IBD Pathology Flashcards

1
Q

Name 4 important pathologic components of normal small bowel

A

Villi
Intraepithelial lymphocytes (~20/100)
Paneth cells
Brunners glands in duodenum

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2
Q

Where are lymphoid aggregates?

A

Terminal ileum

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3
Q

Contrast paneth cells from neuroendocrine cells

A

Neuroendocrine cells are on basement membrane of crypts have thinner/smaller nuclei

Paneth cells are closer to lumen and have chunkier pinker nuclei

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4
Q

What are the two diseases in IBD?

A

Crohn’s disease and ulcerative colitis

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5
Q

Describe basic epidemiology of IBD

A

Presents in teens and younger 20s
Most common among caucasians– Norther America, Norther Europe, Australia
3-5 more common in Ashkenazi jews

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6
Q

What are four large factors in pathogenesis in IBD?

A

Genetics, microbial factors, environmental factors, immune dysfunction

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7
Q

What gene is strongly associated with Crohn’s disease? What is its function?

A

NOD2 on chromosome 16. Detects MDP and binds to bacterial peptidoglycans and initiates NF-kB and MAPK-dependent gene transcritipn

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8
Q

IBD associated genes are involved in responses to what type of bacteria?

A

Mycobacteria including M. Tuberculosis and M. Leprae

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9
Q

What are the features of chronicity in IBD? (4)

A

Architectural distortion
Basal lymphoplasmacytosis
Paneth cell metaplasia (left side only)
Pyloric metaplasia (terminal ileum/cecum)

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10
Q

What are other causes of chronic mucosal injury? (3)

A

Ischemia
XRT/chemo
Chronic infection

Chronic mucosal injury does not mean it is IBD. Need clinical/endoscopic findings or full thickness section

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11
Q

What does “activity” in IBD mean?

A

Activity refers to the presence of neutrophils– They are never normal in lamina propria or crypt epithelium

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12
Q

Describe the different lesion patterns of crohn disease vs. ulcerative colitis

A

Crohn’s disease: skip lesions with transmural inflammation, ulcerations and fissures

UC: continuous colonic involvement that goes rectum up with pseudopolyps and ulcers

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13
Q

What is presentation of Crohn’s disease?

A

Intermittent attacks of diarrhea, fever and abdominal pain that are interrupted by asymptomatic periods that last for weeks-months

Smoking is a strong exogenous risk factor for development of Crohn’s

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14
Q

What are most common sites of chohn’s disease?

A

It can occur anywhere in GI tract….but most common sites are terminal ileum, ileocecal valve and cecum.

Small intestine alone=40%
SI+colon=30%

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15
Q

What are major perianal complications of Crohn’s? How common is it?

A

35-45% of patients are affected

Major complications include fissures, fistulas, abscesses and stenosis

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16
Q

What are the macroscopic features of Crohn’s disease? (6)

A

Skip lesions
Cobblestoning
Strictures (due to hypertrophy of muscular propria)
Creeping fat
Fissures
Fistulas (due to transmural inflammation)

17
Q

What are the microscopic features of Crohn’s disease? (5)

A

Transmural inflammation: from mucosa to serosa
Features of chronic mucosal injury
Active disease: cryptitis or crypt abscesses
Knife-like ulcerations
Non-Caveating epithelioid granulomas (35%)

18
Q

Where is ulcerative colitis usually present?

A

Limited to colon and rectum (though can get backwash ileitis)
If entire colon is diseased– pancolitis
If just rectum: ulcerative proctitis

19
Q

What are macroscopic features of UC? (3)

A

Abrupt transition between diseased/uninvolved colon
Ulcers and inflammatory pseudopolyps
Mucosal bridges: fusion of tips of polyps

No fissures, fistulas, mural thickening, serositis or non-neoplastic strictures

20
Q

What are the microscopic features of UC?

A

Chronic mucosal damage
If active, cryptitits, crypt abscesses
Diffuse inflammatory process limited to mucosa and superficial subucosa

21
Q

How do you tell Crohn’s and UC apart microscopically?

A

Crohn’s: Transmural inflammation from mucosa to serosa

UC: Diffuse inflammatory process limited to mucosa and superficial submucosa. Mucularis propria is spared

22
Q

What is a mucin-granuloma or crypt-rupture granuloma?

A

Describes crypts that are destroyed by neutrophilic infiltrate. It can occur in either UC or Crohn’s.

DO NOT CONFUSE WITH EPITHELIOID GRANULOMA OF CROHN’S

23
Q

What is backwash ileitis?

When do you see it?

A

Incompetence of ileocecal valve due to severe colonic disease results in retrograde flow of colonic contents into distal ileum, leading to inflammation.

Backwash ileitis is observed in UC patients with pancolitis

24
Q

What is the relationship between IBD and colorectal carcinoma?

A

Duration of IBD is associated with risk of developing colorectal carcinoma

25
Q

What is best marker for risk of carcinogenesis?

A

Dysplasia

26
Q

What are the types of dysplasia? Which one can be seen on endoscopy?

A

Can be flat or raised.

Flat– Not endoscopically visible

27
Q

What is DALM?

A

DALM is endoscopically visible dysplasia associated lesion or mass

28
Q

What is strategy for flat dysplasia?

A

If low grade, repeat in 6 months. If still see dysplasia then colectomy.
If high grade dysplasia, do a colectomy