1. Inflammatory Bowel disease
SR-f
Cont
LECTURE 14

2. • Crohn disease and ulcerative colitis are
chronic relapsing inflammatory disorders of
unknown orgin, collectively known as
idiopathic inflammatory bowel disease (IBD),
which share many common features.

3. IBD
• Inflammatory
• Chronic
• Relapsing
• Autoimmune ?
• Idiopathic

4. They result from an abnormal local immune response against the
normal flora of the gut, and probably against some self antigens, in
genetically susceptible individuals.
The pathogenesis of IBD involves genetic susceptibility, failure of
immune regulation, and triggering by microbial flora.

5. Crohn Disease
“terminal ileitis” or
“regional enteritis

6. •A systemic inflammatory
disease with
predominant intestinal
involvement.

7. • When fully developed , Crohn disease is
characterized by:
• Sharply limited transmural involvement of
the bowel by an inflammatory process with
mucosal damage
• Presence of noncaseating granulomas
• Fistula formation

8. Common symptoms of Crohn's disease:
•abdominal pain
•diarrhoea
•weight loss

9. Less common symptoms include:
• poor appetite
• fever,
• night sweats
• rectal pain/rectal bleeding

10. ExtraintEstinal
symptoms
Some patients with Crohn's disease also develop
symptoms outside of the
gastrointestinal tract;these
symptoms include:
• arthritis
• skin rash
• inflammation of the iris of the eye.

11. Ulcerative
Colitis

12. • Ulcerative Colitis is an ulceroinflammatory
disease affecting the colon, which is
limited to the mucosa and
submucosa, except in the most severe
cases.

13. • It begins in the rectum and extends
proximally in a continuous fashion
sometimes involving the entire colon.

15. Epidemiology
• More common in USA & Western countries.
The incidence has risen in recent decades.
More common among whites. No sex
predilection. A peak incidence between ages
20-25 years. Has a familial association.

16. Morphology
• Gross:
• Rectum & Sigmoid --may involve entire colon.
• The lesions are continuous.
• inflammatory destruction of the mucosa with
macroscopic appearance of :
• Hyperemia, edema, and granularity with
friability and easy bleeding.

17. • With severe active disease:
• Extensive and broad based ulceration in the
distal colon.
• Pseudopolyps
• Toxic megacolon

18. • A diffuse, predominantly mononuclear
inflammatory infiltrate in the lamina propria
and Crypt abscesses.

19. Complications:
Perforation, peritonitis, abscess
• Toxic megacolon
• Venous thrombosis
• Carcinoma

20. Clinical features
• Bloody mucoid diarrhea
• Cramps
• Tenesmus
• Colicky lower abdominal pain
• Fever
• Weight loss

21. Extra-intestinal symptoms
• Migratory polyarthritis,
• sacroilitis,
• ankylosing spondilitis,
• uveitis,
• erythema nodosum and
• hepatic involvement (pericholangitis and
primary sclerosing cholangitis).

22. Diagnosis
•Endoscopy
•Biopsy

23. Comparison of CD &UC
• Crohn disease and ulcerative colitis differ in
many respects, including the natural history of
the disease, pathological aspects, and in the
types of therapies and responses to
treatment.

24. Comparisons of various factors in Crohn's disease and ulcerative
colitis
Crohn's DiseaseCrohn's Disease Ulcerative ColitisUlcerative Colitis
Involves terminal ileumInvolves terminal ileum CommonlyCommonly SeldomSeldom
Involves colon?Involves colon?
Involves rectum?Involves rectum?
UsuallyUsually
SeldomSeldom
AlwaysAlways
UsuallyUsually
Bile duct involvement?Bile duct involvement? Not associatedNot associated Higher rate of PrimaryHigher rate of Primary
sclerosing cholangitissclerosing cholangitis
Distribution of DiseaseDistribution of Disease Patchy areas ofPatchy areas of
inflammationinflammation
Continuous area ofContinuous area of
inflammationinflammation
EndoscopyEndoscopy Linear and serpiginousLinear and serpiginous
(snake-like) ulcers(snake-like) ulcers
Continuous ulcerContinuous ulcer
Depth of inflammationDepth of inflammation May be transmural, deepMay be transmural, deep
into tissuesinto tissues
Shallow, mucosalShallow, mucosal

25. FistulaeFistulae,, abnormalabnormal
passageways betweenpassageways between
organsorgans
CommonlyCommonly SeldomSeldom
BiopsyBiopsy Can haveCan have granulomagranulomatata Crypt abscesses andCrypt abscesses and
cryptitiscryptitis
Surgical cure ?Surgical cure ?
SmokingSmoking
Often returnsOften returns
following removal offollowing removal of
affected partaffected part
Higher risk for smokersHigher risk for smokers
Usually cured byUsually cured by
removal of colon,removal of colon,
Lower risk for smokersLower risk for smokers
Autoimmune diseaseAutoimmune disease Generally regarded asGenerally regarded as
an autoimmunean autoimmune
diseasedisease
No consensusNo consensus
Cancer risk?Cancer risk? Lower than ulcerativeLower than ulcerative
colitiscolitis
HigherHigher than Crohn'sthan Crohn's
Comparisons of various factors in Crohn's disease and
UC (Cont.)

26. Features UC CD
Morphologic
Distribution Diffuse,mucosal
&submucosal,
left sided
Focal, trans-
mural, right
sided
Mucosal atrophy Marked Minimal
Cytoplasmic mucin ↓ Preserved
Lymphoid aggregate Rare Common
Edema Minimal marked

27. Features UC CD
Morphologic
Hyperemia Extreme Minimal
Granuloma Absent 60% present
Fissuring Absent Present
Crypt abscess Common Rare
Lymph nodes Reactive Granulomas

29. Acute Appendicitis
The appendix is a normal true diverticulum of
the cecum that is prone to acute and chronic
inflammation. Acute appendicitis is most
common in adolescents and young adults, but
may occur in any age group. The lifetime risk for
appendicitis is 7%;
males are affected slightly more often than
females.

30. • Despite the prevalence of acute appendicitis,
the diagnosis can be difficult to confirm
preoperatively and may be confused with
mesenteric lymphadenitis, acute salpingitis,
ectopic pregnancy, mittelschmerz (pain
caused by minor pelvic bleeding at the time
of ovulation), and Meckel diverticulitis.

31. Pathogenesis
Acute appendicitis is thought to be initiated by
progressive increases in intraluminal pressure
that compromise venous outflow. In 50% to
80% of cases, acute appendicitis is associated
with overt luminal obstruction,
usually caused by a small stone-like mass of
stool, or fecalith, or, less commonly, a
gallstone, tumor, or mass of worms (oxyuriasis
vermicularis).

32. • Ischemic injury and stasis of luminal
contents, which favor bacterial proliferation,
trigger inflammatory responses
including tissue edema and neutrophilic
infiltration of the lumen, muscular wall, and
periappendiceal soft tissues.

33. Morphology
In early acute appendicitis subserosal vessels are
congested and there is a modest perivascular
neutrophilic infiltrate within all layers of the
wall.
The inflammatory reaction transforms the normal
glistening serosa into a dull, granular,
erythematous surface.

34. • Diagnosis of acute appendicitis requires
neutrophilic infiltration of the muscularis
propria.

35. • In more severe cases a prominent
neutrophilic exudate generates a serosal
fibrinopurulent reaction. As the process
continues, focal abscesses may form within
the wall (acute suppurative appendicitis).

36. • Further appendiceal compromise leads to
large areas of hemorrhagic ulceration and
gangrenous necrosis that extends to the
serosa creating acute gangrenous
appendicitis, which is often followed by
rupture and suppurative peritonitis.

37. Clinical Features
• Typically, early acute appendicitis produces
periumbilical pain that ultimately localizes to
the right lower quadrant, followed by
nausea, vomiting, low-grade fever, and a
mildly elevated peripheral white cell count

38. Charles Heber Mc Burney
American
surgeon

39. • Regrettably, these signs and symptoms are
often absent, creating difficulty in clinical
diagnosis. In some cases, a retrocecal
appendix may generate right flank or pelvic
pain, while a malrotated colon may give rise
to appendicitis in the left upper quadrant. In
other cases the peripheral leukocytosis may
be minimal or, alternatively, so great that
other causes are considered.

40. • The diagnosis of acute appendicitis in young
children and the very elderly is particularly
problematic, since other causes of abdominal
emergencies are prevalent in these
populations, and the very young and old are
also more likely to have atypical
clinical presentations.

41. • Given these diagnostic challenges, it should
be no surprise that even highly skilled
surgeons remove normal appendices. This is
preferred to delayed resection of a diseased
appendix, given the significant morbidity and
mortality associated with appendiceal
perforation. Other complications of
appendicitis include pyelophlebitis, portal
venous thrombosis, liver abscess, and
bacteremia.