|
|
|
|
|
|
|
| Adenoma of Small Intestine | ||
| Etiology • Presumably same sequence of loss of heterozygosity as seen in adenomas of colon. •The dysplasia-adenoma-carcinoma sequence occurs in the setting of increasing loss of heterozygosity in genes involved in: DNA replication accuracy(mismatch repair)-Chromosomes 2 and 3; tumor suppression-Chromosomes 5,18, and 17; and oncogene activation-chromosomes 5,17,and 18 | ||
| Pathogenesis •Two pathways are commonly hypothesized to account for the known environmental, dietary and genetic predispositions to intestinal carcinoma. Both eventuate in loss of gene heterozygosity •The first of these postulate mucosal damage either through dietary induction of increased bile acid production or the direct affect of dietary and environmental carcinogens. This leads to increased mucosal cellular proliferative activity and an increase risk for gene match failure •The second postulates a direct genotoxic affect possibly mediated through production of oxygen free radicals •As increased numbers of defective gene growth regulators are formed, increased abnormal cellular activity eventuates in carcinoma • Same factors are presumably at work in small bowel lesions; although reason for low incidence unknown., | ||
| Epidemiology • Rare lesions. • Seen in familial polyposis coli particularly in periampullary region. | ||
| General Gross Description •Localized proliferations of dysplastic epithelium which are initially flat, but with increased growth project from the mucosa forming polyps. •Adenomas are classified by their gross appearance as either sessile(flat) or pedunculated(having a stalk). •Small adenomas(<0.5mm) have a smooth tan surface.Penduculated polyps have a head with a cobblestone or lobulated red-brown surface Sessile polyps have a more delicate villous surface much like a sea anemone. •Pedunculated polyps are more likely to be tubular or tubulovillous histologic type and sessile lesions are more like villous adenomas •While it is impossible to predict the presence or absence of carcinoma based on the gross appearance of polyps, larger polyps have a higher incidence of concurrent malignancy than small polyps. Sessile polyps have a higher incidence of malignany than pedunculated polyps of the same size. •Examples: | ||
| General Microscopic Description •By definition adenomas are composed of dysplastic epithelium. The nuclei are enlarged, cugar-shaped with an increase in nuclear chromatin, increased N/C ration, crowding and loss of polarity withing glands. There is often a decrease inmucous production. •Three subtypes of adenomas are recognized: tubular; tubulovillous: and villous. •Villous adenomas have more than 50% of the dysplastic epithelium arranged in tall fingerlike villous projection similar to the villi seen in normal small intestinal mucosa. •Tubular adenomas have more than 75% of their epithelium arranged in tube like fashion which when cut accross looks like rows of transected gunbarrels. •Tubulovillous lesions have 25-50% villous component the rest being tubular. •Pedunculated adenomas are predominantly tubular with an increasing villous component as they grow larger. •Sessile adenomas are predominantly villous. •As a general rule, adenomas become more sessile as they become larger, and sessile lesions have a higher degree of dysplasia that tubular lesions. •Examples: | ||
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 809-818. This link will directly take you to the relevant new literature Adenoma of Small Intestine
| Synopsis by: Martin Nadel M.D. (T64000M82611)[546]
| |
|
|
|
|
|
|