rectal polyps

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rectal polyps

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Colonic Polyps : 

Colonic Polyps Dr Stuart Collins Colorectal Registrar Gold Coast Hospital

Polyp : 

a discrete mass of tissue that protrudes into the lumen of the bowel. Can be divided into 3 types Non-neoplastic Harmatomatous Neoplastic Polyp

Non-neoplastic : 

Hyperplastic Inflammatory pseudopolyps Submucosal Non-neoplastic

Hyperplastic Polyps : 

Most common non-neoplastic polyp in the colon Difficult to distinguish macroscopically from adenoma Do not exhibit dysplasia (large hyperplastic polyps can co-exist with foci of adenomatous change) results from decreased epithelial cell turnover and accumulation of mature cells on the surface. They may occur singly but more often are multiple, Usually small (less the 5mm) Histologically, they are composed of well-formed glands and crypts lined by non-neoplastic epithelial cells. The delayed shedding of surface epithelial cells leads to infoldings of the crowded epithelial cells and fission of the crypts, creating a serrated epithelial profile and an irregular crypt architecture Hyperplastic Polyps

Hyperplastic Polyposis Syndrome : 

Characterised by multiple, large and/or large proximal hyperplastic polyps Can be associated with serrated adenomas, adenomas or mixed hyperplastic/adenomatous polyps Who criteria ≥ 5 hyperplastic polyps prox to sigmoid colon, (2 have to be > 1cm in diam) Proximal hyperplastic polyps in an individual with a 1st degree relative with HPS >30 hyperplastic polyps throughout colon Hyperplastic Polyposis Syndrome

Inflammatory Pseudopolyps : 

Irregular islands of intact Mucosa that are the result of mucosal ulceration and regeneration that occurs in IBD Not dysplastic Not themselves a risk factor for Ca (although IBD is a risk factor) Inflammatory Pseudopolyps

Submucosal Polyps : 

Lymphoid aggregates Hemangiomas Lipomas – most common Yellow colour Softness when probed Submucosal Polyps

Harmatomatous PolypsA benign (noncancerous) tumor-like growth consisting of a disorganized mixture of cells and tissues normally found in the area of the body where the growth occurs. : 

Juvenile polyps Consist of lamina propria and dilated cystic glands rather than an increase number of epithelial cells Usually removed because of bleeding risk Can be diagnosed at any age but more common in childhood Peutz-Jeghers polyps Lesion of glandular epithelium supported by smooth muscle cells Assoc with Peutz-Jeghers syndrome Usually benign but can undergo malignant transformation Pts with PJS have an inc risk of both GIT and non-GIT tumours Cumulative risk of 50% by 60yrs Harmatomatous PolypsA benign (noncancerous) tumor-like growth consisting of a disorganized mixture of cells and tissues normally found in the area of the body where the growth occurs.

Neoplastic Polyps:Adenomatous Polyps : 

Intraepithelial neoplasms Familial predisposition 4 fold greater risk among 1st degree relatives Prevalence 20-30% before 40yrs 40-50% after 60yrs Separated in to 3 subtypes on the basis of epithelial architecture (considerable overlap) Tubular glands Villous – villous projections Tubulovillous – mixture of the above Neoplastic Polyps:Adenomatous Polyps

Tubular Adenoma : 

80% of adenomas Exhibit more than 75% tubular architecture Composed of dysplastic columnar epithelium (deeply stained) which lines the glands Can be sessile (usually small) of pedunculated Sessile lesions are more likely to harbor high grade dysplasia or be malignant Pedunculated adenoma has a stalk which can act like a buffer zone for invasion Dysplasia is classified as low or high depending on nuclear atypia, cytological distortion, crowding and gland formation Tubular Adenoma

Serrated Adenomatous Polyps : 

Benign neoplastic lesion with mixed histological features of both hyperplastic and adenomatous polyps Characterised by colonic crypts with saw-tooth serrated configuration but nuclear atypia makes them adenoma Can contain areas of significant dysplasia Serrated Adenomatous Polyps

Villous Adenoma : 

Accounts for 5-15% Contain more than 50% villous Architecture Occur in older persons Velvety or cauliflower-like masses project above surrounding normal mucosa When invasion occurs there is no stalk to act as buffer zone Villous Adenoma

Tubulovillous Adenoma : 

Account for 5-15% of polyps Contain 25 – 50% villous architecture Risk of harboring in situ or invasive carcinoma if proportionate to the villous component Tubulovillous Adenoma

Adenoma-Carcinoma Hypothesis : 

Most if not all colon cancers arise within previously benign adenomas Evidence to support this hypothesis comes in the form of Epidemiological – prevalence of adenomas within a population parallels the prevalence of colon cancer. Age distribution curves indicate the development of adenomatous polyps precedes carcinoma by 5-10 years clinicopathologic – in patients with FAP who have hundreds of thousands of polyps – cancer is inevitable molecular genetics studies – progression from adenoma to carcinoma results form accumulation of molecular genetic alterations (activation of oncogenes, inactivation of tumour suppressor genes and participation of so-called stability genes) Adenoma-Carcinoma Hypothesis

Slide 15: 

The accumulation of mutations, rather than their occurrence in a specific order, is more important

Risk factors for focal cancer within a polyp : 

More Villous histology Increasing polyp size – cancer is rare in tubular adenoma <1cm High grade dysplasia These 3 risk factors are interdependent Risk factors for focal cancer within a polyp

Adenoma with Advance Pathological Features : 

Serve as risk factors for developing future CRC Adenomatous polyps >1cm in diameter Adenomatous polyps with high grade dysplasia Adenomatous polyps with >25% villous histology Adenomatous polyps with invasive cancer Adenoma with Advance Pathological Features

Familial Adenomatous Polyposis (FAP) : 

Responsible for <1% of CRC Autosomal dominant condition Characterised by the development of hundreds of thousands of adenomas in the colorectum Almost all patients will develop CRC if not treated Caused by mutation in the APC (adenomatous polyposis coli) gene APC gene has dual function Promotes cell migration and adhesion Gatekeeper protein for cell proliferation Familial Adenomatous Polyposis (FAP)

Hereditary Nonpolyposis Colorectal Cancer (HNPCC) : 

Autosomal dominant syndrome People with HNPCC inherit one mutant DNA repair gene (first hit) Cells in some organs are susceptible to a second somatic mutation (second hit) which inactivates the normal allele Increase risk of colorectal cancer and extraintestinal cancer (particularly the endometrium) Colonic malignancies are often multiple and not usually associated with pre-existing adenomas Hallmark of HNPCC is mutations in DNA repair genes leading to microsatellite instability Hereditary Nonpolyposis Colorectal Cancer (HNPCC)

Microsatellite Instability : 

Involved in 10-15% of sporadic CRC and in the HNPCC Microsatellites are fragments of repeat sequences in the human genome These sequences are prone to misalignment during DNA replication Some sequences are located in coding or promoter regions in genes involved in regulation of cell growth Defective DNA mismatch repair gene – leads to accumulation of mutations in growth-regulating genes culminating in the emergence of CRC Microsatellite Instability

Malignant Polyps : 

Polyps with invasive carcinoma in which the invasion is confined to the submucosa (T1) Accounts for 2-12% of colonoscopic polypectomies and 4 -9% of those in colorectal resections Incidence of malignancy according to size of polyp <5mm – negligible 6mm – 15mm – 2% 16mm – 25mm – 19% 26mm – 35mm – 43% >35mm – 76% Malignant Polyps

Anatomic landmarks of malignant polyps : 

Haggitt et al proposed a morphological classification according to depth of invasion in the polyp Level 0 Carcinoma in situ or intramucosal carcinoma. Not invasive. Level 1 Carcinoma invading through muscularis mucosa into submucosa, but limited to the head of the polyp. Level 2 Carcinoma invading the level of the neck of the adenoma. Level 3 Carcinoma invading any part of the stalk. Level 4 Carcinoma invading into the submucosa of the bowel wall below the stalk of the polyp, but above the muscularis propria. Anatomic landmarks of malignant polyps

Risk of Lymph node metastases : 

Pedunculated polyps Haggitt level 0 – 0% Level 1-3 - <1% Level 4 – 12-25% (all polyps with invasive carcinoma) Sessile polyps - Kudo level for submucosal invasion Sm1 – 3% Sm2 – 8% Sm3 – 23% Risk of Lymph node metastases

Predictors of LN metastases for sessile lesions : 

Invasion to SM3 Lymphovascular invasion Site in the lower 1/3 of the rectum Predictors of LN metastases for sessile lesions

Management of malignant polyps : 

Pedunculated Haggitt 1-3 – complete excision or snaring Level 4 – should be treated as sessile lesions Sessile Invasive Ca <2cm in diameter – snares in one piece (need microscopic margin of 2mm) If lesion is removed piecemeal – need oncologic resection Sessile lesion that has high risk factors (lymphovascular invasion, Sm3, lower 1/3 rectum ) should have oncologic resection In lower 1/3 resections – alternative is full thickness per anal excision with chemoradiation postoperatively Management of malignant polyps

Malignant colorectal polyps that should have an oncologic resections : 

Lesions in the colon and middle and upper 1/3 of rectum Pedunculated Haggitt 4, Sm3 Sessile polyps removed with margin <2mm Sessile lesions removed piecemeal Sessile lesions – Sm3 Sessile lesions with lymphovascular invasion Lesions in distal 1/3 rectum Pedunculated Haggitt 4, Sm3 Pedunculated polyps with lymphovascular invasion All sessile polyps Malignant colorectal polyps that should have an oncologic resections

Follow up (NHMRC guidelines) : 

Follow up (NHMRC guidelines)

Guidelines for FAP : 

Screening until polyposis develops or until 35 years of age then every 3 years Population based screening after 55 years Guidelines for FAP

References : 

Nivatvongs S. Surgical management of malignant colorectal polyps. Surg Clin N Am 82 (2002) 959 – 966 Levine JS et al. Adenomatous polyps of the colon. NEJM 2006 355:2551-7 Nascimbeni R et al. Risk of lymph node metastasis in T1 carcinoma of the colon and rectum. Dis Colon Rectum 2002 45:200-6 Vasen HFA et al. Guidelines for the clinical management of FAP. Gut 2008;57 704-13 Schulmann K et al. Colonic cancer and polyps. Best practice and research clinical gastroenterology 2002;16 91 -114 Up to date. www.uptodate.com Kumar et al. Robbin’s pathologic basis for disease. 2007 NHMRC clinical practice guideline for the prevention, early detection and management of colorectal cancer 2005. References

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