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PA23.5-7 | Intestinal TB, Appendicitis, IBD & Malabsorption — SDL Guide (Part 3)

Ulcerative Colitis — Pathology and IBD Comparison

A four-panel pathology diagram shows ulcerative colitis distribution, gross colon changes, mucosal-limited inflammation, microscopic crypt abscesses, and a concise comparison with Crohn disease. — **Panel A:** Colon and rectum, rectum always involved, continuous proximal spread, no skip lesions, small bowel spared, rare backwash ileitis. **Panel B:** Friable hemorrhagic mucosa, broad shallow ulcers, pseudopolyps, lead-pipe colon, loss of haustrations. **Panel C:** Mucosa, submucosa, muscularis propria, serosa, mucosal and superficial submucosal inflammation, no transmural involvement, Crohn transmural inset. **Panel D:** Crypt abscesses, neutrophils within crypts, crypt architectural distortion, goblet cell depletion, no granulomas. **Bottom comparison strip:** Crohn disease: any GI tract, skip lesions, transmural inflammation, granulomas may occur; Ulcerative colitis: colon and rectum, continuous disease, mucosal inflammation, crypt abscesses, no granulomas.

Ulcerative colitis (UC):

Distribution: Always involves the rectum (proctitis) and extends proximally in a continuous, uninterrupted pattern — never skip lesions. Limited to the colon and rectum (never small bowel, except 'backwash ileitis').

Gross morphology:
• Mucosal disease only (rarely submucosal) — no transmural involvement.
• Pseudopolyps (inflammatory polyps) — islands of regenerating mucosa surrounded by ulcerated areas; pathognomonic of UC.
• Lead-pipe colon on barium — loss of haustrations due to fibrosis and muscular hypertrophy (chronic disease).
• Friable, haemorrhagic mucosa with broad shallow ulcers.

Microscopy:
• Crypt abscesses — neutrophils within crypts, the histological hallmark of UC.
• Crypt architectural distortion — branching, shortened, irregular crypts (chronic change).
• Goblet cell depletion.
• No granulomas.
• Mucosal and submucosal inflammation only.

IBD Comparison Table — The High-Yield Summary:

Feature	Crohn Disease	Ulcerative Colitis
Distribution	Any GI, skip lesions	Colon/rectum, continuous
Depth	Transmural	Mucosal
Ulcers	Deep longitudinal fissures	Broad shallow
Microscopy hallmark	Non-caseating granulomas	Crypt abscesses
Fistulae	Very common	Rare (toxic megacolon risk)
Pseudopolyps	Occasional	Characteristic
Cancer risk	Small (small bowel > colon)	High (pancolitis >10 yr)
Surgery	Not curative	Colectomy = cure

A four-panel comparison diagram shows gross and microscopic differences between Crohn disease and ulcerative colitis, including cobblestoning, fissures, pseudopolyps, continuous ulceration, transmural granuloma, and crypt abscess. — **Panel A:** Crohn disease gross specimen: skip lesions, cobblestone mucosa, deep linear fissures, thickened bowel wall, stricture/narrowed lumen.. **Panel B:** Ulcerative colitis gross specimen: continuous mucosal ulceration from rectum proximally, pseudopolyps, shallow ulcers, friable mucosa, no skip lesions.. **Panel C:** Crohn disease microscopy: transmural inflammation, mucosa, submucosa, muscularis propria, serosa, fissuring ulcer, lymphoid aggregates, non-caseating granuloma.. **Panel D:** Ulcerative colitis microscopy: mucosa-limited inflammation, superficial submucosal extension, crypt abscess, neutrophils in crypt lumen, crypt distortion, mucosal ulceration, absence of granuloma..

IBD — Complications and Extraintestinal Manifestations

⚑ AI image — pending faculty review (auto-QA score 9/10; best of 3 attempts)

Four-panel medical diagram comparing Crohn disease and ulcerative colitis complications with shared extraintestinal manifestations of inflammatory bowel disease. — **Panel A:** Overview of IBD distribution: Crohn disease skip lesions involving terminal ileum/colon; ulcerative colitis continuous inflammation from rectum.. **Panel B:** Crohn disease complications: transmural inflammation, fibrotic stricture, obstruction, perianal fistula, enterovesical fistula, abscess, short bowel syndrome, small bowel adenocarcinoma risk.. **Panel C:** Ulcerative colitis complications: continuous mucosal colitis, toxic megacolon greater than 6 cm, perforation risk, colorectal cancer risk after long-standing pancolitis, haemorrhage, stricture.. **Panel D:** Extraintestinal manifestations: peripheral arthropathy, ankylosing spondylitis/sacroiliitis, erythema nodosum, pyoderma gangrenosum, uveitis, episcleritis, primary sclerosing cholangitis, anaemia..

Complications of IBD:

Crohn disease:
• Stricture and obstruction (fibrosis — 'fibrostenotic' phenotype).
• Fistulae — perianal fistulae, enterovesical, rectovaginal.
• Abscess formation.
• Short bowel syndrome after repeated surgical resections.
• Small bowel adenocarcinoma (rare but elevated risk vs general population).

Ulcerative colitis:
• Toxic megacolon — acute transmural inflammation → colonic dilatation > 6 cm → risk of perforation. Medical emergency. Barium enema and colonoscopy contraindicated.
• Colorectal cancer — risk rises steeply with pancolitis > 10 years (cumulative 10-20% at 20 years). Dysplasia surveillance colonoscopy is mandatory.
• Haemorrhage.
• Stricture (less common than Crohn).

Extraintestinal manifestations (shared by both, commoner in Crohn):
• Joints: peripheral arthropathy (parallels gut activity), ankylosing spondylitis/sacroiliitis (independent of activity).
• Skin: erythema nodosum (parallels gut activity), pyoderma gangrenosum (independent).
• Eyes: uveitis, episcleritis.
• Liver: primary sclerosing cholangitis (PSC) — strongly associated with UC (70% of PSC patients have UC); risk of cholangiocarcinoma.
• Blood: anaemia (iron/B12 deficiency or chronic disease).

SELF-CHECK

A 32-year-old presents with bloody diarrhoea for 8 weeks. Colonoscopy shows continuous mucosal erythema and friability from the rectum to the splenic flexure with multiple small pseudopolyps. Biopsy shows crypt abscesses and goblet cell depletion without granulomas. What is the most serious long-term complication to counsel this patient about?

A. Perianal fistula formation

B. Small bowel adenocarcinoma

C. Colorectal cancer with pancolitis duration

D. Primary biliary cirrhosis

Reveal Answer

Answer: C. Colorectal cancer with pancolitis duration

This is ulcerative colitis (continuous rectal disease, pseudopolyps, crypt abscesses, no granulomas). The most serious long-term complication is colorectal cancer, risk rising to 10-20% with pancolitis lasting >20 years, requiring regular dysplasia surveillance colonoscopy. Perianal fistulae are a feature of Crohn, not UC. PSC is associated with UC but is a hepatic complication, not the most serious intestinal complication. Primary biliary cirrhosis is not specifically associated with UC.

Malabsorption Syndrome — Causes and Pathophysiology

A three-panel medical diagram explains malabsorption syndrome through villous injury, classified causes, and key mechanisms such as coeliac disease, pancreatic insufficiency, bile salt defects, SIBO, and lactase deficiency. — **Panel A:** Small intestinal lumen, normal villi, blunted villi, reduced absorptive surface, unabsorbed fat droplets, carbohydrates, proteins, vitamins, minerals, steatorrhoea, weight loss, nutritional deficiencies. **Panel B:** Mucosal disease, coeliac disease, tropical sprue, Whipple disease, luminal phase defects, pancreatic exocrine insufficiency, bile salt deficiency, bacterial overgrowth, SIBO, enzyme deficiency, lactase deficiency. **Panel C:** Gliadin, immune-mediated villous atrophy, anti-tTG antibodies, pancreatic lipase deficiency, fat malabsorption, bile salt deconjugation, impaired micelle formation, lactose malabsorption, osmotic diarrhoea.

Malabsorption syndrome is defined as failure of the small intestine to absorb nutrients (fat, carbohydrates, proteins, vitamins, minerals) adequately. The cardinal clinical features are steatorrhoea (bulky, greasy, offensive stools), weight loss, and nutritional deficiencies.

Classification of causes:

Mucosal (absorptive surface) diseases:
• Coeliac disease (gluten-sensitive enteropathy) — immune-mediated villous atrophy triggered by gliadin (gluten component); anti-tissue transglutaminase (anti-tTG) and anti-endomysial antibodies; HLA-DQ2/DQ8 association.
• Tropical sprue — chronic malabsorption in tropical countries (India, SE Asia, Caribbean); likely infectious/bacterial cause; responds to tetracycline + folate.
• Whipple disease — rare; caused by Tropheryma whipplei; PAS-positive macrophages in lamina propria; systemic (arthritis, neurological).

Luminal phase defects:
• Pancreatic exocrine insufficiency — chronic pancreatitis, cystic fibrosis; deficient lipase → fat malabsorption.
• Bile salt deficiency — cholestatic liver disease, terminal ileum resection (bile salt reabsorption site), bacterial deconjugation.

Bacterial overgrowth:
• Small intestinal bacterial overgrowth (SIBO) — motility disorders, blind loops, strictures; bacteria deconjugate bile salts and consume nutrients.

Enzyme deficiency:
• Lactase deficiency — commonest worldwide; lactose malabsorption → osmotic diarrhoea; high prevalence in South Asians.

Structural reduction:
• Short bowel syndrome — after extensive surgical resection.