IBD Flashcards
IBD definition
mucosal inflammatory conditions with chronic or recurring immune response and inflammation of the gastrointestinal (GI) tract
two types of IBD
Ulcerative Colitis (UC): mucosal inflammation confined to rectum and colon Crohn’s Disease (CD): transmural inflammation of GI tract that can affect any part from the mouth to the anus
epidemiology of IBD
most prevalent in western countries
both sexes affected equally
peak incidence in second (CD) or third decade (UC)
etiology of IBD
combination of immunologic, infectious, genetic, environmental factors - immune dysregulation, microflora of GI tract may trigger
immunologic etiology of IBD
both autoimmune and non-autoimmune mechanisms
innate immune system involves intestinal barrier function, is associated with secretions in response to stimuli
gut wall infiltrated by WBCs - granuloma formation
cytokine disregulation
microbial etiology of IBD
luminal microorganisms thought to be important in initiation of inflammation however no definitive infectious etiology
-shift toward more proinflammatory bacteria
-increased density of microflora
-potential loss of tolerance to normal GI flora
-bacterial antigens/ligands may induce and
propagate inflammation
-“microbiome” - ecological community of commensal, symbiotic, and pathogenic microorganisms
genetic etiology in IBD
high concordance rate in monozygotic twins
first degree relatives have 20x risk of IBD
not a single gene phenomenon
psychological etiology in IBD
stess may correlate with disease flares and impact QOL
environmental etiology in IBD
“hygiene hypothesis”: cleaner conditions in developed countries expose patients to fewer pathogens/antigens at a young age - potentially altered immune response when encountered later in life
diet (potential association - causality unclear)
smoking - potentially protective in UC (reduced disease activity, fewer flares); associated with an increase frequency and severity of CD
Drug related etiology of IBD
NSAIDs - may trigger disease occurrence or lead to flares, unclear whether COX-2 selective agents are associated with a decreased risk, generally avoid NSAIDs in pts with IBD
antibiotics - potential association, however causal relationship unclear
UC pathophysiology
confined to rectum and colon and affects mucosal and submucosal layers (more superficial than CD)
-abscess formation in mucosal crypts, coalescence results in ulceration
extension and coalescence of ulcers may surround areas of normal tissue
mucosal damage and friability can result in substantial diarrhea and bleeding
complications of UC
local, systemic and extraintestinal complications
local - hemorrhoids, anal fissures, perirectal abcesses
other major complications: colonic perforation (can be w/wo toxic megacolon), massive colonic hemorrhage, colonic stricture
toxic megacolon
complication of UC - severe and potentially fatal
segmental or total colonic distention with acute colitis and signs of systemic toxicity
increase depth of ulceration
vasculitis and thrombosis
colonic dilation and potential perforation
associated with fever, tachycardia, abdominal distention, elevated WBCs
colonic dysplasia/colorectal cancer (CRC)
risk of colonic dysplasia w transition to CRC is 5x greater in UC
cumulative risk of CRC is up to 20-30% at 30 years
screening colonoscopy with biopsies recommended at 8 years after UC onset and every 1-2 years after that
CD pathophysiology
transmural inflammation
anywhere in GI tract (terminal ileum most common)
often discontinuous (normal bowel separating diseased bowel)
deep, elongated ulcers, cobblestone appearance
bowel wall injury may be extensive, associated with luminal narrowing
complications of CD
small bowel stricture and obstruction possible
fistula common (20-40% lifetime risk) - fistula = pathologic connection between bowel and another tissue (skin, another segment of GI tract, bladder, or vagina)
less bleeding than UC (although anemia possible)
risk of carcinoma is increased, but not to the extent of UC
nutritional deficiencies common - weight loss, growth failure in children, iron deficiency anemia, vit B12 def., folate def., hypoalbuminemia, hypokalemia, osteomalacia
extraintestinal manifestations of IBD
hepatobiliary - common (5-95% incidence) - hepatic: fatty liver, pericholangitis, autoimmune hepatits, cirrhosis; biliary - primary sclerosing cholangitis (PSC), cholangiocarcinoma, cholelithiasis
occular - iritis, uveitis, episcleritis, conjuctivits
bone and joint - arthritis: asymmetrical, migratory, typically involes one/few large joints and parallels disease activity; may be at increase risk for metabolic bone disease and osteoporosis (nutrient definiciences, inflammation, hypogonadism, use of CSs)
hematologic - anemia
coagulation - increase risk of VTE; higher during flares, consider prophylaxis if admitted for flare
dermatologic and mucocutaneous - variety of skin and mucosal lesions
clinical presentation of UC
highly variable; may include intermittent illness and periods of remission diagnosis made on clinical suspicion and confirmed by endoscopy (colonoscopy or sigmoidoscopy) and biopsy disease extent (location of inflammation) determined by endoscopy
signs and symptoms of UC
abdominal cramping
frequent BMs +/- blood +/- mucous (can range from frequent small volume to profuse diarrhea)
weight loss
paradoxical constipation possible
fever/tachycardia (esp. in severe disease)
extraintestinal: blurred vision/ocular signs; arthritis; dermatologic manifestations
physical examination of UC
hemorrhoids, anal fissures, perirectal abscesses may be present
dermatologic/ocular findings
lab tests for UC
decreased Hb/HCT
increased ESR/CRP
leukocytosis, hypoalbuminemia (severe dz)
(+) perinuclear antineutrophil cytoplasmicantibodies
fecal calprotectin and fecal lactoferrin
types of UC
distal (left-sided): distal to splenic flexure
extensive: extending proximal to splenic flexure
proctitis: involving the rectal area
proctosigmoiditis: involving rectum and sigmoid colon
pancolitis: involving majority of colon
UC disease classification
determined by s/sxs
- Mild: under 4 stools/day (+/- blood); no systemic disturbance; normal ESR
- Moderate: over 4 stools/day; minimal systemic disturbance
- Severe: over 6 stools/day with blood; evidence of systemic disturbance (fever, tachycardia, anemia, or ESR over 30 mm/h)
- Fulminant: over 10 stools/day with continuous bleeding; toxicity (severe systemic disturbances); abdominal tenderness; need for transfusion; colonic dilation
clinical presentation of CD
highly variable, characterized by periods of remission and exacerbation
typical presentation includes diarrhea and abdominal pain - hematochezia in around 50% (less if no colonic involvement), should suspect diagnosis in children with impaired growth, esp. if associated w abdominal pain
diagnosis involves clinical evaluation in addition to endoscopic (upper and lower), laboratory, radiologic testing
s/sxs of CD
malaise, fever abdominal pain frequent BMs hematochezia fistula weight loss/malnutrition arthritis
PE of CD
abdominal mass/tenderness
perianal fissure, fistula
laboratory tests with CD
Hb/HCT
increased WBCs, ESR, CRP
(+) anti-Saccharomyces cervisiae antibodies
fecal calprotectin and fecal lactoferrin
CD disease classification
no global classification system
CDAI (crohn’s disease activity index) - used to gauge response to therapy and determine remission
treatment guidelines often use “clinical picture”
mild-moderate: ambulatory with minimal other symptoms (dehydration, systemic toxicity, loss of body weight, abdominal tenderness), no obstruction
moderate-severe: patients who fail therapy for mild-moderate
disease, or those with fever, weight loss, abdominal pain/tenderness, vomiting, obstruction, anemia
severe-fulminant: persistent symptoms or evidence of systemic toxicity despite corticosteroid or biologic treatment, or presence of cachexia, rebound tenderness, intestinal obstruction, or abscess
IBD treatment overview
pharmacologic therapy, surgical therapy, nutrition support, treatment of complications, avoiding drugs that may exacerbate IBD
goals of therapy: highly individualized; may include:
-resolve acute inflammation/treatment of disease flare
*resolve and/or prevent complications
-maintain remission
*alleviate extraintestinal manifestations
-avoid need for surgical palliation/cure (patient priority)
-surgical palliation/cure
-maintain QOL
inducing and maintaining remission** is an important ascept of therapy to improve outcomes and QOL and reduce complications - mucosal healing may be associated with better long term outcomes
nonpharm therapy for IBD
nutrition support - no specific diet shown to be beneficial, address nutritional deficiencies, impaired absorption (enteral supplementation if necessary, parenteral nutrition - avoid unless absolutely necessary, supplement vitamin/mineral deficiencies), probiotic therapy
surgery - resecting areas of inflammation, rates in UC may be around 5-30%, indications for surgery in CD are less established
