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INFLAMMATORY BOWEL DISEASE (IBD)

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

• Signs and Symptoms


TREATMENT
VIDEOS
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