Two pathways are commonly hypothesized to account for the known environmental, dietary and genetic predispositions to colorectal carcinoma. 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.
Villous adenomas are sessile lesions with a papillary surface similar to a sea anemone.
Partly polypoid lesions may be seen but these have a broad base rather than a stalk. In villous adenomas the fingerlike proliferation resembles the villi of normal small intestinal mucosa except that the normal epithelial tissue covering is replaced by dysplastic epithelium. These cells have enlarged cigar-shaped nuclei with increased nuclear chromatin, crowding and pseudopalisading. Mucin production is often decreased but some lesions show a marked increase in mucin. They are usually discovered as a result of a workup for occult blood loss, anemia or during a screening colonoscopy.