Monthly Archives: August 2010

Diverticular Disease

Diverticular Disease

Acquired  – lack or have attenuated muscularis propria due to focal weakness in the wall

Multifactorial pathogenesis including:

-increased intraluminal pressure

-colonic wall aging

-motor dysfunction

-lack of dietary fiber

Other diverticula to be aware of:

Esophageal

Meckel’s

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Angiodysplasia

Angiodysplasia

Clinical

-right colon most commonly, occasionally small intestine

-presents as chronic intestinal bleed, anemia and weight loss

- reported to be association with aortic stenosis

-fairly frequent cause of bleeding in the elderly

-3 types

-I  – most common, >55yrs, right colon

-II – 20s and 30s  – stomach and proximal bowel

-III – positive family hx -  GI tract lesions, oral mucosa and skin lesion

Pathogenesis

-acquired.vascular ectasia due to partial intermittent occlusion of submucosal veins

Gross Appearance

-one or multiple lesion  -sharply delineated red, flat or slightly raised,  mucosal lesion with scalloped edges and a prominent draining vein

Histology

-dilated, tortuous submucosal veins with distended branches piercing through the muscularis mucosa, connecting with dilated capillaries between the crypts in the lamina propria

-ectatic small vessels may fill the entire mucosa

-surface mucosa erosion and acute chronic inflammation

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Ischemic Colitis

Ischemic Colitis

Causes of Ischemic Colitis

-damage to colon secondary to decreased blood flow.
-patients are usually in their 7th decade
-usually atherosclerosis related
-torsion and strangulation rare as causes
-acute fulminant disease with progression to transmural necrosis is rare
-chronic ischemia may lead to progressive stenosis and obstruction
-resolution in 50%, but also high recurrence rate

Distribution of lesions

-most common sites: the splenic flexure and descending colon and sigmoid colon
-any site can be involved
-rectum is the least likely

Microscopic findings on biopsy

-superficial mucosal necrosis
-hyalinized lamina propria
-withered or atrophic crypts
-pseudomembranes
-chronic ulcers or strictures

Ischemic Colitis Differential Diagnosis

-pseudomembranous colitis
-enterohemorrhagic e.coli
-NSAID damage
-radiation colitis

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Crohns Disease

Crohns Disease

-1/3 present before the age of 20, 1/5 after the age of 50
-M:F=1:1
-cramping pain , non bloody diarrhea, fever, malaise, anorexia.
-hemorrhage and hematochezia uncommon
-dyspepsia, wt loss, hypoalbuminemia and iron deficiency anemia ( upper GI tract involvement)
-anal and perianal fistulas and fissures
-extraintestinal manifestations  – migratory  polyarthiritis, ankylosing spondylitis, cholngitis, uveitis, erythema nodosum, amyloid.

Causes of Crohns Disease

-etiology unknown
-chornic inflammatory  relapsing and remitting disease of the GI tract
- strong genetic predisposition -  17-35x the risk in siblings of patients

Crohns Disease Appearance

- inflammation anywhere from mouth to anus
creeping fat  subserosal fat contracted over the areas of involvement
-areas of firm, thickened and pipelike bowel
-interloop adhesions
-aphthous erosions
-longitudinal “rake “ ulcers
-cobblestoning
-inflammatory polyps
-fissures
-fistulas
-rectal sparing

Crohns Disease Microscopic Appearance

- biopsy:
-discrete foci of  inflammation and architectural changes adjacent to histologically normal crypts
-basal lymphoplasmacytic infiltrates
-aphthous lesions often associated with underlying lymphoid aggregates
-variability of inflammation within a single biopsy and among biopsy fragments from the same anatomic location
-may or may not see granuloma on biopsy
-panneth cell metaplasia

-resection ( in addition to the above):
-neural hyperplasia
-submucosal fibrosis
-transumural inflammation
-ulcers separated by histological normal mucosa
-lymphoid aggregates in subserosa and submucosa
-fissures, sinuses and fistulas
-granulomata

Crohns Disease Differential Diagnosis

Infectious colitis

-    most common cause of apthous ulcers of small  and large intestine
-    lack of significant chronic inflammation
-    absence of crypt distortion and basal lymphocytosis
-    no epithelial granulomata except for TB and Yersinia, but those have to be diagnosed on clinical history

Ischemic colitis

-history is KEY – elderly patients with atherosclerosis, Left-sided distribution of lesions as the left side of the colon is more vulnerable to ischemia

-no granulomata
-lamina propria neutrophillic infiltrate but no crypt abscesses of cryptitis
-intramucosal hyalinization

Ulcerative Colitis

- involves the colon only

- transmural inflammation

Medication associated colitis

- ie. NSAIDS, penicillamine, sulfasalazine, and methyldopa
-lack active inflammation
-no mucosal architectural distortion
-may resemble Crohn’s because it also has abrupt transition between ulcerated and non ulcerated areas

Diverticular disease associated segmental colitis

-commonly in sigmoid
-diverticula seen on colonoscopy
-foreign body type granulomata, cryptitis and crypt abscesses
-colitis is seen in the distribution of  the diverticula

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Cancer

Neoplastic complications of Iinflammatory Bowel Disease

Epithelial dysplasia in Ulcerative Colitis

Mod Path 2003 : 16(4): 347-358. by Robert Odze

Ulcerative colitis associated epithelial dysplasia

-incidence increases with duration of the disease

-risk is highest with ulcerative pan-colitis – the greatest extent

-presence of sclerosing cholangitis might also be a risk factor

- softer risk factors include: early age of onset, Family History of colon cancer, folate deficiency

-  patients who have had Ulcerative Colitis for 7-8 years should be entered in a screening program

- systematic, multiple mucosal biopsies increase the rate of detection

- dysplasia lesions  classified as either flat or raised  (DALM – dysplasia associated lesion or malignancy).

- dysplastic epithelium further classified into low and high grade dysplasia

-Management guidelies depend on  probabilities of 1. coexistant carcinoma and 2. progression onto carcinoma

DALM – dysplasia associated lesion or malignancy

-flat dysplasia , if low grade, is followed. If high grade, goes to colectomy.

-DALM – dysplasia associated lesion or malignancy – is broken down to adenoma-like polypoid sporadic  ( isolated polypoid lesions similar in appearance to sporadic adenoma) , adenoma like polypoid dysplastic lesion related to the underlying IBD and non adenoma like . Polypoid sporadic  is treated with polypectomy,  and there is increasing evidence that polypoid IBD associate lesions can also be treated with polypectomy, provided there is no associated flat dysplasia.

-non adenoma like lesions are treated with colectomy

Crohn’s Disease Cancer

-increased risk of adenocarcinoma ( 4x-20x)

- adenocarcinoma may arise in a morpholocially normal bowel, in areas of stricture and within fistula tracts, making diagnosis difficult.

-multiple synchronous and metachornous adenocarcinomas may occr and involve large and small intestines

-overall mortality in Crohn’s  from cancer is high -80%

well-differentiated tumors may extend from fistula tracts and may endoscopically be misinterpreted as adenoma

-symptomatically, adenocarcinoma may mimic a Crohn’s relapse – delay in diagnosis

-unlike in ulcerative colitis there is no standard surveillance strategy due to technical diffculties in surveying the bowel

-prophylactic resection  ( for dysplasia) is not recommended because of risk of post op complications

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Extraintestinal Manifestations

Inflammatory bowel disease extraintestinal manifestations

All inflammatory bowel diseases can have:

- Migratory Polyarthritis, Ankylosing spondylitis, Cholangitis, Uveitiis

Crohn’s Disease

- erythema nodosum, amyloid

Ulcerative Colitis

- primary sclerosing cholangitis

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