IBD: Crohn's Disease and Ulcerative Colitis (PDF)

Lecture Material is adapted from © 2017 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 3: Inflammation and Tissue Repair Module 4: Clinical Models Dr. Romeo Batacan Jr. MPAT12001 Medical Pathophysiology Lec...

Lecture Material is adapted from © 2017 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 3: Inflammation and Tissue Repair Module 4: Clinical Models Dr. Romeo Batacan Jr. MPAT12001 Medical Pathophysiology Lecture Series Copyright © 2017 Wolters Kluwer Health | Lippincott Williams &Wilkins  Inflammatory Bowel Diseases: Crohn Disease and UlcerativeColitis Clinical Pathophysiology Diagnosis Treatment manifestations Inflammatory bowel diseases (IBD) Chronic, relapsing inflammatory bowel disorders of unknown origin (idiopathic) Genetic etiology Autoimmunity (Immune reactions to intestinal flora) Abnormal T-cell responses Alterations of epithelial barrier functions Most common in small and large intestine Can occur anywhere in GI tract Most common forms of IBD Crohn Disease Ulcerative Colitis  Crohn Disease Pathophysiology Idiopathic chronic granulomatous inflammatory disorder Family history, environmental factors (smoking, diet, microorganisms) Affects any part of the digestive tract from mouth to anus Most common in small intestine Recurrent condition  Crohn Disease Pathophysiology Australia: ~ 28000 (Craft AJ, Gordon C, Tiziani A. Understanding pathophysiology. 1st ed. Chatswood, Mosby;2011) Non-continuous penetrating ulcerations and fibrosis (skip lesions) Ulcerations can produce longitudinal and transverse inflammatory fissures that extend into the lymphatics  Crohn Disease Pathophysiology Inflammation begins in the mucosa and submucosa Increased permeability and vascular changes: Edema and fibrosis Cellular response develops Granulomas form to wall off effected area Bowel segment become further inflamed Interior surface thicken Edema, fibrosis, granuloma Can lead to bowel obstruction Ingested food can’t pass through, emergency Ulcers (due to poor perfusion) form and lead to Fistula: abnormal passage between 2 segments of bowel or epithelial tissue Abscess: a pocket of purulent exudate, containing pus External surfaces can form adhesions, limiting bowel function  Crohn Disease Clinical Manifestations Rapid stool transition time Intestinal edema Fibrosis Loss of absorptive function Symptoms depend on location of affected area Abdominal pain Diarrhea Malnutrition Occult blood in stool Bowel obstruction Systemic manifestations Fever Weight loss Fatigue Anaemia may result from malabsorption of vitamin B12 and folic acid  Crohn Disease DiagnosticCriteria History and physical examination Difficult to differentiate from ulcerative colitis Similar risk factors and theories of causation as ulcerative colitis Endoscopic examination to check mucosa involvement Radiography/CT to check abscesses, fistulas, obstruction Stool cultures to rule out infection  Crohn Disease Treatment Treatment is symptomatic (symptom management) Pharmacologic treatment Suppress inflammation Suppress immune response Dietary changes Avoid foods that irritate bowel During exacerbations: High in calories and protein Low in fat and fiber Surgical treatment Remove damaged bowel Repair fistula Increased risk of small intestine and colorectal cancer Ulcerative colitis Chronic inflammatory disease of the colon Only in large intestine Does not affect other GI tract Mainly mucosal layer (can extend to submucosa) Idiopathic disease Suggested causes: Infectious, immunologic (anticolon antibodies), dietary, genetic (supported by family studies and identical twin studies) Australia: around 33000 (Craft AJ, Gordon C, Tiziani A. Understanding pathophysiology. 1st ed. Chatswood, Mosby; 2011)  Ulcerative Colitis Pathophysiology Chronic inflammation begins in rectum and ascends the descending colon Continuous superficial areas of ulceration (does not skip) Inflammation invades superficial mucosa: friability (easily bleeds) Mucosa erythematous and granular Hemorrhagic lesions, abscesses, necrotic tissue, ulceration Repeated cycle of ulceration alternating with the deposition of granulation tissue during the healing phase Pseudopolyps: raised inflammatory tissue Perforation, obstruction, and massive hemorrhage can result Craft AJ, Gordon C, Tiziani A. Understanding pathophysiology. 1st ed. Chatswood, Mosby; 2011  Ulcerative Colitis Clinical Manifestations Symptoms are related to large intestine irritability and friability Functional losses are related to the extent of inflammation Most common symptoms: Diarrhea Rectal bleeding Abdominal pain Systemic manifestations Fever Weight loss Fatigue Anaemia  Ulcerative Colitis Diagnosis History and physical examination Diarrhoea (10 to 20/day), bloody stools, cramping http://radiopaedia.org/articles/lead-pipe-sign Severity is based on the number of bowel movement Loss of haustral markings with rectal bleeding and systemic manifestations Mild: 4/day, no systemic manifestations Severe: >4/day, systemic manifestations, low blood albumin Endoscopic examination: mucosal erythema (redness) Radiographs Colonic dilation, ulceration, perforation, obstruction Complete blood count (anemia)  Ulcerative Colitis Treatment Treatment is symptomatic (symptom management) Pharmacologic treatment Suppress inflammation Suppress immune response Antidiarrheal medication Dietary changes Healthy diet (avoid milk, caffeine, spicy food) Adequate fluid intake Surgical treatment If perforation or obstruction occur Increased risk of colon cancer, higher than Crohns