Chronic mucosal inflammation beginning at the rectum and extending proximally in a continuous pattern.
Also known as: UC, ulcerative colitis, ulcerative proctitis, pancolitis
Overview
Chronic, idiopathic, immune-mediated inflammatory bowel disease characterized by continuous mucosal inflammation that begins in the rectum and extends proximally to a variable extent. Inflammation is limited to the mucosa and submucosa.
Epidemiology
Incidence 10-20 per 100,000/year in North America; prevalence ~500 per 100,000 (more common than Crohn). Bimodal peaks at 15-30 and 50-70. Slight male predominance. Higher in Ashkenazi Jews, Northern European descent.
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Question 1GastrointestinalMedium
A 55-year-old man with ulcerative colitis is hospitalized with 8 bloody stools per day, a temperature of 39.0°C, and diffuse abdominal tenderness. WBC is 18,000/mm3 and albumin is 2.4 g/dL. Stool studies, including Clostridioides difficile testing, are negative. Abdominal radiograph shows no colonic dilation. He has received intravenous methylprednisolone for 72 hours with minimal improvement. Which of the following is the most appropriate next step in management?
AIntravenous ciclosporin or infliximab
BHigh-dose oral mesalamine induction
CContinued intravenous methylprednisolone
DUrgent full colonoscopy with biopsies
EIntravenous vedolizumab induction
Reveal answer & full explanation
Correct answer: A — Intravenous ciclosporin or infliximab
AIntravenous ciclosporin or infliximab✓
BHigh-dose oral mesalamine induction
CContinued intravenous methylprednisolone
DUrgent full colonoscopy with biopsies
EIntravenous vedolizumab induction
Why Intravenous ciclosporin or infliximab is correct
This is acute severe ulcerative colitis by Truelove and Witts criteria: more than 6 bloody stools per day with systemic toxicity (fever, leukocytosis, hypoalbuminemia)
Failure to respond to intravenous corticosteroids by about 72 hours (the Oxford day-3 assessment) defines steroid-refractory disease
Per current ACG guidance, the next step after intravenous steroid failure is medical rescue therapy with intravenous ciclosporin or infliximab, with surgical consultation for colectomy if rescue fails
Delaying rescue therapy after steroid failure increases the risk of complications and emergency colectomy
Negative stool studies and the absence of colonic dilation on the radiograph make medical rescue, rather than urgent surgery, appropriate here
Why the others are wrong
Urgent full colonoscopy with biopsies — full colonoscopy carries a substantial perforation risk in acute severe colitis and adds little once infection is excluded; if mucosal assessment is needed, a limited flexible sigmoidoscopy is used instead (buzzword-matching on 'get tissue before escalating therapy')
Continued intravenous methylprednisolone — continuing steroids beyond 72 hours of nonresponse does not improve outcomes and only delays effective rescue therapy (premature closure on 'give the steroids more time')
High-dose oral mesalamine induction — mesalamine induces remission in mild-to-moderate ulcerative colitis and is inadequate for acute severe disease (right-drug-wrong-severity)
Intravenous vedolizumab induction — vedolizumab is an effective biologic for moderate-to-severe ulcerative colitis, but its gut-selective anti-integrin effect has a slow onset over weeks, too slow to rescue steroid-refractory acute severe colitis, where a rapid response is needed to avoid colectomy (right-drug-class-wrong-tempo)
Question 2GastrointestinalMedium
A 45-year-old man with ulcerative colitis involving the entire colon (pancolitis) for 15 years undergoes surveillance colonoscopy that shows mild chronic inflammation. Multiple biopsies from a flat area of the transverse colon are read as 'indefinite for dysplasia' by a single pathologist. He is maintained on mesalamine and remains clinically well. Which of the following is the most appropriate next step in management?
AProceed to colectomy
BEndoscopic resection of the flat area
CContinue annual surveillance
DIncrease mesalamine and repeat in 12 months
ERepeat colonoscopy in 3-6 months
Reveal answer & full explanation
Correct answer: E — Repeat colonoscopy in 3-6 months
AProceed to colectomy
BEndoscopic resection of the flat area
CContinue annual surveillance
DIncrease mesalamine and repeat in 12 months
ERepeat colonoscopy in 3-6 months✓
Why Repeat colonoscopy in 3-6 months is correct
'Indefinite for dysplasia' is a noncommittal pathology read with high interobserver variability, frequently driven by active inflammation; it is not itself an indication for surgery.
Per AGA/SCENIC guidance, optimize inflammation control and repeat colonoscopy in 3–6 months, ideally with chromoendoscopy and expert gastrointestinal-pathologist review, before any management change.
This confirms or refutes true dysplasia before committing the patient to a major intervention.
Why the others are wrong
Continue annual surveillance — defers reassessment far too long for an indefinite read; premature closure that under-responds to the finding.
Increase mesalamine and repeat in 12 months — controlling inflammation is reasonable, but a 12-month interval delays needed re-evaluation (right-idea-wrong-timing).
Proceed to colectomy — surgery is reserved for confirmed high-grade (or multifocal/endoscopically unresectable low-grade) dysplasia, not an unconfirmed indefinite read; anchoring on cancer risk.
Endoscopic resection of the flat area — endoscopic resection is used to remove a visible, well-demarcated lesion, but these biopsies came from flat, inflamed mucosa with no discrete lesion described, and an indefinite read has not established dysplasia; it must first be confirmed or refuted on repeat colonoscopy, ideally with chromoendoscopy, after inflammation is controlled (treating an equivocal read as confirmed dysplasia).
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Family history (HLA-DR2, multiple susceptibility loci)
NON-smoking — smoking is PARADOXICALLY PROTECTIVE; cessation can precipitate first flare
Appendectomy for appendicitis in childhood or adolescence is protective
NSAID use can trigger flares
Stress and infections may trigger relapses but do not cause UC
Pathophysiology
Aberrant Th2-skewed mucosal immune response to commensal microbiota in genetically susceptible hosts. Epithelial barrier dysfunction, increased permeability, and dysregulated regulatory T cells. Continuous mucosal inflammation starts at the rectum and progresses proximally without skip lesions.
Clinical presentation
Symptoms
Bloody diarrhea (HALLMARK)
Tenesmus and urgency
Lower abdominal cramping, especially LLQ
Passage of mucus and pus
Fatigue, weight loss, fever in moderate/severe disease
Distension and absent bowel sounds suggest toxic megacolon
Extraintestinal findings as above
Classic findings
Young adult with weeks of bloody diarrhea, tenesmus, and urgency; LLQ tenderness; flexible sigmoidoscopy reveals continuous mucosal inflammation starting at the rectum.
Composite of clinical (bloody diarrhea, urgency), endoscopic (continuous mucosal erythema, friability, ulceration starting at rectum), and histologic (crypt distortion, basal plasmacytosis, crypt abscesses; NO granulomas) findings, after exclusion of infection. Severity by Truelove and Witts criteria or Mayo Score.
Labs
CBC (anemia, leukocytosis, thrombocytosis as inflammatory marker)
CRP, ESR
BMP, albumin (severity)
LFTs (screen for PSC — alk phos disproportionately elevated)
Stool studies — C. diff, culture, ova/parasites; CMV biopsy in steroid-refractory cases
Fecal calprotectin (>250 supports active inflammation; useful for monitoring)
Serology: pANCA+/ASCA- pattern supports UC over Crohn
Moderate-severe disease: oral corticosteroids as an induction bridge, and start advanced therapy early (anti-TNF, vedolizumab, IL-12/23 or IL-23 antagonist, S1P modulator; JAK inhibitor after anti-TNF) rather than gradual step-up (AGA 2024)
Severe (hospitalized): IV corticosteroids (methylprednisolone 40-60 mg/day or hydrocortisone)
Maintenance with 5-ASA, immunomodulators, or biologics depending on response
Second-line / adjunct
Biologics: anti-TNF (infliximab, adalimumab, golimumab), vedolizumab (anti-integrin, gut-selective), ustekinumab (anti-IL-12/23), risankizumab/mirikizumab (anti-IL-23) for moderate-severe disease or steroid-refractory
JAK inhibitors: tofacitinib, upadacitinib — induction and maintenance after anti-TNF failure or intolerance (boxed warning: serious infection, mortality, malignancy, MACE, thrombosis)
S1P receptor modulators: ozanimod, etrasimod — oral agents for induction and maintenance
Immunomodulators (azathioprine, 6-MP) — maintenance, often in combination with biologics
Cyclosporine or infliximab — rescue therapy for acute severe UC failing 3-5 days of IV steroids
Surgery: total proctocolectomy with ileal pouch-anal anastomosis (IPAA) — CURATIVE; for medically refractory disease, multifocal or endoscopically unresectable dysplasia, cancer, or toxic megacolon
Complications
Toxic megacolon — colonic dilation >6 cm with systemic toxicity; surgical emergency; avoid antimotility agents, opioids, anticholinergics, barium enema
Severe hemorrhage
Perforation
Colorectal cancer — risk rises 8-10 yr after diagnosis with extensive colitis; surveillance colonoscopy every 1-3 yr
Strictures (less common than Crohn; if present, exclude malignancy)
Pouchitis after IPAA (treat with ciprofloxacin or metronidazole)
VTE — risk 3× baseline during flares; prophylax hospitalized patients
PANCE pearls
Bloody diarrhea + urgency + tenesmus in a young adult = UC until proven otherwise.
Continuous inflammation starting at the rectum distinguishes UC from Crohn (skip lesions, terminal ileum).
Smoking and appendectomy are paradoxically PROTECTIVE for UC. Smoking cessation can trigger first flare.
Acute severe UC (Truelove-Witts): ≥6 bloody stools/day + ≥1 systemic sign (fever, tachycardia, anemia, ESR >30) — admit, IV steroids, day-3 reassessment for rescue therapy.
Day-3 (Oxford/Travis) rule on IV steroids: >8 stools/day, OR 3-8 stools/day with CRP >45 mg/L, predicts ~85% colectomy → start rescue infliximab or cyclosporine; failure → colectomy.
Toxic megacolon: stop antimotility, opioids, anticholinergics; bowel rest; broad-spectrum antibiotics; serial abdominal exams and films; surgical consultation.
Colectomy is CURATIVE for colonic UC (unlike Crohn).
CRC surveillance: chromoendoscopy or high-definition white-light colonoscopy every 1-3 yr starting 8 yr after diagnosis (immediately upon PSC diagnosis).
Hospitalized IBD patients require VTE prophylaxis even during active bleeding — DVT risk outweighs minor bleeding risk.
Dysplasia on surveillance: visible, well-demarcated, completely resectable lesion (even high-grade) → endoscopic resection, then chromoendoscopic surveillance at 3-6 months and annually; invisible dysplasia on random biopsies → repeat high-definition chromoendoscopy by an IBD expert; multifocal or unresectable dysplasia → colectomy; indefinite for dysplasia → optimize inflammation control, expert GI pathology review, and repeat colonoscopy in 3-6 months (SCENIC; AGA 2021).
References
ACG 2025 — Rubin DT et al. ACG Clinical Guideline Update: Ulcerative Colitis in Adults. Am J Gastroenterol 2025;120:1187-1224
AGA 2024 — Singh S et al. AGA Living Clinical Practice Guideline on Pharmacological Management of Moderate-to-Severe Ulcerative Colitis. Gastroenterology 2024;167:1307-1343
ECCO 2022 — Raine T et al. ECCO Guidelines on Therapeutics in Ulcerative Colitis: Medical Treatment. J Crohns Colitis 2022;16:2-17
SCENIC 2015 — Laine L et al. SCENIC International Consensus Statement on Surveillance and Management of Dysplasia in Inflammatory Bowel Disease. Gastroenterology 2015;148:639-651
AGA 2021 CPU — Murthy SK et al. AGA Clinical Practice Update on Endoscopic Surveillance and Management of Colorectal Dysplasia in Inflammatory Bowel Diseases: Expert Review. Gastroenterology 2021;161:1043-1051
Travis 1996 — Travis SP et al. Predicting outcome in severe ulcerative colitis. Gut 1996;38:905-910
AGA 2019 — Ko CW et al. AGA Clinical Practice Guidelines on the Management of Mild-to-Moderate Ulcerative Colitis. Gastroenterology 2019;156:748-764
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