1. UC & CD are disorders of modern society: their frequency in developed countries has been increasing since the mid-20 th century. Children: CD is more prevalent than UC The highest incidence & prevalence: Northern Europe & North America A westernized environment & lifestyle: Smoking, high fat & sugar diets, stress, & high socioeconomic status UC: Smoking is associated with milder disease, fewer hospitalization, & a reduced need for medications. UC: Appendectomy in early life is associated with a decreased incidence CD: Appendectomy in early life is associated with a increased incidence

2. Genetic influences: play a greater role in CD than in UC Is genetic screening indicated to assess the risk of UC? NO, (given the large number of implicated genes & the small additive effect of each) Human Microbiome project aims to define the composition of the intestinal microbiota in conditions of health & disease. The density of microbiota is greater in IBD patients than in healthy control subjects.

3. Risk factors for CRC: – Long duration of the disease (regardless of clinical activity) – Extensive involvement – Severe inflammation – A young age at onset – The presence of PSC – Family history of CRC Surveillance colonoscopy for patients at risk: there is no clear evidence that such surveillance increases survival. Pancolitis: inflammation up to ileocecal valve, with occasional limited involvement of the distal ileum (Backwash ileitis) Better detection of suspicious mucosal patterns & dysplasia: Chromoendoscopy, NBI, & autofluorescence imaging

4. UC: – Proctitis may present with constipation – A small area of inflammation surrounding the appendiceal orifice (cecal patch) can be identified in patients with left sided colitis, proctosigmoiditis, or proctitis. – Cancer: up to 20-30% after 30 years CD: – Video capsule endoscopy – Single balloon enteroscopy – Double balloon enteroscopy

5. Pillcam SB capsule (originally named the M2A capsule)

6. Indication for surgery: – Failure of medical therapy – Intractable fulminant colitis – Toxic megacolon – Perforation – Uncontrollable bleeding – Intolerable side effects of medication – Stricture that are not amenable to endoscopic therapy – Unresectable high-grade or multifocal dysplasia – DALM (Dysplasia associated lesion or mass) – Cancer – Growth retardation in children

7. Unlike CD, UC may respond to probiotics: – Escherichia coli strain Nissle 1917 (200 mg/day) – VSL#3 (3600 colony-forming units/day/for 8 weeks) Pouchitis: – An inflammation caused by an immune response to the newly established microbiota in the ileal pouch (dysbiosis). – Metronidazole, ciprofloxacin, rifaximin. – Probiotics can be effective for preventing recurrence. – Pouch failure is a condition requiring pouch excision or permanent diversion.

8. Suppository: Rectum Foam enema: Proximal sigmoid Liquid enema: Splenic flexure Rectal 5-ASA induces earlier & better results than oral mesalazine in the treatment of active proctitis. In active left-sided colitis there is proximal colonic stasis & fast colonic transit through the inflamed colon. This results in reduced exposure of the distal colon to the oral agent. The combination of both oral & rectally delivered 5-ASA has greater efficacy & speed of response in patients with distal colitis than either administration route used alone. Cyclosporine is only a bridge. The expanding use of anti-TNFa agents has not decreased the need for colectomy for UC patients.

9. Do not forget these etiologies of acute pancreatitis in a patient with IBD: – AZA – 6-MP – 5-ASA – Sulfasalazine – Steroid Granuloma may be seen: – CD – TB – Lymphoma – Behcet's disease – Yersinia

10. Toxic megacolon: – Colonic distension ( supine film >6 cm ) – Plus at least 3 of the following: T >38ºC HR >120 Neutrophilic leukocytosis >10,500 Anemia – PLUS at least 1 of the following: Dehydration Altered sensorium Electrolyte disturbances Hypotension Systemic toxicity Decreased incidence Smooth muscle inflammation  paralyzes  dilatation Hydrocortisone 100 mg/tid-qid Third generation + Metronidazole