Neoplastic Colonic polyps- Colonic Adenoma; Familial Syndromes

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Neoplastic Colonic polyps- Colonic Adenoma; Familial Syndromes

  1. 1. Benign Neoplastic Colonic Polyps Colonic Adenomas Colorectal Adenomas Lecture 15 Dr Mohammad Manzoor Mashwani BKMC Mardan
  2. 2. Classification- Neoplastic Polyps • Benign polyps • Adenomas • Malignant lesions (Polyps) Adenocarcinoma Squamous cell carcinoma of the anus
  3. 3. Adenomas • A benign epithelial tumor in which the cells form recognizable glandular structures or in which the cells are derived from glandular epithelium.
  4. 4. Colonic adenoma The most common and clinically important neoplastic polyps are colonic adenomas, benign polyps that give rise to a majority of colorectal adenocarcinomas. Most adenomas, however, do not progress to adenocarcinoma.
  5. 5. Adenomatous Polyps Adenomas By definition they are dysplastic and have malignant potential. Time for development of adenomas to cancer is about 7 to 10 years.
  6. 6. Epidemiology epithelial dysplasia. • Colorectal adenomas are characterized by the presence of • These growths range from small, often pedunculated polyps to large sessile lesions. • There is no gender predilection, • present in nearly 50% of adults living in the Western world • beginning age 50. • surveillance colonoscopy starting at age 50. • Because persons with a family history are at risk for developing colon cancer earlier in life, they typically are screened at least 10 years before the youngest age at which a relative was diagnosed . • While adenomas are less common in Asia, their frequency has risen (in parallel with an increasing incidence of colorectal adenocarcinoma) as Western diets and lifestyles become more common.
  7. 7. Types of adenomas On the basis of epithelial structure 1. Tubular adenomas 2. Villous adenomas 3. Tubulovillous adenomas 4. Sessile Serrated adenomas Endoscopic classification: 1. Sessile – base is attached to colon wall usually large 2. Pedunculated – mucosal stalk is interposed between the polyp and the wall 3. Flat – height less than one-half the diameter of the lesion. Depressed lesions appear to be particularly likely to harbor high-grade dysplasia or be malignant even if small. Pathologic classification: I. Low grade dysplasia II. High grade dysplasia
  8. 8. Gross Morphology • Size- 0.3 to 10 cm in diameter and • can be pedunculated or sessile, • with the surface of both types having a texture resembling velvet or a raspberry, due to the abnormal epithelial growth pattern.
  9. 9. Microscopy • Histologically, the cytologic hallmark of epithelial Dysplasia is nuclear hyperchromasia, elongation, and stratification. These changes are most easily appreciated at the surface of the adenoma, because the epithelium fails to mature as cells migrate out of the crypt. Pedunculated adenomas have slender fibromuscular stalks containing prominent blood vessels derived from the submucosa. The stalk usually is covered by nonneoplastic epithelium, but dysplastic epithelium is sometimes present.
  10. 10. Morphology Classification: tubular, tubulovillous, or villous. • Tubular adenomas- small, pedunculated polyps composed of small, rounded or tubular glands. Villous adenomas- larger &sessile, covered by slender villi • Tubulovillous adenomas- have a mixture of tubular and villous elements. • Sessile serrated Adenomas- serrated architecture throughout the full length of the glands, including the crypt base, associated with crypt dilation and lateral growth. • In hyperplastic polyps serrated architecture is confined to the surface. Larger size(>4cm) & high grade dysplasia are risk for malignancy in polyps.
  11. 11. Colonic adenomas. A, Pedunculated adenoma .B, Adenoma with a velvety surface. C, Lowmagnification photomicrograph of a pedunculated tubular adenoma.
  12. 12. Tubular adenoma with a smooth surface and rounded glands. Active inflammation is occasionally present in adenomas, in this case, crypt dilation and rupture can be seen at the bottom of the field.
  13. 13. Dysplastic epithelial cells (top) with an increased nuclear-to-cytoplasmic ratio, hyperchromatic and elongated nuclei, and nuclear pseudostratification.
  14. 14. Villous adenoma with long, slender projections that are reminiscent of small intestinal villi .
  15. 15. Sessile serrated adenoma lined by goblet cells without typical cytologic features of dysplasia. This lesion is distinguished from a hyperplastic polyp by extension of the neoplastic process to the crypts, resulting in lateral growth.
  16. 16. Familial syndromes I. Familial Adenomatous Polyps • Familial adenomatous polyposis (FAP) is an autosomal dominant disorder marked by the appearance of numerous colorectal adenomas by the teenage years. It is caused by mutations of the adenomatous polyposis coli gene (APC). A count of at least 100 polyps is necessary for a diagnosis of classic FAP, and as many as several thousand may be present
  17. 17. Familial Adenomatous Polyps • Except for their remarkable numbers, these growths are morphologically indistinguishable from sporadic adenomas. Colorectal adenocarcinoma develops in 100% of patients with untreated FAP, often before age 30. As a result, prophylactic colectomy is standard therapy for persons carrying APC mutations. However, patients remain at risk for extra intestinal manifestations, including neoplasia at other sites.
  18. 18. Familial Adenomatous Polyposis • Specific APC mutations are also associated with the development of other manifestations of FAP and explain variants such as Gardner syndrome and Turcot syndrome. • Clinical features of Gardner syndrome: • Intestinal polyps, osteomas of mandible, skull, and long bones; epidermal cysts; desmoid (tendon-like ; musculoaponeurotic) and thyroid tumors; and dental abnormalities, including unerupted and supernumerary teeth.
  19. 19. Familial Adenomatous Polyposis • Turcot syndrome is rarer and is characterized by intestinal adenomas and tumors of the central nervous system. • Two thirds of patients with Turcot syndrome have APC gene mutations and develop medulloblastomas. • The remaining one third have mutations in one of several genes involved in DNA repair and develop glioblastomas. Some patients who have FAP without APC loss have mutations of the base excision repair gene MUTYH.
  20. 20. II.Hereditary Nonpolyposis Colorectal Cancer • Hereditary nonpolyposis colorectal cancer (HNPCC), also known as Lynch syndrome, originally was described as familial clustering of cancers at several sites including the colorectum, endometrium, stomach, ovary, ureters, brain, small bowel, hepatobiliary tract, and skin. • Colon cancers inpatients with HNPCC tend to occur at younger ages than for sporadic colon cancers and often are located in the right colon.
  21. 21. Familial adenomatous polyposis. A, Hundreds of small colonic polyps are present along with a dominant polyp (right).
  22. 22. Familial adenomatous polyposis. B, Three tubular adenomas are present in this single microscopic field.

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