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31 Cards in this Set

  • Front
  • Back
Ulcerative colitis
recurrent acute and chronic inflamm disorder with extensive ulcers of colon and involvement of extracolonic sites. M=F, most often in 2nd and third decades of life. Familial clustering. disease for life
Gross Pathology of Ulcerative Colitis
starts in the rectum and extends proximally and in continuity.merging ulcers and sloughing. pseudopolyps. no skip areas.
histopathology of UC
cryptitis and crypt abcess that coalesce to undermine mucosa. Marked goblet cell depletion. Regeneration.
For dx: incr #plasma cells at the base of the mucosa bw the terminal end of the crypt or gland and mucosa. basilar plasmacytosis. irregular contours of crypts or glands bc of every crypt or gand is coated by a sheath and when damaged crypt cannot regenerate in a normal shape.
Two most important: irreg branched crypts/glands and basilar plasmacytosis.
primarily mucosal based unlike crohns that is transmural.
Granulomatous Colitis
chron's disease. large bowel is involved 40% of the time, in about half of these only large intestine involved
Gross Pathology of Chron's disease
segmental, predominately right sided (contrast to UC). may not involve rectum whatsoever (opposite of UC)
Histopathology of CD
transmural lyphoid aggregates, granulomas, edema, fissures, minimal mucosal atrophy, skip regions
Rectal bleeding in UC vs CD
common in UC not in CD
Abdominal pain in UC vs CD
left sided in UC, right sided in CD
Sigmoidoscopy in UC vs CD
abn majority of UC, abn in <50% of CD
Anal problems in UC vs CD
rare in UC and more frequent in CD
Distribution in UC vs CD
UC-left sided, diffuse, mucoasl and submucosal. Crohns- right sided and skipped areas and transmural
Rectal disease UC vs CD
UC- almost always, CD 50%
Granulomas UC vs CD
UC-absent, CD- usu present
Lymphoid aggregates UC vs CD
rare in UC, common in CD
Edema in UC vs CD
UC- minimal, CD-prominent
Fissures in UC vs CD
Absent in UC and common in CD
Internal fistulae
UC-absent, CD common
Diverticular disease
hypertrophy of Teniae coli and circular muscle with flask shaped sacs of mucosa and submucosa protruding along the side of tanieae. Complications include inflammation, pericolic abcess, and hemorrhage. sigmoid involvement most common
Hyperplastic polyp
usu asymptomatic , often in rectum, usu multiple, less than 5 mm, sessile -no stalk, on mucosal fold crest, elongated glands with papillary infolding small basal nuclei and abundant mucin. no atypia
Juvenile polyp
more common in children, single or multiple, rectum is most common site, pedunculated, focally ulcerated, smooth surface round polyp, on sectioning-numerous cysts. Dilated crypts embedded in excess lamina propria which shows purulent inflammation
Colonic Adenomas
benign. sharply circumscribed elevations of dysplasti epithelium, pedunculated or sessil, tubular villous or tubovillous. Reduced mucus, increased N;C ratio, hyperchromasia, high mitotic rate, stratification
Adenoma-Carcinoma Sequence
2/3 of all adenocarcinomas arise in adenomas
Most are over 2 cm-larger are more likely to harbour cancer
Most are villous or tubovillous.
Degree of dysplasia
Colonic Carcinoma
peaks in the 7th decade, 45% have 5 yr survival.
Gross pathology of Colonic Carcinoma
Left: circumfrential mapkin ring constriction, obstruction
Right: Exophytic-polypoid growth, anemia
Classic glandular adenocarcinoma. Colloid (or mucinous)*variant- has worse prognosis. Signet ring variant.
Familial Adenomatous Poluposis
Autosomal dominant. Adenomas appear in 2-3rd decades. Bleeding mucus discharge, diarrhea. Polyps usu less than 1 cm....LOTS of them. approx half have colonic carcinoma upon presentation of symptoms. Prophylactic colectomy at Dx
Lynch Syndromes
AD inheritance of colorectal carcinoma with young age at diagnosis, right sided predominance, & multiplicity
Associated with Kidd (18q 11-12)
8 times more common than FAP
May be associated with “Flat” adenomas
2 genetic pathways of colon cancer
Suppressor Pathway Genetic changes in APC, beta-catenin, & TCF4 80% sporadic colon cancers FAP
Mutator Pathway Multiple genetic changes in DNA mismatch repair gene system Results in microsatellite instability 10-20% sporadic cancers Many cases of CUC cancers
Normal mechanisms of colon cancer
APC protein binds ß-catenin Glycogen synthase kinase then phosphorylates ß-cat Then, ß-cat can be degraded
5 normal DNA mismatch repair genes They reduce mutations, especially at microsatellites
Supressor pathway
Most often, mutation in APC gene results in abnormal truncated protein
50% of cases with normal APC gene, mutation in -cat gene resulting in abnormal protein
In either case, no phosphorylation
 -cat builds in cytoplasm & moves to nucleus
 -cat binds TCF4
This results in upregulation of #genes. eg bcl-1 & PPAR
mutator pathway
Most often, hypermethylation (& inactivation) of hMHL1 promotor
Increased tendency for more mutations, especially at microsatellites, a few of which are near important genes.