Inflammatory bowel disease (IBD) is a group of chronic inflammatory conditions of the gastrointestinal tract that disrupt the ability to digest food and absorb nutrients. The two main types of IBD are ulcerative colitis, which causes inflammation of the inner lining of the large intestine and rectum, and Crohn's disease, which causes transmural inflammation that may affect any part of the gastrointestinal tract from mouth to anus. Diagnosis involves a review of symptoms, physical examination, blood tests, stool tests, endoscopy, biopsies and imaging studies to determine if inflammation is present and if other causes can be ruled out.

1. INFLAMMATORY BOWEL
DISEASE
KIRSHA K S
Asst. Professor
KMCH College of Pharmacy,
Coimbatore 1KIRSHA K S

2. • Inflammatory bowel disease (IBD) is a group of idiopathic
chronic, relapsing-remitting inflammatory intestinal
conditions
• Disrupt body’s ability to digest food, absorb nutrition and
eliminate waste
Crohn’s Disease Ulcerative Colitis
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3. ULCERATIVE COLITIS
• Limited to the large intestine
(colon) and the rectum.
• The inflammation occurs only in the
innermost layer of the lining of the
intestine.
• Usually begins in the rectum and
lower colon, but may also spread
continuously to involve the entire
colon.
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4. CROHN’S DISEASE
• Transmural inflammation (inflammation may
extend through the entire thickness of the
bowel wall) of GI mucosa affect any part of
the GI tract.
• Most commonly affects the end of the small
intestine (the ileum) where it joins the
beginning of the colon.
• Appear in “patches,” affecting some areas of
the GI tract while leaving other sections
completely untouched.
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5. CROHN’S DISEASE ULCERATIVE COLITIS
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6. INDETERMINATE COLITIS
• In some individuals, it is difficult
to determine whether their IBD
is Crohn’s disease or ulcerative
colitis.
• In these rare cases, people are
given the diagnosis of
indeterminate colitis (IC).
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8. EPIDEMIOLOGY
• The peak age of onset of UC and CD is between 15 and 30
years.
• A second peak occurs between the ages of 60 and 80.
• The male to female ratio for UC is 1:1 and for CD is 1.1–1.8
• The risk of UC in smokers is 40% that of nonsmokers .
Smoking is associated with a twofold increased risk of CD
• If a patient has IBD, the lifetime risk that a first-degree
relative will be affected is ~10%.
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9. IBD
Mucosal Immune
System
(Immuno-Regulatory
Defect)
Environmental
Triggers
(luminal bacteria,
infection, NSAIDs,
smoking)
Genetic
predisposition
ETIOLOGY
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10. 10KIRSHA K S

11. • DIET : fat intake, fast food, milk and fiber consumption
• INFECTION
CD: mycobacterium paratuberculosis
UC: after episodes of infective diarrhoea
• ENTERIC MICRO FLORA: The intestinal microbiota, which is dominated by bacteria,
but also includes viruses, fungi and protozoa, is crucial for development of the host
immune system but also appears to be the target of the inflammatory response
during IBD. The composition of the intestinal microbiota appears to be altered
during disease,
• GENETICS
o Linkage of human lymphocyte antibody (e.g. IL10RA and IL10RB)
oFirst degree relatives are more prone
oGreater in monozygotic twins
•ANTIBIOTICS: precipitate relapse of disease due to change in enteric micro flora
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12. • CIGARETTE SMOKING
o Smokers are 40% as likely as non-smokers to develop UC
o Active smokers are half as likely to be hospitalized as nonsmokers, and
former smokers are 50% more likely to be hospitalized and twice as likely
as current smokers or those who have never smoked to require colectomy
• APPENDECTOMY
o Protective effect of nearly 70% of appendectomy for the development of UC
o Pts who developed UC after appendectomy were less likely to develop
recurrent disease than those with colitis
• STRESS : Triggers relapse in IBD by activating inflammatory mediators at
enteric nerve endings in the gut wall
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14. LOCATION FOR UC
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15. LOCATION FOR CD
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16. PATHOGENESIS
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17. PATHOPHYSIOLOGY
TRIGGERING EVENTS
DYSREGULATED INFLAMMATORY AND IMMUNE RESPONSE IN
GENETICALLY SUSCEPTIBLE PERSONS
AMPLIFICATION OF IMMUNE RESPONSE
RELEASE OF INFLAMMATORY MEDIATORS
RELEASE OF TNF ALPHA,
PROINFLAMMATORY
INTERLEUKINS
MUCOUS BREAKDOWN AND CONTINUOS EXPOSURE
TO LUMEN DIETARY OR BACTERIAL ANTIGENS
IMPAIRED HANDLING OF MICROBIAL
ANTIGENS BY THE IMMUNE SYSTEM
INFLAMMATION 17KIRSHA K S

18. INFLAMMATION
INFLAMMATION INFLAMMATION + SUBSEQUENT INJURY OF
TISSUE (CRYPTITIS)
LOSS OF FINE VASCULAR
PATTERN
ULCERATIONS, EXUDATES,
PSEUDOPOLYPS
ULCERATIVE COLITIS
CRYPT ABCESS INFLUX +
EPITHELIAL NECROSIS
FOCAL APHTHOID ULCERATION
INFLUX AND PROLIFERATION OF
INFLAMMATORY MEDIATORS
TRANSMURAL INFLAMMATION
LYMPHEDEMA AND BOWEL WALL THICKENING
CROHN’S DISEASE
INFLAMMATION
LOSS OF FINE VASCULAR
PATTERN
INCREASED MUCOSAL
FRIABILITY
ULCERATIONS, EXUDATES,
PSEUDOPOLYPS
ULCERATIVE COLITIS
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19. SYMPTOMS
 Altered bowel movements
o Increased stool frequency
o Decreased stool consistency
 Abdominal pain
- LLQ cramping, relieved with
defecation
- Tenesmus
 Hematochezia (Blood in stool)
 Altered bowel movements
oChronic or nocturnal diarrhea
 Abdominal pain
oPostprandial RLQ abdominal pain
oDistension
 Weight loss
 Fever
ULCERATIVE COLITIS
CROHN’S DISEASE
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20. • As the lining of the intestine becomes inflamed and
ulcerated, it loses its ability to adequately process food and
waste or absorb water, resulting in loose stools
(diarrhea), and in severe cases weight loss.
• Inflammation can cause small sores (ulcers) to form in the
colon and rectum. These can join together and become
large ulcers that bleed, resulting in bloody stools. Blood
loss can eventually lead to anemia if unchecked.
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21. CLINICAL FEATURES
Colon only
Rectal involvement
Mucosal disease
Diffuse ulceration, granularity,
friability, bleeding, exudate
No fistulas or Granulomas
Any segment
Rectal sparing
Skip lesions
Transmural
Aphthous ulcers, serpiginous ulcers,
cobble stoning
Fistulae
Granulomas
UC CD

22. EXTRAINTESTINAL MANIFESTATIONS
ULCERATIVE COLITIS
Pyoderma
Gangronesum
Erythema Nodosum
Aphthous Ulcer
Iritis Uveitis

23. EXTRAINTESTINAL MANIFESTATIONS
CROHN’S DISEASE
Sweet’s syndrome Iridocyclitis Episcleritis
Uveitis
Pyoderma Gangronesum
Erythema Nodosum

24. ULCERATIVE COLITIS vs CROHN’S DISEASE
A Comparison of Complications
CROHN’SU.C.COMPLICATION
Usually non-massiveUsually massiveBleeding1
Early Obstruction
common
Late
Hose pipe appearance
‘Fibrosis’
Stenosis
Thick wall
2
Common +++Rare Perforation3
Common +++Rare Penetration → fistula4
Rare Common +++Malignant Change5
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25. DIAGNOSIS
• The diagnosis of IBD in adults requires a comprehensive
physical examination and a review of the patient’s history.
• Various tests, including blood tests, stool examination,
endoscopy, biopsies, and imaging studies help exclude other
causes and confirm the diagnosis.
http://www.worldgastroenterology.org/guidelines/global-guidelines/inflammatory-bowel-disease-ibd/inflammatory-bowel-disease-ibd-english
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26. Patient History
• Ask about symptoms — diarrhea (blood, mucus), abdominal pain, vomiting, weight loss, extra
intestinal manifestations, fistulas, perianal disease (in CD), fever.
• Inquire as to whether any of the presenting symptoms has occurred at any time in the past
(not uncommonly, flares of disease have gone undiagnosed in the past).
• Duration of current complaints, nocturnal awakening, missing work or usual social activities.
• Inquire about possible extra intestinal manifestations
• Identify whether mood disorders are present, or stressful situations known to precipitate IBD.
• Recent and past medical problems — intestinal infection.
• History of tuberculosis (TB) and known TB contacts.
• Travel history.
• Medications — antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and others like
corticosteroids for acne.
• Family history (IBD, celiac disease, colorectal cancer, TB).
• Cigarette smoking.
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27. Physical Examination
General:
• General well-being
• Pallor
• Cachexia
• Nutritional status
• Pulse rate and blood pressure
• Body temperature
• Body weight and height
Abdominal region:
• Mass
• Distension
• Tenderness, rebound, guarding
• Altered bowel sounds (obstruction)
• Hepatomegaly
• Surgical scars
Perianal region:
• Tags
• Fissures
• Fistulas
• Abscess
• Digital rectal examination
(assess for anal strictures,
rectal mass)
Extra intestinal inspection — mouth, eyes, skin, and joints
• Aphthous ulcers
• Arthropathy
• Uveitis, Episcleritis
• Erythema Nodosum
• Pyoderma gangrenosum
• Sweet’s disease (acute neutrophilic dermatosis)
• Primary sclerosing cholangitis (manifestations of
chronic liver disease)
• Metabolic bone disease
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28. Stool Examination
• Routine fecal examinations and cultures should be carried out to eliminate
bacterial, viral, or parasitic causes of diarrhea.
• Testing for Clostridium difficile (should be considered even in the absence of
antecedent antibiotics) — should be carried out within 2 hours of passage of
stools.
• A check for occult blood or fecal leukocytes should be carried out if a patient
presents without a history of blood in the stool.
• Lactoferrin, α1-antitrypsin, Calprotectin : to rule out intestinal inflammation.
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29. Blood Examination
Complete blood count (CBC). ESR, C-reactive protein; levels correlate
imperfectly with inflammation and disease activity.
• Serum ferritin : elevated in active IBD
• Transferrin saturation: The soluble transferrin
receptor (sTFR) assay is also a good measure of
iron stores.
• Electrolytes and albumin, ferritin (may indicate
absorption or loss problems), calcium,
magnesium, vitamin B12.
• Decreased serum cobalamin — may indicate
malabsorption.
Perinuclear antineutrophil cytoplasmic antibody
(p-ANCA) and anti-Saccharomyces cerevisiae
antibodies (ASCA) for cases of unclassified IBD.
• Positive p-ANCA and negative ASCA tests
suggest UC.
• Negative p-ANCA and positive ASCA tests
suggest CD
Celiac antibody testing should be pursued unless
presentations include obviously nonceliac features
such as fistulas, perineal disease, and blood in the
stool.
Human immunodeficiency virus (HIV) — additional
opportunistic infection work-up, hepatitis B virus
(HBV), hepatitis C virus (HCV), varicella zoster
virus (VZV), immunoglobulin G (IgG)
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30. Imaging and Endoscopy
Plain abdominal radiography:
Can establish presence of colitis and its
extent.
Used when bowel obstruction or perforation
is expected.
Excludes toxic megacolon.
Barium double-contrast enema/barium small-
bowel radiography:
Can be useful for identifying fistulas.
Can provide an anatomic “road-map” prior to
surgery.
Sigmoidoscopy, colonoscopy:
Examine for ulcers, inflammation, bleeding,
stenoses.
Upper gastrointestinal endoscopy:
In case of upper gastrointestinal symptoms
(nausea, vomiting, epigastric pain).
As upper gastrointestinal disease may be
more common in pediatric CD, this is more
routine in children.
Dual-energy X-ray absorptiometry (DEXA):
For assessing bone mineral density in selected
cases.
Chest radiography:
To exclude pulmonary TB and also to allow a search
for free air under the diaphragm in case of
perforation
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31. Magnification and chromoendoscopy:
To allow more accurate detection and
characterization of dysplastic lesions and
assessment of the severity of mucosal disease
Magnetic resonance cholangio-
pancreatography (MRCP):
If there is evidence of cholestasis, or suspected
PSC (Primary Sclerosing Colangitis).
Capsule endoscopy:
Allows evaluation of the entire small intestine, thus
improving the diagnosis and differential diagnosis
of IBD.
Double-balloon, single-balloon, and spiral
enteroscopy:
• To treat small-bowel strictures or for
assessment of obscure bleeding in CD.
Cross-sectional imaging:
Computed tomography (CT), ultrasonography, magnetic resonance imaging (MRI; including CT
enterography and MRI enterography).
Helpful for determining the extent and severity of disease and for assessing perforating
complications of CD.
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32. DIFFERENTIATING BETWEEN UC AND CD
cobblestone
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34. 34KIRSHA K S

35. DIFFERENTIAL DIAGNOSES FOR ULCERATIVE COLITIS
AND CROHN’S DISEASE
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36. MANAGEMENT
The goal of treatment is to:
• Improve and maintain patients’ general well-being
• Treat acute disease:
– Eliminate symptoms and minimize side effects and long-term adverse
effects
– Reduce intestinal inflammation and if possible heal the mucosa
• Prevent complications, hospitalization, and surgery
• Maintain good nutritional status
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37. The approach to treatment must be tailored to the
individual. Factors that determine the approach to
treatment include:
• Disease severity
• Anatomic location of disease
• Previous response to medication
• Side effects of medication
• Co-morbidities (other diseases or medical conditions that
the person has)
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38. PHARMACOLOGICAL MANAGEMENT
AMINOSALICYLATES
• Anti-inflammatory agents
o 5-aminosalicylic acid (5-ASA),
o Mesalazine
o Sulfasalazine
CORTICOSTEROIDS
o Intravenous : (Methylprednisolone,
Hydrocortisone).
o Oral : (Prednisone, Prednisolone, Budesonide,
Dexamethasone).
IMMUNE MODIFIERS
• Thiopurines
o Azathioprine
o Mercaptopurine
• Calcineurin Inhibitors
o Cyclosporine A (CSA)
o Tacrolimus
• Methotrexate (MTX)
BIOLOGICS
• Anti-tumor necrosis factor (anti-TNF) agents
o Infliximab
o Adalimumab
o Certolizumab
• Adhesion molecule antagonists
oVedolizumab
ANTIBIOTICS
o Metronidazole
o Ciprofloxacin
PROBIOTICS
o VSL#3
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40. Symptomatic therapy and supplements
• Antidiarrheals such as loperamide (Imodium) if colitis is not fulminant;
cholestyramine if the patient has previously undergone ileal resection.
• Analgesics such as acetaminophen, or even codeine if acetaminophen is
insufficient.
• Nutritional supplementation for those with malnutrition, or during periods of
reduced oral intake.
• Vitamin B12 replenishment for those with deficiency.
• Vitamin D supplementation if the local area does not allow sun exposure for
much of the year— and for patients on Thiopurines who are using sunscreens.
• Routine vitamin D and calcium supplementation for corticosteroid users.
• Routine multivitamin supplementation for all.
• For chronic iron-deficiency anemia, parenteral iron should be administered
(either as weekly intramuscular shots or dosing with intravenous iron) if oral
iron is not tolerated.
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41. Distal UC Extensive UC Crohn’s Disease
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42. CROHN’S DISEASE
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43. ULCERATIVE COLITIS
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44. TERMS TO KNOW
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45. • Perforated bowel—chronic inflammation of the intestine may weaken the
intestinal wall to such an extent that a hole develops
• Toxic mega colon—severe inflammation that leads to rapid enlargement of
the colon
• Fistula—ulcers on the wall of the intestine that extend and cause a tunnel
(fistula) to another part of the intestine, the skin or another organ.
• Stricture—a narrowing of a section of intestine caused by scarring, which can
lead to an intestinal blockage
• Abscess—a collection of pus, which can develop in the abdomen, pelvis, or
around the anal area
• Perforated bowel—chronic inflammation of the intestine may weaken the
wall to such an extent that a hole develops
• Pseudo polyps are projecting masses of scar tissue that develop from
granulation tissue during the healing phase in repeated cycle of ulceration
• Tenderness is pain or discomfort when an affected area is touched
• Abdominal guarding is the tensing of the abdominal wall muscles
to guard inflamed organs within the abdomen from the pain of pressure upon
them. The tensing is detected when the abdominal wall is pressed.
Abdominal guarding is also known as 'défense musculaire
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46. • Clostridium difficile : Bacteria that can infect the bowel
and cause diarrhoea. The infection most commonly affects
people who have recently been treated with antibiotics. It
can spread easily to others.
• Fecal markers include a biologically heterogeneous group
of substances that either leak from or are actively released
by the inflamed mucosa.
• Fecal Lactoferrin is an iron-binding protein, which is
mainly neutrophil derived, but may also be secreted by
several mucosal epithelial cell types
• Calprotectin, a proinflammatory proteins can be detected
and measured in the stool due to leukocyte shedding in the
intestinal lumen.
• Alpha-1-antitrypsin is a protease inhibitor produced by
the liver, macrophages, and intestinal epithelium
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47. END
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