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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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