Pathology Colon

Front 1

Ulcerative colitis

Back 1

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

Front 2

Gross Pathology of Ulcerative Colitis

Back 2

starts in the rectum and extends proximally and in continuity.merging ulcers and sloughing. pseudopolyps. no skip areas.

Front 3

histopathology of UC

Back 3

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.

Front 4

Granulomatous Colitis

Back 4

chron's disease. large bowel is involved 40% of the time, in about half of these only large intestine involved

Front 5

Gross Pathology of Chron's disease

Back 5

segmental, predominately right sided (contrast to UC). may not involve rectum whatsoever (opposite of UC)

Front 6

Histopathology of CD

Back 6

transmural lyphoid aggregates, granulomas, edema, fissures, minimal mucosal atrophy, skip regions

Front 7

Rectal bleeding in UC vs CD

Back 7

common in UC not in CD

Front 8

Abdominal pain in UC vs CD

Back 8

left sided in UC, right sided in CD

Front 9

Sigmoidoscopy in UC vs CD

Back 9

abn majority of UC, abn in <50% of CD

Front 10

Anal problems in UC vs CD

Back 10

rare in UC and more frequent in CD

Front 11

Distribution in UC vs CD

Back 11

UC-left sided, diffuse, mucoasl and submucosal. Crohns- right sided and skipped areas and transmural

Front 12

Rectal disease UC vs CD

Back 12

UC- almost always, CD 50%

Front 13

Granulomas UC vs CD

Back 13

UC-absent, CD- usu present

Front 14

Lymphoid aggregates UC vs CD

Back 14

rare in UC, common in CD

Front 15

Edema in UC vs CD

Back 15

UC- minimal, CD-prominent

Front 16

Fissures in UC vs CD

Back 16

Absent in UC and common in CD

Front 17

Internal fistulae

Back 17

UC-absent, CD common

Front 18

Diverticular disease

Back 18

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

Front 19

Hyperplastic polyp

Back 19

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

Front 20

Juvenile polyp

Back 20

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

Front 21

Colonic Adenomas

Back 21

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

Front 22

Adenoma-Carcinoma Sequence

Back 22

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

Front 23

Colonic Carcinoma

Back 23

peaks in the 7th decade, 45% have 5 yr survival.

Front 24

Gross pathology of Colonic Carcinoma

Back 24

Left: circumfrential mapkin ring constriction, obstruction
Right: Exophytic-polypoid growth, anemia

Front 25

Histopatholgy

Back 25

Classic glandular adenocarcinoma. Colloid (or mucinous)*variant- has worse prognosis. Signet ring variant.

Front 26

Familial Adenomatous Poluposis

Back 26

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

Front 27

Lynch Syndromes

Back 27

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

Front 28

2 genetic pathways of colon cancer

Back 28

Suppressor PathwayGenetic changes in APC, beta-catenin, & TCF480% sporadic colon cancersFAP
Mutator PathwayMultiple genetic changes in DNA mismatch repair gene systemResults in microsatellite instability10-20% sporadic cancersMany cases of CUC cancers

Front 29

Normal mechanisms of colon cancer

Back 29

APC protein binds ß-cateninGlycogen synthase kinase then phosphorylates ß-catThen, ß-cat can be degraded
5 normal DNA mismatch repair genesThey reduce mutations, especially at microsatellites

Front 30

Supressor pathway

Back 30

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

Front 31

mutator pathway

Back 31

Most often, hypermethylation (& inactivation) of hMHL1 promotor
Increased tendency for more mutations, especially at microsatellites, a few of which are near important genes.