Inflammatory bowel disease Notes

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This Osmosis High-Yield Note provides an overview of Inflammatory bowel disease essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Inflammatory bowel disease:

Crohn's disease

Microscopic colitis

Protein losing enteropathy

Ulcerative colitis

NOTES NOTES INFLAMMATORY BOWEL DISEASE GENERALLY, WHAT IS IT? PATHOLOGY & CAUSES DIAGNOSIS ▪ Immune-mediated inflammatory bowel conditions ▪ More common in White people of Jewish descent ▪ Usually presents in young people, 15–35 ▪ Up to 25% of people with inflammatory bowel disease have affected first-degree relative DIAGNOSTIC IMAGING CAUSES MEDICATIONS ▪ Gut microbiome alterations ▪ “Western” style diet: high processing/ sugar/fat content RISK FACTORS ▪ Crohn’s disease: smoking ▫ Smoking may be protective for Ulcerative colitis ▪ Endoscopy LAB RESULTS ▪ Biopsy TREATMENT ▪ Anti-inflammatory medications; antibiotics; immunosuppressants SURGERY ▪ Surgical resection OTHER INTERVENTIONS ▪ Dietary changes SIGNS & SYMPTOMS ▪ ▪ ▪ ▪ Chronic diarrhea, frequently bloody/mucous Abdominal pain Fever, weight loss, anemia Extraintestinal manifestations ▫ Arthritis, uveitis OSMOSIS.ORG 255
CROHN'S DISEASE osms.it/crohns-disease PATHOLOGY & CAUSES ▪ AKA Crohn disease, regional enteritis ▪ Chronic, immune-related disorder → excessive immune response to unknown trigger → transmural inflammation anywhere along gastrointestinal (GI) tract, mouth to anus ▪ Compare to ulcerative colitis ▫ Only affects colon, rectum; superficial lesions; autoimmune disorder where tissue is directly attacked by immune system ▪ Frameshift mutation in nucleotide-binding oligomerization domain-containing protein 2 (NOD2)/ caspase recruitment domaincontaining protein 15(CARD15) ▫ Excessive inflammatory response → tissue damage ▪ Unknown immune response trigger → T helper (Th) 1 cells release inflammatory cytokines ▫ Interferon (IFN) gamma, tumor necrosis factor (TNF) alpha → inflammatory response → cytokines recruit macrophages → further inflammatory mediators released (proteases, platelet activating factor, free radicals) → further inflammation → healthy tissue destroyed → inflammatory cells invade intestinal mucosa → ulcer, granuloma form → transmural inflammation → intestinal lumen; fistula formation, narrowing ▪ Fistula, stricture formation ▫ Serosal layer involvement → fistula ▫ Most common: enterovesical, enterocutaneous, enterovaginal, enteroenteric fistulae ▪ Scattered inflammation → cobblestone appearance ▪ Most commonly affects terminal ileum, colon CAUSES ▪ Unclear; mycobacterium paratuberculosis, pseudomonas, listeria implicated SIGNS & SYMPTOMS ▪ Unpredictable patterns of flares, remissions ▪ Abdominal pain; most common in right lower quadrant (ileal inflammation) ▪ Fatigue, fever, nausea, vomiting ▪ Chronic diarrhea; may/may not be bloody ▫ Gross bleeding rare; upon microscopy, bleeding common ▪ Malabsorption, weight loss, vitamin deficiencies ▪ Up to 20% of cases present with inflammatory eye, skin, joint lesions ▫ Uveitis, erythema nodosum, pyoderma gangrenosum, cholelithiasis (impaired bile reabsorption), arthritis ▪ Perianal abscesses, phlegmon, fistulae ▫ Perianal fistulas (up to 30%) ▫ Enterovesical fistulae → recurrent UTI, pneumaturia ▫ Enteroenteric fistulae → asymptomatic ▫ Enterovaginal fistulae → passage of fecal matter through vagina ▫ Enterocutaneous fistulae → draining of bowel contents unto skin ▪ Intestinal obstruction (up to 30%) Figure 33.1 Pyoderma gangrenosum on the leg of an individual with Crohn’s disease. 256 OSMOSIS.ORG
Chapter 33 Inflammatory Bowel Disease MNEMONIC: CHRISTMAS Features of Crohn’s disease Cobblestones High temperature Reduced lumen Intestinal fistulae Skip lesions Transmural: all layers, may ulcerate Malabsorption Abdominal pain Submucosal fibrosis Figure 33.3 Gross pathology of a resected colon involved by Crohn’s disease. The severe and prolonged inflammation has led to a cobblestone appearance of the colonic mucosa. DIAGNOSIS DIAGNOSTIC IMAGING ▪ Endoscopy LAB RESULTS ▪ Biopsy ▫ Cobblestone appearance, intermittent lesion pattern, pseudopolyps, aphthous ulcers OTHER DIAGNOSTICS ▪ Barium enema TREATMENT MEDICATIONS ▪ Anti-inflammatory medications → sulfasalazine ▫ For colonic symptom management ▪ Antibiotics → metronidazole ▫ Reduce bacterial overgrowth, antiinflammatory effect ▪ Immunosuppressants → prednisone, azathioprine ▫ Only if no response to antibiotics ▪ Antidiarrheals ▪ Methotrexate, anti-TNF agents ▫ Refractory disease SURGERY ▪ Surgical removal of affected tissue ▫ High relapse rate ▫ Short bowel syndrome: complication of resection OTHER INTERVENTIONS ▪ Nutritional supplementation, support Figure 33.2 Histological appearance of Crohn’s disease. The lamina propria is expanded by chronic inflammatory cells and there is a non-caseating granuloma present. OSMOSIS.ORG 257
MICROSCOPIC COLITIS osms.it/microscopic-colitis DIAGNOSIS PATHOLOGY & CAUSES ▪ Idiopathic chronic inflammation of colon → watery diarrhea ▪ Associated with celiac disease, autoimmune diseases, NSAIDs, smoking ▪ More common in individuals who are biologically female ▪ Unknown trigger → abnormal collagen metabolism → dysfunctional epithelium → alteration in barrier function → mucosal inflammation → decreased sodium absorption, increased chloride secretion → secretory diarrhea TYPES Collagenous ▪ More common in older individuals who are biologically female ▪ Dense subepithelial collagenous layer; increased intraepithelial lymphocytes, inflammatory infiltrate in lamina propria Lymphocytic ▪ Increased intraepithelial lymphocytes, inflammatory infiltrate in lamina propria SIGNS & SYMPTOMS ▪ ▪ ▪ ▪ ▪ Abdominal pain Chronic watery diarrhea No weight loss Fecal urgency, incontinence Anemia DIAGNOSTIC IMAGING Endoscopy ▪ Non-specific findings, normal mucosa LAB RESULTS ▪ Biopsy of colonic mucosa ▫ Inflammatory changes in lamina propria, intraepithelial lymphocytic infiltration, dense subepithelial collagenous layer ▪ Elevated inflammatory markers (nonspecific) ▫ Erythrocyte sedimentation rate, myeloperoxidase ▪ Autoantibodies ▫ Anti-thyroid peroxidase (TPO), antinuclear (ANA), antineutrophil cytoplasmic (ANCA), anti Saccharomyces cerevisiae (ASCA), rheumatoid factor (RF) TREATMENT MEDICATIONS ▪ Avoid NSAIDs, other medications associated with microscopic colitis ▪ Antidiarrheals ▫ Loperamide, bismuth salicylate ▪ Corticosteroids ▫ Budesonide, prednisone ▪ Bile acid sequestrants ▫ Cholestyramine SURGERY ▪ Surgical resection (ileostomy) 258 OSMOSIS.ORG
Chapter 33 Inflammatory Bowel Disease Figure 33.4 Histological appearance of collagenous colitis. The subepithelial basement membrane is markedly thickened. Figure 33.5 Histological appearance of lymphocytic colitis. There is an increase in the number of intraepithelial lymphocytes (>20/100 epithelial cells). PROTEIN LOSING ENTEROPATHY osms.it/protein-losing-enteropathy PATHOLOGY & CAUSES SIGNS & SYMPTOMS ▪ Inflammatory GI conditions → loss of serum proteins into GI tract ▪ Mucosal injury → epithelial inflammation, → mucosal permeability → protein exudates across epithelium → proteins in GI tract degraded into amino acids (AA) ▪ Lymphatic obstruction/venous stasis → increased hydrostatic pressure in lymphatics → lymph leaks into intestinal lumen → reduced chylomicron reabsorption → decrease in fat soluble vitamins → protein deficiency ▪ Hyponatremia, peripheral edema, ascites ▪ Serosal effusions (pleural and pericardial) ▫ Dyspnea, cough, chest pain ▪ Steatorrhea, bloating, flatulence, abdominal pain ▪ Weight loss, chronic diarrhea CAUSES ▪ Inflammatory bowel disease ▫ Crohn’s disease, ulcerative colitis ▪ Malabsorptive diseases ▫ Tropical sprue, celiac sprue ▪ Infectious diseases ▫ C. difficile → pseudomembranous colitis ▪ GI malignancies DIAGNOSIS LAB RESULTS ▪ Consider in individuals with edema, hypoalbuminemia ▪ Increase in alpha-1 antitrypsin clearance ▪ Exclude other causes of hypoproteinemia ▫ Renal disease → proteinuria ▫ Hepatic disease → impaired protein synthesis ▫ Malnutrition TREATMENT OTHER INTERVENTIONS ▪ Low fat, high protein diet; supplement medium chain triglycerides (MCT) OSMOSIS.ORG 259
ULCERATIVE COLITIS osms.it/ulcerative-colitis PATHOLOGY & CAUSES ▪ Autoimmune disease → superficial ulcer formation; continuous, circumferential inflammation in colonic, rectal mucosa ▪ Most common inflammatory bowel disease; may present at any age ▪ Compare to Crohn’s disease ▫ Usually affects young people, affects entire GI tract; causes transmural inflammation; patches of inflamed mucosa, cobblestone appearance ▪ CD8+ cell activation → destruction of cells in mucosal, submucosal colonic layers ▫ Associated with perinuclear antineutrophil cytoplasmic antibodies (p-ANCAs) ▪ Multifactorial origin ▫ Environmental stimuli + excessive sulfide-producing bacteria + genetic predisposition ▪ More common among white people, especially of Eastern European descent ▪ More common in young individuals who are biologically female CAUSES ▪ Unclear; autoimmune reaction against colonic flora, molecular mimicry, increased sulfide production implicated ▪ Environmental factors contribute to acute flares COMPLICATIONS ▪ Toxic megacolon, anal fissures, perirectal abscess 260 OSMOSIS.ORG MNEMONIC: ULCERATIONS Features of Ulcerative colitis Ulcers Large intestine Carcinoma (risk of) Extraintestinal manifestations Remnants of old ulcers (pseudopolyps) Abscesses in crypts Toxic megacolon (risk of) Inflamed, red, granular mucosa Originates at rectum Neutrophil invasion Stool is bloody SIGNS & SYMPTOMS ▪ Acute flares, remissions; gradual onset ▫ Risk of relapse related to person’s age at diagnosis ▪ Severity determined by frequency of bowel movements, degree of inflammation, systemic symptoms ▪ Colicky, left lower quadrant pain ▪ Diarrhea; frequently grossly bloody, mucous ▪ Rectal tenesmus, incontinence, urgency, bleeding ▫ Tenesmus: Latin teinesmos; to strain ▪ Fever, fatigue, weight loss, anemia, dehydration ▪ Extraintestinal manifestations ▫ Arthritis (most common); uveitis; erythema nodosum; pyoderma gangrenosum; primary sclerosing cholangitis; arterial, venous thromboembolisms
Chapter 33 Inflammatory Bowel Disease DIAGNOSIS ▪ > four weeks active diarrhea + inflammatory findings on endoscopy + chronic inflammatory changes on biopsy ▪ Biopsy ▫ Crypt abscesses LAB RESULTS ▪ Anemia ▪ Elevated inflammatory markers ▫ Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) Figure 33.6 A pancolectomy specimen from an individual with ulcerative colitis. OTHER DIAGNOSTICS ▪ Clinical diagnosis; exclude other causes of colitis ▫ Infections (e.g. parasites, Clostridium difficile), STIs, radiation, medications TREATMENT MEDICATIONS ▪ Anti-inflammatory medications ▫ Sulfasalazine, mesalamine ▪ Immunosuppressors ▫ Corticosteroids, azathioprine, cyclosporine ▪ TNF blocking agent SURGERY ▪ Colectomy only if disease localized Figure 33.7 Abdominal radiograph demonstrating toxic megacolon, a complication of ulcerative colitis. Figure 33.8 The clinical appearance of erythema nodosum; a cutaneous manifestation of inflammatory bowel disease. OSMOSIS.ORG 261
Figure 33.9 Histological appearance of active ulcerative colitis in a colonic biopsy. There is active inflammation causing crypt destruction. Cryptitis and crypt abscesses are also present. 262 OSMOSIS.ORG

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This Osmosis High-Yield Note provides an overview of Inflammatory bowel disease essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Inflammatory bowel disease by visiting the associated Learn Page.