inflammatory bowel disease

1. INFLAMMATORY
BOWEL DISEASE
SMS 2044

2. INFLAMMATORY BOWEL DISEASE
IBD is a group of inflammatory
conditions of large intestine ,in
some cases small intestine.

3. Intestines - Pathology
Idiopathic Inflammatory
Bowel Diseases
Etiology & Pathogenesis
Crohn’s disease
Ulcerative Colitis

4.  Etiology & Pathogenesis
 Characterized by= A chronic, relapsing inflammatory
conditions
 unknown etiology.
 Speculations involve= Genetic factors,
 Unknown infectious agents,
 Special susceptibility factors, altered immuno-reactivity to
dietary
Idiopathic Inflammatory Bowel
Diseases

5. Idiopathic Inflammatory Bowel
Diseases

Distinguished into two clinicopathologic entities:
 Crohn’s disease (CD)
 Ulcerative colitis (UC)
 Crohn’s disease (CD)
 Transmural granulomatous inflammation of the bowel,
with mucosal ulcerations, fissures & fistulas in Young
(20s)whites Females
 Skip lesions (cobble stone app.)
 Ulcerative colitis (UC)
 Crypt abscesses, psudopolyps & ↑risk of carcinoma
(adenocarcinoma)

6. Intestines - Pathology
Idiopathic Inflammatory Bowel Diseases
(CD) (UC)
Fissuring Ulcer
noncaseating granulomas

7. ULCERATIVE COLITIS
 Ulcerative colitis (Colitis ulcerosa, UC) is a form of
inflammatory bowel disease (IBD).
 Ulcerative colitis is a form of colitis, a disease of the
intestine, specifically the large intestine or colon, that
includes characteristic ulcers, or open sores, in the
colon.
 The main symptom of active disease is usually
diarrhea mixed with blood, of gradual onset.
 however, a systemic disease that affects many parts
of the body outside the intestine

9. AETILOGY
 Exact cause is unknown.
 Several causes have been suggested .it
includes
1. Genetic Factors
2. Environmental Factors
3. Auto Immune Disease
4. Several Other Theories

10. Genetic factors
 A genetic component to the etiology of ulcerative
colitis can be hypothesized based on the
following
1. Aggregation of ulcerative colitis in Families.
2. Diet: as the colon is exposed to many different
dietary substances which may encourage
inflammation.
3. Other childhood exposures or infections

11. Autoimmune disease
4. Some sources list ulcerative colitis as an
Autoimmune disease
Disease in which immune system malfunctions,
attacking some parts of body.
This suggests cause of disease is in colon itself,
not in immune system.

12. Pathological Feature
 Ulcerative colitis involves only the mucosa; it is
characterized by the formation of crypt abscesses and a
coexisting depletion of goblet cell mucin.
 In severe cases, the submucosa may be involved; in
some cases, the deeper muscular layers of the colonic
wall is also affected.
 Increased cellular infiltrate in the lamina propria,more
extensive and extends diffusely towards the deeper part
(transmucosal)
 Accumulation of plasma cells near the mucosal base, in-
between the crypt base and the muscularis mucosae (basal
plasmacytosis

13.  An irregular surface or a villiform surface and a disturbed
crypt architecture.
 Mucosal atrophy characterized by a combination of crypt
drop-out and shortening of crypts.
 Mucosal ulcerations and erosions, mucin depletion,
 Paneth-cell metaplasia and diffuse thickening of the
muscularis mucosae

14. H&E stain of a colonic biopsy showing a crypt
abscess:a classic finding in ulcerative colitis

17. Patients with ulcerative colitis
can occasionally have
aphthous ulcers involving the
tongue, lips, palate and
pharynx
Endoscopic image of ulcerative colitis
showing loss of vascular pattern of the
sigmoid colon, granularity and some
friability of the mucosa.

18. CLASSIFICATION
Extent of involvement
 The disease is classified by the extent of involvement,
depending on how far up the colon the disease extends.
1.Distal colitis
a. Proctitis: Involvement limited to the rectum.
b. Proctosigmoiditis: Involvement of the rectosigmoid colon, the
portion of the colon adjacent to the rectum.
c. Left-sided colitis: Involvement of the descending colon, which runs
along the patient's left side, up to the splenic flexure and the
beginning of the transverse colon.
2.Extensive colitis, inflammation extending beyond the
reach of enemas:

19. 1. Mild disease : fewer than 4 stools daily,no signs of
systemic toxicity,normal ESR,mild abdominal pain.
2. Moderate disease :more than 4 stools daily,minimal
signs of toxicity,anaemia,moderate abdominal
pain,low grade fever.
3. Severe disease :more than 6 bloody stools,evidence
of toxicity with fever,tachycardia,elevated ESR
4. Fulminant disease :more than 10
stools,bleeding,toxicity,abdominal tenderness,blood
transfusion requirement.unless treated will lead to
death.
Severity of disease

20. Clinical presentation
1. Diarrhoea mixed with blood and mucus.
2. Gradual onset.
3. Signs of weight loss.
4. Different degrees of abdominal pain ranging
from mild discomfort to severely painful
cramps.

21. Extraintestinal features
1. Iritis
2. Episcleritis
3. Aphthous ulcers involving
tongue,lips,palate,pharynx.
4. Arthritis
5. Ankylosing spondylitis
6. Erythema nodusum
7. Deep venous thrombosis
8. Pulmonary embolism
9. Auto immune hemolytic anaemia
10. Clubbing of fingers

22. Diagnosis
1. Complete blood count-
anaemia,thrombocytosis,high platelet count.
2. Electrolyte studies-hypokalemia,hypomagnesia
3. Renal function tests
4. Liver function tests
5. X-ray
6. Stool culture
7. ESR
8. C-reactive protein

23. Crohn's Disease

24. Definition:Definition:
Crohn's disease (also known as regional
enteritis) is a chronic, episodic, inflammatory
condition of the gastrointestinal tract characterized
by:
 Transmural inflammation (affecting the entire wall
of the involved bowel) and skip lesions (areas of
inflammation with areas of normal lining between).
 Crohn's disease is a type of inflammatory bowel
disease (IBD) and can affect any part of the
gastrointestinal tract from mouth to anus; as a
result,

25. Introduction to Crohn’s disease:
 This is a chronic inflammatory disease which causes
stomach pains, diarrhoea, and weight loss.
 The disease is characterised by periods of activity and
remissions.
 It typically affects the lower part of the small intestine (ileum)
or the large intestine (colon), but it can affect any part of the
digestive system.

26. Classification:
 Based on location.

27. Classification
Based on behaviour of
disease
Stricturing disease.
Penetrating disease.
Inflammatory disease.

28. Cause
 The exact cause of Crohn's disease is unknown.
 However, genetic and environmental factors
have been invoked in the pathogenesis of the
disease.
 Mutations in the CARD15 gene (also known as
the NOD2 gene) are associated with Crohn's
disease and with susceptibility to certain
phenotypes of disease location and activity.

29. Cause contd..
 Abnormalities in the immune system
 Many environmental factors.
 Diets
 Smoking
 Methods of hormonal contraception
 Some bacteria:
Eg Mycobacterium avium subsp. Paratuberculosis,
mannose, anti saccharomyces cerevisiae antibodies
and E. coli

30. Pathology:
Odeomatous and thickened bowel wall
Cobblestone
Patchy inlammation
Skip lessions
Transmural inflammation
Mucosal damage (transmural)
Well demarcated regions
Noncaseating granulomas
Formation of fissures
narrowed lumen (obstruction)
H and E section of colectomy showing transmural inflammation.

31. Cobblestone

33. www.freelivedoctor.com

34. Clinical Features
 Ileal Crohn’s Disease
Abdominal pain
Diarrhea
Weight loss
 Crohn’s colitis
Bloody diarrohea
Passage of mucus
Lethargy
Malaise
Anorexia
Weight loss

35. Chronic course may lead to:
 Fibrosing strictures
- terminal ileum
- fistulas other areas
 Protein loss
 Vit B12 loss
 Bile salt loss
- steatorrhea
Complications:

36. Complications:
Severe, life-threatening inflammation of
colon.
Perforation of the small intestine or colon.
Life-threatening acute haemorrhage.
Fistulae and perianal disease.
linear serpentine ulcers
Cancer.

37. Investigations:
 Endoscopic image of Crohn's colitis showing deep ulceration.

38. Contd…..
 Bacteriology
 Barium studies
 Other investigations
 X-ray
 Radio labelled white cell scan
 Ultrasound
 MRI scans

39. Contd..
 CT scan showing Crohn's disease in the fundus of the stomach.

40. ULCERATIVE
COLITIS
CROHN’S
Age Any Any
Sex m=f M=f
Anatomical
distribution
Colon only Any part of G.I
Presentation Bloody
diarrhoea
Variable; pain diarrhoea,
Weight loss
Risk factors more common in
non smokers
More common in smokers
Comparison of UC and CD

41. Treatment of
Inflammatory Bowel
Disease

42. TREATMENT
Treatment for IBD may include:
DIETARY CHANGES
LIFESTYLE CHANGES
DRUG THERAPY SURGERY

43. Dietary Changes
 Taking specific nutritional supplements,
 Limiting dairy products,
 Eating low-fat foods,
 Avoiding foods high in undigestible fiber
 Low-salt diet
 Following doctor-recommended diets and
 Eating smaller, more frequent meals.

44. LIFESTYLE CHANGES
.
Taking
rest
nonsmoking
Stress reductionDoing exercise

45. Drug Therapies
5-Aminosalicylates (5-ASA): Aminosalicylates are
A group of medicines that can help to control the symptoms
of some inflammatory bowel (gut) diseases.
Glucocorticoids (steroids)
 Antibiotics
Immunosuppressants
 Biological Therapy

46. Aminosalicylates
 Sulfasalazine (5-aminosalicylic acid and
sulfapyridine as carrier substance)
 Mesalazine (5-ASA), e.g. Asacol, Pentasa
 Balsalazide (prodrug of 5-ASA)
 Olsalazine (5-ASA dimer cleaves in colon)
 Oral, rectal preparation

47. What is Irritable Bowel Syndrome(IBS)?
 A group of functional bowel disorders
 Chronic abdominal complaints without a structural or
biochemical cause
 Constitutes a major health problem with gastrointestinal
(GI) symptoms
 The cause of IBS is unknown.
 Affects up to ~20 % adults in the industrialized world
 The condition is more frequent in women.
 The direct medical costs of IBS are ~ $ US 8 billion in the
US each year.

48. Clinical Manifestation
 Usually affects individuals younger than 45.
 Decreased incidence in older individuals
 Women are 2-3 times more likely to have IBS.
[80% patients are women]

50. Findings
 The main finding is abdominal pain during morning
hours – which may be in the hypogastrium (25%),
right (20%), left (20%), and epigastrium (10%).
 Other findings may include defecation straining,
urgency or a feeling of incomplete bowel movement,
bloating, and passing mucus.

51. Treatments
 High-fiber diets.
 Anticholinergic drugs inhibit gastrocolic reflex
(ipratropium bromide).
 Anti-diarrheals (loperamide).
 Chloride Channel Activators – lubiprostone.
 Anti-depressants – SSRIs (fluoxetine).
 Serotonin Receptor Agonist and Antagonists –
Alosetron, Tegaserod.