ( Inflm. Loops of bowel or abscesses).

7. -PR =perianal abscess, skin tags, fissures & fistulae sp. with colitis. -Sigmoidoscopy= rectum may be spared or may be indistinguishable from UC. Take biopsies. Clinical feature of UC -Presentation is variable depending on the extent & severity of the disease. -Bloody diarrhea with mucus & occasionally only blood &mucus. Lower abdominal pain. -Urgency & tensmus in proctitis without constitutional symptom.

8. -Anorexia ;nausea & lethargy in total colitis. -Slight abdominal distension & tenderness. -PR= normal or tender with blood in the examining finger. -Mild colitis=up to 4 motions per day. -Mod. Colitis=4-6 motions per day. -Severe Colitis = more than 6 motions per day, patient very ill temp. >37.5, pulse >90, Hb <10 g./dl., ser. Albumin <30 g./l. & under nutrition. Anorexia, nausea

9. * Fulminent colitis may cause toxic mega- colon with perforation or septicemia. Extra-intestinal manifestations of IBS (Related to disease activity & more in UC.) -Clubbing of fingers, E. nodosum, pyoderma gangrenosum & oral aphthus ulcers. -Episcleritis, conjunctivitis, iritis & uveitis. -Monoarthritis, sacro-ilitis & ankylosing spondylitis. -Fatty liver, chronic hep., cirrhosis, autoimmune hep. scl.cholanhitis, cholanioCa.

10. -Portal pyaemia &liver abscess. -Auto-immune hemolytic anemia, vasculitis & thrombosis of portal & mesenteric veins. -Amyloidosis. * *** Relapses in UC are precipitated by:- Stress, intercurrent infection, G.E, antibiotics & NSAIDs. Investigations in IBD. -anemia( multifactorial), raised WBC, ESR & CRP. -stools ex. To exclude bacterial ,protozal & helmithic infections.

11. -Low serum albumin & abnormal LFT. -Blood culture in suspected septicemia. -Stool culture if diarrhea persist despite Tr. -Plain abd. X-ray in toxic megacolon. -Ba.enema : shortening, narrowing & loss of haustrations of colon, granular appearance of colon, pseudopolyps & filling defects. Avoided in acute cases. -Sigmoidoscopy: engorged hyperemic mucosa which bleed spontaneously in severe cases. -Colonoscopy: assesses extent & severity of disease

12. and take multiple biopsies to distinguish between UC & CD. -Small bowel Ba. follow- through ( abn. Mucosal pattern, skipped lesions, deep ulcers & narrowing_string sign.) - US fore masses & CT for abscesses & bowel thickening. Diff. diag : - Small bowel disease: chronic diarrhea, malabsorption & malnutrition, ileocecal Tb.,

13. actinomycosis, yersinia, appendicitis & append. Abscess, lymphoma &Ca caecum. -Infective diarrhea :salmonella, shigella, campylobacter., E.coli hagic colitis, GN & Chlamydia proctitis, pseudomembraneous, herpes simplex & amebiasis. -Noninfecive colitis: ischemic, radiation, diffuse lymphoma, behcet, NSAID, diverticulitis & colonic Ca. Management of IBS. Medical :well balanced diet with protein and energy. Maintain fluid & elect. balance.

14. -Low fat & milk if malabsorption. High fibre avoided in mall bowel disease, it is beneficial in proctitis & constipation. Iron, folic acid, B12,Vit. D & Ca supplements. -Drugs: Mild CD treated symptomatically with antidiarrheal.In acute CD admit for induction of remission with Prednsolone 40-60 mg/ day for 2W & reduce to 10-20mg for 6-8 w. Azathioprin for maintenance of steroid induced remission or if Prednsolone fails. Sulphasalasine ( 5ASA) & mesalasine for maintenance of remiss. In colonic CD . Methotrexate, ciclosp & TNF Abs.for those who do not respond to a.m. drugs.

15. -Antibiotics & Metronidazole bacterial colonization & perianal disease. -Surgery is required in 80% CD but should be avoided & conservative with minim. resection ( stricture & fistulae, abscess, perforation , toxic megacolon & severe extensive colonic disease if no response to med . TR..). Unlike UC surgery is not curative. -Medical management in UC: In severe active colitis--- fluid & elect. correction, blood & plasma transfusion , nutrition, S/C heparin to prevent DVT, blood culture & antibiotics if septicemia is suspected.

16. -Parentral methylprednsolone or oral Prednsolone ( 40-60) for 2W to induce remission & maintain on (5ASA) to prevent relapse. If no response use azathioprin. If no response then surgery. Azathioprin is also used for patients who require high dose steroids for Maintaince. -Steroid suppositories for proctitis & steroid enema for mild proctocolitis. If no response or if the patient can not retain enema; use systemic steroids. 5ASA can induce remission in mild & mod. colitis but less effective.

17. - Surgery for UC : Emergency proctocolectomy or colectomy Ist.& later proctosigmoidectomy for toxic dilatation, perforation & hage ,. Acue severe UC failing to med. TR , colonic abscess stricture & long standing total colitis & severe extra-intestinal not responding to med. TR are another indications. Complications of IBS: -Fistulae, fissures, abscess & local perforation in CD. -Toxic colonic dilatation. - Perforation in toxic dilt.

18. -Massive hage is rare. -Ca colon (3-5%) specially in extensive colitis of > 10 years. -Amyloidosis. Course in IBS: - R elapses & remiss. Mortality is twice as common as in normals in CD & is associated with surgery. -Prognosis is good in proctitis & worse with severe colitis. Mortality 15-25 % in fulmin. colitis

124. -Low serum albumin & abnormal LFTs. -Blood culture in suspected septicemia. -Stool culture if diarrhea is persistent. =In colitis plain in toxic dilatation of colon, Ba enema : avoided in acute cases.There is narrowing, shoryening, loss of haustration , ulceration, pseudo polyps &granular appearance. -Sigmoidoscopy :engorged hyperemic mucosa which bleeds spontaneously or or touch

125. -Colonoscopy: To assess extenty & severity of the disease, to distinguish between UC &CD & take multiple biopsies. -Small bowel follow through in CD( skipped lesions, abnormal mucosa, deep ulcerations & narrowing ( string sign) -CT for abscesses & bowel thickening & US for masses. Diff. Diagnosis: -CD of small bowel: chronic diarrhea, malabsorption, malnutrition, ileocecal Tb.,

126. actinomycosis, appendicitis &abscess, Yesinia ielitis, lymphoma & Ca cecum. -Colitis: infective colitis ( salmonella, shigella, campylobacter, E. coli hemorrhagic colitis, G.N.& Chlamydia proctitis, pseudomembr.colitis & amebiasis.) AND noninfective colitis ( ischemic, radiation, Behcets, NSAIDs, Ca colon & diverticulitis )

134. IBD includes UC & CD: -There is overlap between them & could be spectrum of the same disease & in 10% of colitis it is difficult to say which is which. -Common in the west .F=M. 20-40 ys. -Relapses & remissions. Aetiology Genetic & enviromental factors are implicated -Familial -Genetic associated with HLAB27. - Dietary: low residue & high sugar diet.

135. - Smoking in CD. UC more common in non smokers. -Transmissible agent e.g. measels-mycob.Tb. -Multifocal angiitis—infarction. -Bacterial endotoxins liberating NO3 causing damage. -Luminal Ag. Evocing immune response causing inflammatory response through cytokins & free O2 radicals.

136. Pathogenesis Involves activation of macrophages in response to dietary element or bacterial product with release of inflammatory cytokins with activation & attraction of polymorphs, plasma cells & lymphocytes leading to inflammation & ulceration. Pathology General: -In CD whole GIT is involved sp. Terminal ileum &

137. ascending colon are commonly affected while proctitis is rare. In UC proctitis is invariable & backwash ileitis is rare. Macroscopic: -In CD small bowel is thickened with skipped lesions & deep ulcers. Aphthus ulcers, abscesses & fistulae are common. Fulminant colitis & toxic diltation can occur. In UC there is confluent colitis with extensive ulceration and pseudopolyps.

138. Microscopy In CD there is transmural non casiating granuloma of the bowl &L. nodes with infrequent crypts abscesses & normal goblet cells. In UC there is superficial chronic inflammatory infiltrate, no granuloma with loss of goblet cells & crypt abscesses. Clinical picture In UC clinical picture is variable depending on the site, extent & severity of the disease.

139. -bloody diarrhoea with mucus. Occasionally only mucus & blood. There is lower abdominal pain, distension & tenderness. -Urgency & tensmus without constitutional symptoms in proctitis. -Anorexia, malaise & lethergy in total colitis with aphthoid ulcers. *Mild colitis =Up to 4 motions/day. *Mod. Colitis = 4-6 motions/day. *Severe colitis=More than 6 motions/day. Pat. Is very ill , febrile, Hb < 10gm, pulse >90, albumin <30 gm & undernutrition. Fulminant colitis with diltation, perforation & septicaemia can occur. PR= tender with blood.

140. In CD clinical picture is variable depending on the extent & severity of disease ranging from mild disease to severe disease with repeated admission. -Acute or chronic onset with abd. Pain & diarrhoea(80%) with constitutional symptoms of fever, fever,A, N,V, weight loss & fatigue. Colicky pain suggests obstruction. Pain RIF like acute appendicitis. -Features of malabsorption with anaemia, weihgt loss & vitamin deficiency. Aphth. Ulcer -Abd. Ex. Normal or tender with masses -Colitis in CD is similar to UC. -PR: skin tags, perianal abscesses, fissures & fistulae sp. In CD with colitis.

141. Extraintestinal manifestations of IBD. -Clubbing ,E. nodosum, Py. Gangrenosum, Aphthus ulcers & amyloidosis. -A spondylitis, S/ Ilitis & monoarthritis. -Conjunctivitis, episcleritis, iritis & uveitis. -Fatty liver ,chronic hepatitis, cirrhosis, Scler cholangitis, cholangioCa, autoimmune hepatitis, portal pyemia &liver abscess. -Autoimmune hemolytic anemia, vasculitis, thrombosis including portal mesen. Thrombosis.

142. Investigations Aimed at confirming diagnosis, defining disease extent & activity and identifying complications. -Anemia: multifactorial, high ESR & CRP. -Low serum albumin & abn. Liver biochemst. -Stool culture to exclude infections & biood cultures in patients with IBD who develop fever. -Plain abdominal XR if toxic dilatation & perforation are suspected.

143. -BA. E nema: narrow & short colon, loss of haustrations, granular appearance, pseudopolyps & filling defects. Ba. Avoided in active disease. -Sigmoidoscopy: ranges from abnormal vascular pattern in mild colitis to engorged mucosa which may bleeds spontaneously or on touch. Take biopsies. Rectal sparing in CD. -Colonoscopy: In UC the pathology is continuous, while in CD it I patchy, ulcers are deep & strictures are common. Take multiple biopsies

144. -Small bowel follow-through in CD shows skipped lesions, deep ulcers & narrow segments ( string sign). -CT for bowel thickening & abscesses. -US to detect masses. Differential diagnosis -CD should be differentiated from other causes of chronic diarrhoea, malabsosption & malnutrition, ileocaecal Tb., actinomycosis, yersinia, appendicitis & append. Abscess, lymphomas & Ca caecum.

145. -Colitis in UC & CD should be differentiated from infective colitis ( bacterial or amoebic, & pseudomembraneous colitis ) Or non infective colitis ( ischemic, radiation, lymphoma, behcet, Ca & diverticulitis,). Management A-Medical of CD: -Fluid & electrolyte balance. Maintenance of nutrition with low fat & milk diet if there is malabsorption. Iron, folic acid, B12, vit. D & calcium supplements.

395. -Symptomatic treatment with antidiarrhoeals in mild cases. -For severe acute attacks, Prednsolone 40-60 mg. for 1-2 weeks reduced to 10-20 mg. for 6-8 weeks ( Budesonide has less S.E.).