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Inflammatory

Bowel Disease

INTRODUCTION
IBD is an idiopathic disease , probably involving an
immune reaction of the body to its own intestinal tract
Crohns disease (CD)
Ulcerative colitis (UC)

INTRODUCTION
CD is a condition of chronic granulomatous
inflammation potentially involving any location of the
GIT from mouth to anus.
UC is an non granulomatous inflammatory disorder
that affects the rectum and extends proximally to
affect variable extent of the colon.

EPIDEMIOLOGY
UC:
15-40 yrs (Young adults)
No variation between between men and women or
between socioeconomic group
High incidence areas: USA and northern-western
Europe
More common in non-smokers

EPIDEMIOLOGY
CD
1st peak 15-30 years of age, 2nd peak around 60 y
Marginally more common in females
High incidence areas: North America, UK,northern
Europe
More common in smokers

ETIOLOGY
Immunology
Initiating pathogen
Environmental Factors
Genetic factors

SYMPTOMS
UC:
Rectal bleeding or bloody diarrhea
Pain of colonic origin, often left sided and related to defecation
CD:
Diarrhea
Recurrent abdominal pain
Anorectal lesions, Anorexia, Anemia
Malnutrition (weight loss)
Fever

INVESTIGATIONS
Endoscopy
Colonoscopy
Histopathology
Radiology
Hematological tests and microbiological stool test for
infection

LABORATORY INVESTIGATION
UC

CD

ESR elevation

ESR

Hypoalbuminemia

Hypoalbuminemia

Anaemia

Anaemia

Electrolyte imbalance
Leucocytosis

DISTINGUISHING CHARACTERISTICS OF CD AND UC


Feature

UC

CD

Location

Only colon

GIT

Anatomic

Continuous, begins

Skip lesions

distribution

distally

Rectal involvement

Involved in >90%

Rectal spare

Gross bleeding

Universal

Only 25%

Peri-anal disease

Rare

75%

Fistulization

No

Yes

Granulomas

No

50-75%

PATHOLOGIC FEATURES OF CD AND UC


Feature

CD

UC

Transmural inflammation

Yes

Uncommon

Granulomas

50-75%

No

Fissures

Common

Rare

Fibrosis

Common

No

Submucosal inflammation Common

Uncommon

RADIOLOGIC FEATURES OF CD AND UC

UC

CD

Collar button ulcers

Nodularity
Granularity

PATHOPHYSIOLOGY
Bacterial antigens are taken up by specialized M cells, pass
between leaky epithelial cells or enter the lamina propria through
ulcerated mucosa
After processing they are presented on type 1 T-helper cells by
antigen presenting cells (APC) in the lamina propria.
T-cell activation and differentiation results in Th1 T cell mediated
cytokine response

With the secretion of cytokines including gamma interferon (IFN )

PATHOPHYSIOLOGY
Further amplification of T cells perpetuates the inflammatory
process with activation of non immune cells and release of the
important cytokines.
Eg: IL-12, IL-23, IL-1, IL-6 and tumor necrosis factor (TNF)
These pathways occur in all normal individual exposed to
inflammatory insults and this is self limiting in healthy subjects
In genetically predisposed persons, dysregulation of innate
immunity may trigger inflammatory bowel disease.

MANAGEMENT OF IBD
Non-pharmacological
Initial tretment is nonoperative Stop Smoking (for
crohns disease)
Nutrition

PHARMACOLOGICAL
Aminosalicilates (5-ASA): sulfasalazine, mesalazine,
olsalazine
Corticosteroids : Budesonide, presnisolone,
methylprednisolone
Immunosuppressants: azathioprine , 6-mercaptopurine
Antibiotics : metronidazole, ciprofloxacin
Anti diarrhoals : loperamide, Diphenoxylate &
atropine

PHARMACOLOGICAL
Antispasmodic agent: Dicyclomine
Immunoglobulin - nfliximab
Miscellaneous( Total or supplementary parenteral
nutrition, fish oils, sodium cromoglycate, lidocaine,
nicotine trans dermally)
Surgical management

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