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KABERA René,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.
• The small intestine is never involved, except when the distal
terminal ileum is inflamed in a superficial manner, referred to as
backwash ileitis.
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