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Step 2 CK · Internal Medicine · Gastroenterology

Inflammatory Bowel Disease (Clinical)

Diagnose the pattern, then climb the treatment ladder

Gastroenterology·Lower GI Disorders·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy
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Crohn disease vs ulcerative colitis

Two patterns of chronic, relapsing inflammation. Crohn disease is transmural. It can affect any segment from mouth to anus, favors the terminal ileum, and leaves skip lesions, fistulae, and strictures. Ulcerative colitis (UC) is mucosal. It always involves the rectum and spreads continuously and proximally, and it affects the colon only.

Distinguishing Crohn disease from UC
FeatureCrohn diseaseUlcerative colitis
DistributionMouth to anus, terminal ileum favored; skip lesionsRectum always involved; continuous proximal spread; colon only (proctitis to pancolitis)
DepthTransmural; noncaseating granulomasMucosal; crypt abscesses
SymptomsCrampy (often RLQ) pain, often non-bloody diarrhea, weight lossBloody diarrhea, tenesmus, urgency
ComplicationsStrictures with obstruction, fistulae, abscesses, perianal disease; B12 deficiency, gallstonesToxic megacolon; colorectal cancer; PSC association
SerologyASCA positivep-ANCA positive
SmokingWorsens diseaseProtective
SurgeryResection for complications; not curative, and disease recursColectomy is curative

Terminal ileal Crohn disease impairs B12 and bile-acid absorption. The results are B12 deficiency and gallstones (bile-acid loss makes bile lithogenic). Fat malabsorption also raises the risk of calcium oxalate kidney stones.

Making the diagnosis

Ileocolonoscopy with biopsy confirms IBD and defines its pattern.

  • Fecal calprotectin: a noninvasive marker of neutrophilic intestinal inflammation. It is high in IBD and normal in irritable bowel syndrome. It also tracks disease activity and predicts relapse.
  • Serology: ASCA favors Crohn disease; p-ANCA favors UC.
  • CT or MR enterography: maps small-bowel Crohn disease, strictures, and fistulae.

In every IBD flare, test the stool for Clostridioides difficile before escalating immunosuppression. C. difficile often complicates IBD and mimics a flare. Treat it with oral vancomycin or fidaxomicin. A superimposed infection worsens outcomes and raises the risk of colectomy.

Inducing and maintaining remission

  1. 5-ASAMild-to-moderate UC.
  2. CorticosteroidsInduce remission in flares; never used for maintenance.
  3. ImmunomodulatorsAzathioprine/6-MP or methotrexate as steroid-sparing maintenance.
  4. Biologics and small moleculesModerate-to-severe disease.
  5. SurgeryCurative colectomy in UC; resection of complications in Crohn disease.
IBD drugs: role and must-know points
DrugRoleMust-know point
5-aminosalicylates (mesalamine)Induce and maintain mild-to-moderate UC, oral plus topicalTopical rectal therapy is key for proctitis and distal colitis; limited efficacy in Crohn disease
Corticosteroids: oral prednisone, IV methylprednisoloneRapid induction for moderate-to-severe flaresNever used for maintenance because of toxicity
BudesonideIleocecal Crohn diseaseHigh first-pass hepatic metabolism: acts locally in the gut with few systemic effects
Azathioprine, 6-mercaptopurineSteroid-sparing maintenanceCheck TPMT activity first: low activity predicts severe myelosuppression. Monitor CBC and liver enzymes
MethotrexateMaintains Crohn remissionMonitor CBC and liver enzymes; teratogenic
Anti-TNF: infliximab, adalimumabInduce and maintain moderate-to-severe Crohn disease and UC; used for fistulizing diseaseScreen for latent TB and hepatitis B before starting
VedolizumabModerate-to-severe diseaseGut-selective anti-α4β7 integrin
UstekinumabModerate-to-severe diseaseAnti-IL-12/23
JAK inhibitors (tofacitinib)Moderate-to-severe UCOral small molecule; warnings for serious infection and thrombosis

Extraintestinal manifestations

Skin, eyes, joints, and bile ducts. Some of these manifestations flare with the bowel, and others run their own course. That distinction predicts whether treating the colitis will help.

Extraintestinal manifestations and bowel activity
SystemTracks bowel activityIndependent course
SkinErythema nodosumPyoderma gangrenosum (often independent)
EyesEpiscleritisUveitis (often independent)
JointsPeripheral arthritisAxial arthritis: ankylosing spondylitis, sacroiliitis
Liver—Primary sclerosing cholangitis

Primary sclerosing cholangitis (PSC). PSC is tied to UC. It presents with pruritus and cholestatic liver tests, and MRCP shows multifocal strictures with beading of the bile ducts. It raises the risk of both cholangiocarcinoma and colorectal cancer.

Complications: toxic megacolon and cancer

>6 cmcolonic dilation with systemic toxicity = toxic megacolon
8 yearsafter colitis diagnosis: start surveillance colonoscopy

Toxic megacolon. Nonobstructive colonic dilation over 6 cm with systemic toxicity (fever, tachycardia, distension), which threatens perforation.

  • Avoid: antimotility agents such as loperamide, opioids, and colonoscopy, all of which make it worse.
  • Treat: IV steroids, bowel rest, decompression, broad-spectrum antibiotics, fluid and electrolyte correction, and testing for C. difficile.
  • Surgery: colectomy if there is no improvement in 24–72 hours, or for perforation.

In a severe colitis flare with abdominal distension, ordering loperamide or an opioid for "diarrhea control" can precipitate perforation.

Colorectal cancer surveillance. Chronic colitis raises colorectal cancer risk with longer duration, greater extent, and coexisting PSC. The schedule:

  • Begin surveillance colonoscopy about 8 years after colitis diagnosis, then repeat every 1–2 years.
  • With PSC, start at the time of diagnosis.

These cancers arise from flat dysplasia rather than discrete polyps, so random biopsies are taken (chromoendoscopy with targeted biopsies is increasingly used). Dysplasia that cannot be removed endoscopically is an indication for colectomy.