2. •IBD is a chronic condition resulting
from inappropriate mucosal
immune activation (dysregulated
immune response to host intestinal
micro flora).
• It involves chronic inflammation of
all part of digestive tract.
3. Types of IBD
• It involves two types of disorders
1- Ulcerative Colitis-
•It is limited to the
mucosa & sub
mucosa of colon
and rectum.
4. 2- Crohn’s Disease- It affects any segment
of the GIT from the mouth to the anus.
•Transmural
inflammation
of terminal ileum.
•It causes skip
lesions
6. Etiopathogenesis
•It can occur at any age, frequently in teens in
early 30’s, Ulcerative colitis is more common in
males & Crohn’s among females.
•Exact etiology of IBD is not known, but it is
believed that IBD results from combined effect of
Alterations in host response.
Intestinal epithelium dysfunction.
Mucosal immune response.
7. Factors having important role in IBD
1- Genetic Factor
2- Mucosal Immune response - to
bacteria, viruses, or food particles- triggers an
inflammatory reaction.
3- Epithelial Defects
4- Microbiota
8. Genetic Factor
•Evidence that genes have role in IBD are-
•Risk of disease increases when there
is an affected family member
•50% chance of crohn disease in
monozygotic twins
•NOD 2 (Nucleotide oligomerization
binding Domain 2 gene on
chromosome 16 ia associated with
Crohn disease)
9. Mucosal Immune Response
•Defective mucosal immune response plays
significant role in IBD
•T helper cells are activated in crohn
disease, CD4+ T cells are present in
Lamina propria.
•TH1 type in Crohn’s disease
•TH2 & TH17 type in Ulcerative
colitis
10. •Gene “Knock out” studies in colitis
on Mice reviled that multiple immune
abnormalities are responsible for IBD
•Many pro-inflammatory cytokines
such as- TNF, Interferon & IL-10 play
imortant role in pathogenesis of IBD
11. Epithelial Defects
•Defects in intestinal epithelial tight
junction barriers present in Crohn’s
disease & their first degree relatives.
•Some proteins ECM1 (Extracellular
matrix protein 1) are linked to
Ulcerative colitis but not in Crohn’s
disease.
12. Microbiota
•Abundance of microbiota in GI lumen
i.e. 1012 organisms/ml of colon matter.
•Several species (Salmnella, Shigella,
Helicobactor, Clostridia, E. coli)have
been suspected to cause IBD but
without any definite evidence.
13. Other risk factors
•Smoking & use of contraceptive pills
increases the risk of Crohn’s disease
but no such risk for ulcerative colitis.
•People who live in urban areas and
industrialized countries have a higher
risk of getting IBD.
14. Clinical Features
•Symptoms vary according to the
location and severity of the disease, as
well as the type of disease-
• Blood in the stool
• Diarrhea
• Fatigue
• Fever
• Lack of appetite
• Nausea
• Painful or difficult
bowel movements
• Stomach pain and
cramps
• Vomiting
15.
16. Diagnosis
•In order to diagnose IBD, full medical
history of patient is recorded.
•Tests usually include.
-stool culture
-X-rays, if a serious complication is
suspected
-CT Scan
-MRI scans, to detect fistulas in the
small intestine or anal area
17. •Endoscopy
Colonoscopy - to examine the entire colon
Flexible sigmoidoscopy - to examine the
last section of the colon
Upper endoscopy - to examine the food
pipe, stomach, and first part of small
intestine
Diagnosis
18. Complications
Malnutrition with resulting weight
loss
Colon cancer
Fistulas, or ulcers that go through the
bowel wall
Intestinal rupture, or perforation
Bowel obstruction
19. Crohn’s Disease
•It refers to transmural chronic
inflammation of terminal ileum(most
common) ascending & sigmoid colon.
•It affects age group of 20-40 yrs &
women are more affected.
•It tends to run in families
20. •Clinical Features
•Abdominal pain especially rt. Lower
quardent.
•Bloody diarrhea.
•Fever
•Weigh loss
•Malabsorbtion
•Fistulae between lop of intestine
•Stricture
