Pharmacotherapy :

Inflammation Bowel Disease

APT. ELFIA NESWITA, S.FARM.,

M.FARM.
1. Patofisiologi
2. Clinical Presentation
3. Treatment
4. Evaluation of Therapeutic

TUJUAN PERKULIAHAN : UNTUK

MENGETAHUI IBD
There are two forms of IBD:
UC, a mucosal inflammatory condition confined
to the rectum & colon, &
Crohn disease, a transmural inflammation of
GI mucosa that may occur in
any part of the GI tract.

RINGKASAN
The etiologies of both conditions are
unknown, but they may have a
common pathogenetic mechanism.

RINGKASAN
Your best quote that reflects your
approach… “It’s one small step for
man, one giant leap for mankind.”

SKEMA
Factors involved in cause of IBD
include infectious agents, genetics, the environment, and the immune
system

PATHOPHYSIOLOGY
The microflora of the GI tract may provide an environmental trigger to
activate inflammation and are highly implicated in the development of
IBD.

PATHOPHYSIOLOGY
Several genetic markers & loci have been
identified that occur more frequently in
patients with IBD.

PATHOPHYSIOLOGY
The inflammatory response with IBD may
indicate abnormal regulation of the normal
immune response or an autoimmune reaction
to self-antigens.

PATHOPHYSIOLOGY
Th1 cytokine activity is excessive in
CD and increased expression of interferon-γ
in the intestinal mucosa and production
of IL-12 are features of
the immune response in CD.

PATHOPHYSIOLOGY
Tumor necrosis factor-α (TNF-α ) is
a pivotal pro-inflammatory cytokine that is inc
reased in the mucosa and
intestinal lumen of patients with CD
and UC

PATHOPHYSIOLOGY
Antineutrophil cytoplasmic antibodies are found in
a high percentage of patients with
UC and less frequently with CD.

PATHOPHYSIOLOGY
•Smoking appears to be protective for
ulcerative colitis but associated with increased frequency of Crohn
disease

PATHOPHYSIOLOGY
The use of nonsteroidal anti-inflammatory
drugs (NSAIDs) may trigger disease occurrence
or lead to disease flares.

PATHOPHYSIOLOGY
UC and Crohn disease differ in
two general respects: anatomical sites and
depth of involvement within
the bowel wall. T

PATHOPHYSIOLOGY
There is, however, overlap between
the two conditions,
with a small fraction of
patients showing features of
both diseases (Table 26–1).

PATHOPHYSIOLOGY