INFLAMMATORY BOWEL DISEASE (IBD)

KABERA Ren,MD
PGY III Resident Family and Community Medicine National University of Rwanda

PLAN
Introduction

Pathophysiology
Ulcerative colitis Crohn disease Etiology Diagnostic Management

INTRODUCTION
Inflammatory bowel disease (IBD) is an idiopathic disease, probably involving an immune reaction of the body to its own intestinal tract. The 2 major types of IBD are ulcerative colitis (UC) and Crohn disease (CD). As the name suggests, ulcerative colitis is limited to the colon. Crohn disease can involve any segment of the gastrointestinal (GI) tract from the mouth to the anus

INTRODUCTION
Extraintestinal manifestations: iritis, episcleritis, arthritis, and skin involvement, as well as pericholangitis and sclerosing cholangitis. Systemic symptoms are common in IBD and include fever, sweats, malaise, and arthralgias. The rectum is always involved in ulcerative colitis, and the disease primarily involves continuous lesions of the mucosa and the submucosa.

PATHOPHYSIOLOGY
The pathophysiology of IBD is under active investigation.

The common end pathway is inflammation of the mucosal lining of the intestinal tract, causing ulceration, edema, bleeding, and fluid and electrolyte loss.

PATHOPHYSIOLOGY
Many inflammatory mediators: Cytokines, released by macrophages in response to various antigenic stimuli, bind to different receptors and produce autocrine, paracrine, and endocrine effects. Cytokines differentiate lymphocytes into different types of T cells. Helper T cells, type 1 (Th-1), are associated principally with Crohn disease, whereas Th-2 cells are associated principally with ulcerative colitis.

The immune response disrupts the intestinal mucosa and leads to a chronic inflammatory process.[1]

ULCERATIVE COLITIS
In ulcerative colitis, inflammation begins in the rectum and extends proximally in an uninterrupted fashion to the proximal colon, eventually involving the entire length of the large intestine, no skip areas. The rectum is always involved. The mucosa and submucosa are affected.

ULCERATIVE COLITIS
The disease remains confined to the rectum in approximately 25% of cases 75% of cases, ulcerative colitis spreads proximally and contiguously.

Pancolitis occurs in 10% of patients.

ULCERATIVE COLITIS
Even with less than total colonic involvement, the disease is strikingly and uniformly continuous. As ulcerative colitis becomes chronic, the colon becomes a rigid foreshortened tube that lacks its usual haustral markings.

CROHN DISEASE
Crohn disease can affect any portion of the GI tract from the mouth to the anus. It causes 3 patterns of involvement: inflammatory disease, strictures, and fistulas.

This disease consists of segmental involvement by a nonspecific granulomatous inflammatory process.

CROHN DISEASE
The most important pathologic feature of Crohn disease is that it is transmural, involving all layers of the bowel. Crohn disease is discontinuous, with skip areas interspersed between one or more involved areas.

CROHN DISEASE
The 3 major patterns of involvement in Crohn disease:

disease in the ileum and cecum (40% of patients) disease to the small intestine (30% of patients) disease confined to the colon (25% of patients) Rectal sparing is a typical but not constant feature of Crohn disease. However, anorectal complications (eg, fistulas, abscesses) are common.
Much less commonly, Crohn disease involves the more proximal parts of the GI tract, including the mouth, tongue, esophagus, stomach, and duodenum.

CROHN DISEASE
The incidence of gallstones and kidney stones is increased in Crohn disease because of malabsorption of fat and bile salts. Gallstones are formed because of increased cholesterol concentration in the bile, caused by a reduced bile salt pool.

Patients who have Crohn disease with ileal disease or resection are also likely to form calcium oxalate kidney stones.

ETIOLOGY
The triggering event for the activation of the immune response in IBD has yet to be identified. Possible factors related to this event include : Pathogenic organism (as yet unidentified)

Immune response to an intraluminal antigen (eg, protein from cow milk), or an autoimmune process whereby an appropriate immune response to an intraluminal antigen and an inappropriate response to a similar antigen is present on intestinal epithelial cells (ie, alteration in barrier function).

ETIOLOGY
Smoking The risk of developing ulcerative colitis is higher in nonsmokers and former smokers than in current smokers. The onset of ulcerative colitis occasionally appears to coincide with smoking cessation. This does not imply that smoking would improve the symptoms of ulcerative colitis; interestingly, some success in the use of nicotine patches has been reported. Patients with Crohn disease have a higher incidence of smoking than the general population Patients with Crohn disease who continue to smoke appear to be less likely to respond to medical therapy.

DIAGNOSTIC
Signs and Symptoms

TREATMENT

VIDEOS

THANK YOU