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 ESR elevation ESR CD

Hypoalbuminemia
Anaemia Electrolyte imbalance Leucocytosis

Hypoalbuminemia
Anaemia

DISTINGUISHING CHARACTERISTICS OF CD AND UC

Feature
Location Anatomic distribution Rectal involvement Gross bleeding Peri-anal disease Fistulization Granulomas

UC
Only colon Continuous, begins distally Involved in >90% Universal Rare No No

CD
GIT Skip lesions

Rectal spare Only 25% 75% Yes 50-75%

PATHOLOGIC FEATURES OF CD AND UC

Feature
Transmural inflammation

CD
Yes

UC
Uncommon

Granulomas
Fissures Fibrosis

50-75%
Common Common

No
Rare No Uncommon

Submucosal inflammation Common

RADIOLOGIC FEATURES OF CD AND UC

UC Collar button ulcers

CD 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