Inflammatory Bowel Disease

Front 1

*Epidemiology of IBD?

Back 1

more in northern hemisphere and industrialized countries, onset at 16-35 years
CD: female predominant. UC: male predominant.
Caucasian/Ashkenazi have increased risk

Front 2

*Pathogenesis of IBD?

Back 2

enviromental (hygiene, diet, appendectomy (increases CD, decreases UC), abnormal response to flora, acute infection, meds, smoking (decreases UC, increases CD and worsens CD course)
genetics: NOD2/CARD15 (homozyg has 40x RR, heterozyg has 4x RR), IL23R (more Th17 --> inflammation)
immune dysregulation: increased T cells (Th1, 2, 17), defect in innate immunity, defect in adaptive immunity, too much pro-inflammation, too little Treg to deactivate inflammation, ineffective apoptoces, failure to downregulate lymphocyte adhesion

Front 3

*How are CD and UC different clinically?

Back 3

UC: frequent bloody loose stools, urgency, tenesmus, lower abd cramping, incontenance, nocturnal awakening, pallor. comps: toxic megacolon, perforation, EMI

CD:diarrhea, abd pain, fever, weight loss, orthostatic hoTN, tachycardia, cachexia, perianal fissure/absecess. comps: fistulas, intraabdominal abscess, obstruction, perforation, EMI.

Front 4

*How are CD and UC different pathologically?

Back 4

UC: mostly in colon, proximal continuous extension from the rectum, inflammation is limited to the mucosa. mild/mod: erythema, edema, ulcers, erosions. severe: coalescence of ulcers, mucopurulent exudate, pseudopolyps. chronic: mucosal atrophy, muscle hypertrophy, loss of haustra.

CD: patchy, often rectal-sparing, terminal ileum and colon are most commonly affected, full-thickness inflammation. mild: apthoid ulcers, edema, hyperemic spots, loss of vascular pattern. severe: bear claw ulcers, pseudopolys, cobblestoning.

Front 5

*How are CD and UC different radiographically?

Back 5

UC: barium enema-- granular, ulcers, loss of haustra, strictures/dilation. CT--diffuse symmetric thickening, dilation, perf, EMI.

CD: string sign from thickened wall and stricture, CT-- ileal/colon thickening, fat stranding, abscess, obstruction, EMI. CT/enterography-- mucosal detail. MRI-- perianal/rectovaginal fistula

Front 6

How are CD and UC different histologically?

Back 6

UC: early: PMN, lymphocytes, cryptitis, crypt abscesses. chronic: Paneth cell metaplasia, crypt distortion/atrophy, basal lymphoid aggregation, chrnoic inflammatory infiltrate.

CD: non-caseating granulomas, transmural inflammation, fistulas, strictures, creeping fat

Front 7

*What's the differential diagnosis for IBD and ileitis?

Back 7

IBS, inflammation, neoplastic (if >50yo, weight loss, fhx cancer), vascular, infectious, drugs, factitious diarrhea, gyn problems, infiltrative, congenital

Front 8

*What are some extraintestinal manifestations of IBD?

Back 8

rheumatologic (peripheral or axial, metabolic bone disease. CD>UC)
mucocutaneous (pyoderma gangrenosum, erythema nodosum, sweet's syndrome, psoriasis (10% of CD), oral ulcers)
ocular: uveitis, cleritis
hematologic: anemia, hypercoagulation
nephrolithiasis
hepatobiliary: primary and sclerosing cholangitis (liver/bile duct stricture --> cirrhosis, UC>CD), gallstones)

Front 9

Which EMI parallel the disease course and which are independent?

Back 9

parallel: pauciarticular arthropathy, erythema nodosum, sweet's syndrome, episcleritis

independent: polyarticular arthropathy, axial arthropathy, pyoderma gangrenosum, uveitis

Front 10

What do you see on an endoscopy for CD vs. UC?

Back 10

UC: mild: erythema, edema, abnormal vasc patter.
mod: granular, friable, erosions, ulcers
severe: coalescence of ulcers, mucopurulent exudate, pseudopolyps
chronic: mucosal atrophy, muscle hypertrophy, loss of haustra

CD:mild: apthoid ulcers, edema, hypermeic spots, loss of vascular pattern.
mod/severe: deep linear bear-claw ulcers, pseudopolyps, cobblestoning

Front 11

*What are the pharmacological treatments for IBD?

Back 11

5-ASA for UC. inhibits COX, LOX, B cells. safe.
Abx (cipro, metro, rifaxamin). for CD.
steroids. to induce UC and CD remission. decreases lymphocytes and cytokines. AE: Cushing's.
6-MP: for steroid w/drawal, maintenance. purine-analog anti-metabolite. AE: pancreatitis, infection, fever
MTX: induce and maintain CD remission. folate analog anti-metabolite. AE: decreased bp, hepatotox.
cyclosporine. for steroid-refractory UC. downregulates IL-2. AE: infection, HTN, neurotox, renal tox.
natalizumab. to induce/maintain CD remission. alpha-4 integrin Ab. AE: PML
infliximab, adalimumab, cerolizumab. to induce/maintain CD and UC. anti-TNF-alpha. AE: infection, SLE, infusion reaction

Front 12

What's the risk for colon cancer with IBD?

Back 12

30% risk within 35 years, depends on disease extent, severity of inflimmation, pseudopolyps, Fhx, smoking.
5-ASA may decrease the risk.
Colonoscopy surveillance is recommended after 8-10 years, to find dysplasia.

Front 13

What are the complications of IBD with pregnancy?

Back 13

same fertility, 1/3 flare, 2/3 same/improve.
preterm birth, low birth weight, small for gestational age.
most meds (not MTX) are okay