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Intestinal polyps

This document provides an overview of intestinal polyps. It begins with an introduction and relevant anatomy. Polyps are then classified based on size, attachment, and cellular architecture. Both non-neoplastic and neoplastic polyps are discussed. Non-neoplastic polyps include hyperplastic, juvenile, Peutz-Jeghers, inflammatory, Cronkhite-Canada, and Cowden polyps. Neoplastic polyps include adenomatous and syndromic polyps associated with Familial Adenomatous Polyposis (FAP) and Hereditary Nonpolyposis Colon Cancer (HNPCC). The pathogenesis and molecular biology of adenomatous polyps is also reviewed. Management strategies

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Intestinal Polyposis Presented by – Dr. Nihar Chandak
Synopsis Introduction Anatomy Classification • Size • Attachment • Cellular Architecture Non-neoplastic • Hyperplatic polyp • Juvenile polyp • Peutz- Jeghers Syndrome • Inflammatory polyp • Cronkhite-Canada • Cowden Syndrome Neoplastic • Histologic variant • Pathogenesis & molecular biology Adenomatous polyposis Syndrome • FAP • HNPCC Management • Screening • Diagnosis • Treatment Sub- Mucosal Polyps • Lipomas • Pneumatosis cystoides intestinalis • Colitis cystica profunda • Lymphoid aggregates • Carcinoids Management
Introduction • Polyp (Greek polypous, “morbid excrescence”) is a nonspecific clinical term that describes any projection from the surface of the intestinal mucosa into the bowel lumen regardless of its histologic nature. - Schawrtz 10e • Polyps are more common in gastrointestinal tract and are the precursors for the benign and malignant conditions. • Polyp can be either -true polyps or false polyps
Relevant Anatomy
• Polyps are can be categorized according to- 1. Size 2. Character of their attachment 3. Cellular architecture
According to size • Studies have shown that the malignant potential of adenomatous polyps is related to polyp size. • Polyps with larger mass have greater volume of neoplastic cells, hence a higher likelihood of harboring cancer. Those measuring 0.5 cm or less- only 0.5% shown to have malignant potential in an autopsy series smaller than 1 cm- only 1% to 2% contain carcinoma greater than 2 cm- as many as 40% of adenomas contain cancer
According to character of attachment • Sessile- with a broad-based attachment to the colonic wall, or • Pedunculated- attached to the colonic wall by way of a fibrovascular stalk Sessile polyp Pedunculated polyp Diagram representation of cancer-containing polyps
According to cellular architecture • Adenomatous • Tubular adenoma • Tubulovillous adenoma • Villous adenoma • Non- adenomatous • Hamartomatous mucosal • Sub- mucosal
Classification of Intestinal Polyps Mucosal Polyps Sub- Mucosal Polyps Non neoplastic (Hamartomatous) Benign Adenomatous polyps Malignant polyps • Hyperplastic • Juvenile • Peutz-Jeghers • Inflammatory • Cronkhite-Canada Syn • Cowden Syn. • Serrated polyp • Tubular adenoma • Tubulovillous adenoma • Villous adenoma • Carcinoma in situ • Invasive carcinoma • Polypoid carcinoma • Lipomas • Leiomyomas • Colitis cystica profunda • Pneumatosis cystoides intestinalis • Lymphoid aggregates • Lymphoma (primary or secondary) • Carcinoids
Non- Neoplastic polyps Hyperplatic polyp Juvenile polyp Peutz- Jeghers Syndrome Inflammatory polyp Cronkhite-Canada Cowden Syndrome
1. Hyperplastic polyps • MC colonic polyp • Small, less than 1 cm • usually sessile • are common age-related lesions found in about 1/3rd of the population older than 50 years. • most frequently encountered in the distal colon and rectum • carry no significant potential for malignant degeneration • When hyperplastic polyps are found proximal to the rectosigmoid region, one must consider the possibility of a serrated adenoma. Hyperplastic polyp
Hyperplastic polyp Serrated polyp Microscopically Sawtoothed epithelial pattern representing micropapillary luminal infoldings of columnar absorptive cells Same + dysplastic cytologic features of an adenoma Macroscopically Less than 1cm Can be more than 1cm Location Distal to rectosigmoid jn. Proximal to rectosigmoid jn. Malignant potential Are asymptomatic with no malignant potential Can be the precursors to colorectal cancers of the MSI phenotype Treatment and survillence Does not require Requires Sessile serrated adenoma. This view shows basilar crypt dilation, epithelium proliferating in a serrated (saw-toothed) manner, and so-called crypt architectural dysplasia
2. Juvenile polyps • also k/a retention polyps • can occur sporadically or as part of a familial polyposis syndrome • 75% occur in children younger than 10 years of age • Present as single pedunculated cherry- red polyps with a smooth surface and contour • detectable in about 2% of children who do not have symptoms. Juvenile polyps
• often present in the form of hematochezia because they are highly vascularized lesions. • Rectal prolapse may occur with distal lesions, whereas intussusception may be precipitated by proximal juvenile polyps found in the context of familial syndromes. • Individually, these polyps have no malignant potential, but symptomatic polyps should be removed to prevent further complications. • In approx. 10% of patients with juvenile polyposis, there is an increased risk for the early development of cancer.
3. Peutz-Jeghers Syndrome • Autosomal dominant • The gene responsible is on chromosome 19p and encodes a serine/ threonine kinase called LKB1 or STK11. • GI Features: • GI polyps are non-neoplastic hamartomas. • Consists of a supportive framework of smooth muscle tissue covered by somewhat hyperplastic epithelium with no inflammatory cells. • Polyps may be found in the stomach, small intestine, or colon. Gross specimen of a Peutz-Jeghers polyp illustrating a large multilobular lesion.
• Cutaneous manifestations: • Found early in life • consists of dark, macular lesions on the mouth (both on the skin and in the buccal mucosa), nose, lips, hands, feet, genitalia, and anus. • These lesions tend to become less obvious by the time of puberty. • Unlike ordinary freckles, the cutaneous lesions of Peutz-Jeghers syndrome are present from birth. Hyperpigmentation of perioral region and buccal mucosa
• Clinical complication: 1. intestinal obstruction from intussusception • usually develops in infancy or childhood • More prominent in the small intestine 2. Gastrointestinal bleeding 3. Cancer in the small intestine or colon can occur; however, this is an uncommon complication (2% to 10%) -Sabiston 19e • arise from foci of adenomatous epithelium found in some P-J polyps. • There is also an increased risk for extraintestinal malignancies, including cancer of the breast, ovary, cervix, fallopian tubes, thyroid, lung, gallbladder, bile ducts, pancreas, and testicles. Polyp causing intussusception
• Management: • Removal of polyps is the mainstay • Endoscopic techniques should be used when possible. • Surgery may be required for intussusception caused by small- intestinal polyps. • The risk for neoplastic development should be kept in mind, but these patients are not candidates for prophylactic removal of any section of the gastrointestinal tract. • gonadal neoplasms and breast cancer are potential complications that may require surgery.
4. Inflammatory polyps/ Pseudopolyps • Occur most commonly in inflammatory bowel disease • But may also occur after amoebic colitis, ischemic colitis, and schistosomal colitis. • These lesions are not premalignant. • But they cannot be distinguished from adenomatous polyps based on gross appearance and therefore should be removed. • Microscopic examination shows islands of normal, regenerating mucosa (the polyp) surrounded by areas of mucosal loss. • Polyposis may be extensive, especially in patients with severe colitis, and may mimic FAP. Ulcerative colitis
5. Cronkhite-Canada Syndrome • characterized by multiple polyps of the digestive tract with anomalies of ectodermal tissues • Currently considered idiopathic • MC in Japanese descents • male to female ratio is 2:1 • GI manifestation: • Polyps found in Stomach (MC) > large intestine > small intestine > esophagus (Least common) • Are non- malignant • Other manifestation: • anomalies of ectodermal tissues, such as alopecia, atrophy of the nails, or skin pigmentation
6. Cowden Syndrome/ Multiple Hamartoma Syn. • Rare, AD disorder • A/w mutations in PTEN, a tumor suppressor gene • characterized by multiple non-cancerous tumor-like growths called hamartomas, typically found in the skin, mucous membranes (mouth, nasal membranes, GI tract), thyroid gland, and breast tissue. • While the hamartomas are benign, people with Cowden Syndrome are at increased risk of certain forms of cancer, including breast cancer (30-50% risk) thyroid cancer (10% risk) endometrial, kidney cancers.
• Benign ectodermal tumor— tricholemmoma —80% • Macrocephaly—40% • GI polyposis—35% and no risk of GI malignancy benign cutaneous neoplasm that shows differentiation toward cells of the outer root sheath
• Benign Adenomatous polyps • Serrated polyp • Tubular adenoma • Tubulovillous adenoma • Villous adenoma • Malignant Adenomatous polyps • Carcinoma in situ • Invasive carcinoma • Polypoid carcinoma Neoplastic Mucosal Polyps • Syndromic Polyps • Familial Adenomatous Polyp (FAP) • Hereditary Nonpolyposis Colon Cancer (Lynch’s Syndrome)
Introduction • Most colorectal cancers arise in preexisting adenomatous polyps. • Occur in up to 25% of the population older than 50 years of age. • More common on left side. • By definition, these lesions are dysplastic. • abnormalities in crypt architecture (such as irregular branching or crowded “back-to- back” glands) and cytologic detail (enlarged, pleomorphic, and hyperchromatic nuclei with multiple mitoses and pseudostratification) • Heredity plays a role not only in FAP and Lynch syndrome but also in the development of sporadic adenomas. • Several lines of evidence support the assumption that colorectal adenocarcinomas arise from adenomatous polyps.
Histologic variants – according to glandular structure Histologic type Tubular adenomas Villous adenomas Tubulovillous adenomas Characteristics characterized by a complex network of branching adenomatous glands contain fronds or folds of mucosa that have overgrown their underlying stroma and project toward the colonic lumen both histologic types coexist % of total adenomatous polyps 65% - 85% (most common) 5%- 10% (least common) 10%- 25% Malignant potential 5% (have less atypia) 40% (have severe atypia) 22% Location Found anywhere in colon Found mostly in rectum Mostly in rectum Attachment Most often pedunculated Most often sessile
• According to the invasion and degree of dysplasia, polyps can be described as: Carcinoma in situ- when the basement membrane is intact Intramucosal carcinoma- Extension into the lamina propria Invasive carcinoma/ Malignant polyp- Invasion into the muscularis mucosae
Haggitt’s Classification (depth of invasion) Level Depth of invasion Level 0 Carcinoma does not invade the muscularis mucosae (carcinoma-in-situ or intramucosal carcinoma). Level 1 Carcinoma invades through the muscularis mucosae into the submucosa but is limited to the head of the polyp Level 2 Carcinoma invades the level of the neck of the polyp (junction between the head and stalk). Level 3 Carcinoma invades any part of the stalk Level 4 Carcinoma invades into the submucosa of the bowel wall below the stalk of the polyp but above the muscularis propria. • By definition, all sessile polyps with invasive carcinoma are level 4 by Haggitt’s criteria.
Pathogenesis and Molecular Biology • Neoplastic mucosal epithelium evolves through a series of progressive, cumulative molecular and cellular steps that lead to altered proliferation, cellular accumulation, and glandular disarray. • The adenoma–carcinoma sequence is the most accepted pathway taken by neoplasms that have “chromosomal instability.”
• Genetic changes that lead to the development of adenomas (and carcinomas) can be loosely organized into three major classes: 1. loss of tumor-suppressor gene activity 2. alterations in proto-oncogenes 3. abnormalities of genes involved in DNA repair
Genetic change Mechanism Example loss of tumor- suppressor gene activity Tumor-suppressor gene-  acts as the “gatekeeper” of colonic epithelial proliferation  inactivation of this gene will lead to net cellular proliferation and initiation of neoplasia in the colon APC on chromosome 5q is a tumor suppressor gene alterations in proto- oncogenes Cellular proto-oncogene-  play a role in signal transduction and the normal regulation of cell growth.  They function by being turned on when growth is stimulated and then turned off when sufficient growth has been achieved. Mutations of the K-ras oncogene • small adenomas- 9%, • adenomas greater than 1cm - 58% • more common in pedunculated than flat adenomas. abnormalities of genes involved in DNA repair Altered DNA mismatch repair-  creates an inability to repair DNA mismatches and results in a diffuse mutational signature in the tumor called microsatellite instability, or MSI.  This defect leads to the mutational inactivation of several key genes important for maintaining normal cellular behavior. The transforming growth factor- receptor II (TGF-RII) Mutation seen in 85% of MSI colorectal cancers
Evidence for adenoma–carcinoma sequence 1. The prevalence of adenomas and carcinomas is very similar – carcinoma patients are about five years older 2. The distribution of adenomas in the colon is the same as that of cancers (70% left sided) 3. When small cancers are studied, they almost always have adjacent adenomatous tissue 4. Adenomas are found in 1/3rd of specimens resected for colorectal cancer 5. Sporadic adenomas are identical to the adenomas of familial adenomatous polyposis, which is associated with a 100 per cent chance of colorectal adenocarcinoma unless treated 6. Larger adenomas are more likely to be dysplastic and to have higher grades of dysplasia than small adenomas. 7. Incidence of colorectal cancer falls within a screening programme that involves colonoscopy and polypectomy -L n B 26e
• Neoplastic polposis are manifested most commonly in 2 forms- Familial Adenomatous Polpsosis (FAP) Adenomatous Polyposis Syndrome Hereditary Nonpolyposis Colon Cancer HNPCC (Lynch’s Syndrome)
Adenomatous Polyposis Syndrome Familial Adenomatous Polpsosis (FAP) Hereditary Nonpolyposis Colon Cancer HNPCC (Lynch’s Syndrome)
Familial Adenomatous Polpsosis (FAP) Hereditary Nonpolyposis Colon Cancer (Lynch’s Syndrome) Inheritance Autosomal dominant Autosomal dominant Prevalence Less common more common than FAP Clinically patients develop hundreds to thousands of adenomatous polyps shortly after puberty cancers arise in discrete adenomas, but polyposis (i.e., dozens or hundreds of polyps) does not occur Average age at which polps appear 15-20 years 20-30 years Average age at which colorectal cancer appears 30-40 years 40-50 years Genetic abnormality mutation in the APC gene, located on chromosome 5q mutations in mismatch repair genes, most commonly affected genes are MLH1 and MSH2 % of overall colorectal cancers accounts for only about 1% of all colorectal adenocarcinomas. 1%–3% of all colon cancers Life time risk of developing colon cancer 100% 80%
Extracolonic Manifestations Familial Adenomatous Polpsosis (FAP) Hereditary Nonpolyposis Colon Cancer HNPCC (Lynch’s Syndrome) Extracolonic manifestation Endodermal- Adenomas and carcinomas of the  stomach (seen in 90% with FAP),  duodenum,  small intestine,  thyroid  biliary tree Ectodermal-  Epidermoid cysts,  Congenital hypertrophy of the retinal pigment epithelium (CHRPE)  Brain tumors (Turcot Syn.) Mesodermal-  Desmoid tumors,  Fibromas  Osteomas (Gardner Syn.) endometrial carcinoma (most common), ovarian, pancreas, stomach, small bowel, biliary, and urinary tract carcinomas Seen in up to 50 % of patients with FAP Can be used to screen affected families
Skull film demonstrating osteomas of the calvarium Chest radiograph demonstrating multiple fibromas in FAP Congenital hypertrophy of the retinal pigment epithelium (CHRPE)
Gardner Syndrome • Commonly a/w FAP—10%. • Presents with bone, skin, soft tissue and dental abnormalities. • Jaw osteomas are very common. • Other features are epidermoid cysts (50%), exostoses, fibromas, lipomas. • a/w desmoid tumors seen in the scar, abdomen, intraabdominal region and mesenteric fibromatosis. • Congenital hypertrophy of retinal pigment epithelium (CHRPE) —commonly seen. • Often associated with MEN IIb syndrome. mandible demonstrating protuberant mandibular osteomas Mandibular radiograph demonstrating a large osteoma of the mandible
Clinical Features • Most patients do not have symptoms • Overt bleeding (hematochezia)- may occur with larger polyps, which may be evident when the polyps are located distally in the rectum. • Secretory diarrhea with accompanying hypokalemia and hypochlorhydria- common in villous type • Prolapse- common in tubular type • Very large colonic polyps may be associated with obstructive symptoms, such as lower abdominal cramping or alterations in bowel habits, but this is unusual.
Screening policy of FAP • Colonoscopy of blood relatives, including cousins, nephews and nieces, is mainstay of screening. • At-risk family members are offered genetic testing in their early teens. • Should be examined at the age of 10–12 years, repeated every year. • Most of those who are going to get polyps will have them at 20 years, and these require operation. • If there are no polyps at 20 years, continue with 5 yearly examination until age 50 years. • If there are still no polyps, there is probably no inherited gene.
Screening modalities Advantages Disadvantages Fecal occult blood testing  Easy  noninvasive  Low cost  Good sensitivity with repeat testing  May not detect most polyps  Low specificity  Colonoscopy required for positive result  Poor compliance with serial testing Sigmoidoscopy  Examines colon most at risk  Very sensitive for polyp detection in left colon  Does not require full bowel preparation (enemas only)  Invasive  Uncomfortable  Slight risk of perforation or bleeding  May miss proximal lesions  Colonoscopy required if polyp identified Colonoscopy  Examines entire colon  Highly sensitive and specific  Therapeutic  Most invasive  Uncomfortable and requires sedation  Requires bowel preparation  Risk of perforation or bleeding  Costly Double-contrast barium enema  Examines entire colon  Good sensitivity for polyps >1 cm  Examines entire colon  Requires bowel preparation  Less sensitivity for polyps <1 cm  May miss lesions in the sigmoid colon  Colonoscopy required for positive result Computed tomography colonography (virtual colonoscopy)  Noninvasive  Sensitivity may be as good as colonoscopy  Requires bowel preparation  Insensitive for small polyps  Colonoscopy required for positive result
Diagnosis • Stool for occult blood • Colonoscopy, preferable to sigmoidoscopy • because 50% of individuals with advanced proximal neoplasms (adenoma 1 cm; adenoma with villous features or dysplasia; cancer) have no distal neoplasms. • Chromoendoscopy or high-resolution optical methods (e.g., narrow-band imaging, laser confocal endoscopy) to identify flat adenomas. Colonoscopic view of intestinal polyp
• CT colonography, or “virtual” colonoscopy, involves the use of helical CT. • Has the potential advantage of being a rapid and safe method of providing full structural evaluation of the entire colon. • Sensitivity of CT colonography for adenomas greater than 10 mm was 90% • Availability of a genetic diagnosis has changed the approach to this disease. • A mutation in APC can be found in most (90%) of pts of FAP. • Upper GIscopy- as carcinoma of duodenum / periampullary is common in FAP
Diagnosis of HNPCC- Amsterdam criteria 1. three affected relatives with histologically verified adenocarcinoma of the large bowel (one must be a first-degree relative of one of the others) 2. in two successive generations of a family 3. with one patient diagnosed before age 50 years 4. FAP excluded 5. tumors verified by pathological examination • Modified Amsterdam Criteria: • Same as the Amsterdam criteria, except that cancer must be associated with HNPCC (colon, endometrium, small bowel, ureter, renal pelvis) instead of specifically colon cancer
Treatment of FAP • The aim of surgery is to prevent the development of colorectal cancer. • The surgical options are: 1. Colectomy with ileorectal anastomosis (IRA) • Advantages: avoids the temporary stoma avoids the potential compromise to sexual function that accompanies proctectomy. has a lower morbidity and mortality. • Disadvantages: rectum is left and requires regular surveillance Colectomy with ileorectal anastomosis (IRA)
2. Restorative proctocolectomy (RPC) with an ileal pouch-anal anastomosis, the anastomosis may be defunctioned with a loop ileostomy; • Advantage: Safest bcoz of removing the whole colon and rectum (although a small cuff of rectal mucosa may be left behind with a stapled anastomosis). • Disadvantage: Requires temporary stoma formaton 3. Total proctectomy and end ileostomy normally reserved for patients with a low rectal cancer
• It has been found that adenomas can regress in FAP in response to treatment with sulindac (Clinoril). • Even large numbers of polyps regress in patients on 150 to 200 mg of sulindac twice per day • Unfortunately, the polyps reappear when the drug is stopped. • Development of cancer despite treatment with sulindac has been reported.
Treatment of HNPCC • Once detected, adenomas should be completely removed. 1. Endoscopic Snare Polypectomy relatively safe and easily performed when adenomas are small or pedunculated. but is more difficult when polyps are large or sessile. Potential complications include bleeding and perforation of the polypectomy site. Data from the NPS (National Polyp Study) suggested a recurrence rate of 32% to 42% by 3 years after index polypectomy. Endoscopic Snare Polypectomy
2. Segmental surgical resection polypectomy is adequate treatment provided that a margin of more than 2 mm is present, the cancer is not poorly differentiated, and no vascular or lymphatic invasion is noted. When there is uncertainty about the polypectomy margin in the case of pathologically advanced lesions, surgical resection is advised. Carried when there is large sessile villous adenomas (2 cm) that have great potential for malignant degeneration.
Sub-Mucosal Polyps • Submucosal masses can expand to push the colonic mucosa into the bowel lumen and thus appear as polypoid lesions. • Many submucosal lesions are clinically asymptomatic and must be differentiated from neoplastic lesions. • Many submucosal lesions are not detected on endoscopic mucosal biopsy because standard biopsy forceps do not reach beyond the mucosa. • If a submucosal lesion is suspected, multiple biopsy specimens of the same site sometimes provide tissue for diagnosis.
1. Lipomas • are benign fatty tumors that occur throughout the gastrointestinal tract • most commonly found in the cecum near the ileocecal valve • appear endoscopically as soft, smooth polyps that are pliable and deformable. • The overlying mucosa is intact but may be light yellow in appearance. • These are benign lesions that have little clinical significance and are commonly seen in obese patients. Lipomatous infiltration of ileocecal valve seen at colonoscopy & Colectomy specimen showing a large submucosal lipoma cut in cross section.
2. Pneumatosis cystoides intestinalis • consists of multiple airfilled cysts within the submucosa. • Usually an incidental finding in patients with COPD, scleroderma, asymptomatic pneumoperitoneum secondary to recent surgery or instrumentation (in which air or colonic gas diffuses into the cysts) • These sometimes resolve with administration of oxygen. • A far more virulent form of pneumatosis is associated with fulminant mucosal inflammation, ischemia, or necrotizing enterocolitis in children. • These cysts are thought to result from mucosal invasion by gas-producing bacteria.
3. Colitis cystica profunda • Intestinal wall is thickened by submucosal mucus-filled cysts with accumulation of fibroblasts in the lamina propria. • Presents as an ulcerating or mass lesion in the rectosigmoid • May result from the downward displacement of colonic glands during trauma or chronic inflammation followed by healing. • The appearance of aberrant submucosal glandular epithelium and acellular mucous lakes must be distinguished from a colloid carcinoma • Has no malignant potential.
4. Lymphomatous polyposis of the colon • Isolated lymphoid nodules consisting of benign lymphoid tissue may appear as sessile smooth polyps of various sizes • predilection for the distal colon and rectum • usually asymptomatic. • Diffuse nodular lymphoid hyperplasia occurs in children as an incidental finding. • The nodules must be distinguished from primary or secondary lymphoma of the large intestine, which may present as mucosal nodularity. • Flow cytometry of the lymphocytes in the lesion will be helpful; • benign polyposis is polyclonal, • lymphomas are monoclonal and may overexpress cyclin D. Lymphomatous polyposis of the colon
5. Carcinoid tumors of rectum • Isolated, small, yellow-gray submucosal nodules. • Often incidental findings during sigmoidoscopy. • Most are smaller than 1 cm- have little malignant potential. • Lesions larger than 2 cm- more likely to be malignant but seldom give rise to metastases. • Should be treated aggressively with complete excision. • Are usually asymptomatic but may present with hematochezia. • Rectal carcinoid tumors are not associated with the carcinoid syndrome. • Carcinoid tumors in the proximal colon may be locally invasive or metastasize to the liver, liberating vasoactive peptides into the systemic circulation and producing the carcinoid syndrome.

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Intestinal polyps

  • 1.
    Intestinal Polyposis Presented by– Dr. Nihar Chandak
  • 2.
    Synopsis Introduction Anatomy Classification • Size • Attachment •Cellular Architecture Non-neoplastic • Hyperplatic polyp • Juvenile polyp • Peutz- Jeghers Syndrome • Inflammatory polyp • Cronkhite-Canada • Cowden Syndrome Neoplastic • Histologic variant • Pathogenesis & molecular biology Adenomatous polyposis Syndrome • FAP • HNPCC Management • Screening • Diagnosis • Treatment Sub- Mucosal Polyps • Lipomas • Pneumatosis cystoides intestinalis • Colitis cystica profunda • Lymphoid aggregates • Carcinoids Management
  • 3.
    Introduction • Polyp (Greekpolypous, “morbid excrescence”) is a nonspecific clinical term that describes any projection from the surface of the intestinal mucosa into the bowel lumen regardless of its histologic nature. - Schawrtz 10e • Polyps are more common in gastrointestinal tract and are the precursors for the benign and malignant conditions. • Polyp can be either -true polyps or false polyps
  • 4.
  • 5.
    • Polyps arecan be categorized according to- 1. Size 2. Character of their attachment 3. Cellular architecture
  • 6.
    According to size •Studies have shown that the malignant potential of adenomatous polyps is related to polyp size. • Polyps with larger mass have greater volume of neoplastic cells, hence a higher likelihood of harboring cancer. Those measuring 0.5 cm or less- only 0.5% shown to have malignant potential in an autopsy series smaller than 1 cm- only 1% to 2% contain carcinoma greater than 2 cm- as many as 40% of adenomas contain cancer
  • 7.
    According to characterof attachment • Sessile- with a broad-based attachment to the colonic wall, or • Pedunculated- attached to the colonic wall by way of a fibrovascular stalk Sessile polyp Pedunculated polyp Diagram representation of cancer-containing polyps
  • 8.
    According to cellulararchitecture • Adenomatous • Tubular adenoma • Tubulovillous adenoma • Villous adenoma • Non- adenomatous • Hamartomatous mucosal • Sub- mucosal
  • 9.
    Classification of IntestinalPolyps Mucosal Polyps Sub- Mucosal Polyps Non neoplastic (Hamartomatous) Benign Adenomatous polyps Malignant polyps • Hyperplastic • Juvenile • Peutz-Jeghers • Inflammatory • Cronkhite-Canada Syn • Cowden Syn. • Serrated polyp • Tubular adenoma • Tubulovillous adenoma • Villous adenoma • Carcinoma in situ • Invasive carcinoma • Polypoid carcinoma • Lipomas • Leiomyomas • Colitis cystica profunda • Pneumatosis cystoides intestinalis • Lymphoid aggregates • Lymphoma (primary or secondary) • Carcinoids
  • 10.
    Non- Neoplastic polyps Hyperplaticpolyp Juvenile polyp Peutz- Jeghers Syndrome Inflammatory polyp Cronkhite-Canada Cowden Syndrome
  • 11.
    1. Hyperplastic polyps •MC colonic polyp • Small, less than 1 cm • usually sessile • are common age-related lesions found in about 1/3rd of the population older than 50 years. • most frequently encountered in the distal colon and rectum • carry no significant potential for malignant degeneration • When hyperplastic polyps are found proximal to the rectosigmoid region, one must consider the possibility of a serrated adenoma. Hyperplastic polyp
  • 12.
    Hyperplastic polyp Serratedpolyp Microscopically Sawtoothed epithelial pattern representing micropapillary luminal infoldings of columnar absorptive cells Same + dysplastic cytologic features of an adenoma Macroscopically Less than 1cm Can be more than 1cm Location Distal to rectosigmoid jn. Proximal to rectosigmoid jn. Malignant potential Are asymptomatic with no malignant potential Can be the precursors to colorectal cancers of the MSI phenotype Treatment and survillence Does not require Requires Sessile serrated adenoma. This view shows basilar crypt dilation, epithelium proliferating in a serrated (saw-toothed) manner, and so-called crypt architectural dysplasia
  • 13.
    2. Juvenile polyps •also k/a retention polyps • can occur sporadically or as part of a familial polyposis syndrome • 75% occur in children younger than 10 years of age • Present as single pedunculated cherry- red polyps with a smooth surface and contour • detectable in about 2% of children who do not have symptoms. Juvenile polyps
  • 14.
    • often presentin the form of hematochezia because they are highly vascularized lesions. • Rectal prolapse may occur with distal lesions, whereas intussusception may be precipitated by proximal juvenile polyps found in the context of familial syndromes. • Individually, these polyps have no malignant potential, but symptomatic polyps should be removed to prevent further complications. • In approx. 10% of patients with juvenile polyposis, there is an increased risk for the early development of cancer.
  • 15.
    3. Peutz-Jeghers Syndrome •Autosomal dominant • The gene responsible is on chromosome 19p and encodes a serine/ threonine kinase called LKB1 or STK11. • GI Features: • GI polyps are non-neoplastic hamartomas. • Consists of a supportive framework of smooth muscle tissue covered by somewhat hyperplastic epithelium with no inflammatory cells. • Polyps may be found in the stomach, small intestine, or colon. Gross specimen of a Peutz-Jeghers polyp illustrating a large multilobular lesion.
  • 16.
    • Cutaneous manifestations: •Found early in life • consists of dark, macular lesions on the mouth (both on the skin and in the buccal mucosa), nose, lips, hands, feet, genitalia, and anus. • These lesions tend to become less obvious by the time of puberty. • Unlike ordinary freckles, the cutaneous lesions of Peutz-Jeghers syndrome are present from birth. Hyperpigmentation of perioral region and buccal mucosa
  • 17.
    • Clinical complication: 1.intestinal obstruction from intussusception • usually develops in infancy or childhood • More prominent in the small intestine 2. Gastrointestinal bleeding 3. Cancer in the small intestine or colon can occur; however, this is an uncommon complication (2% to 10%) -Sabiston 19e • arise from foci of adenomatous epithelium found in some P-J polyps. • There is also an increased risk for extraintestinal malignancies, including cancer of the breast, ovary, cervix, fallopian tubes, thyroid, lung, gallbladder, bile ducts, pancreas, and testicles. Polyp causing intussusception
  • 18.
    • Management: • Removalof polyps is the mainstay • Endoscopic techniques should be used when possible. • Surgery may be required for intussusception caused by small- intestinal polyps. • The risk for neoplastic development should be kept in mind, but these patients are not candidates for prophylactic removal of any section of the gastrointestinal tract. • gonadal neoplasms and breast cancer are potential complications that may require surgery.
  • 19.
    4. Inflammatory polyps/Pseudopolyps • Occur most commonly in inflammatory bowel disease • But may also occur after amoebic colitis, ischemic colitis, and schistosomal colitis. • These lesions are not premalignant. • But they cannot be distinguished from adenomatous polyps based on gross appearance and therefore should be removed. • Microscopic examination shows islands of normal, regenerating mucosa (the polyp) surrounded by areas of mucosal loss. • Polyposis may be extensive, especially in patients with severe colitis, and may mimic FAP. Ulcerative colitis
  • 20.
    5. Cronkhite-Canada Syndrome •characterized by multiple polyps of the digestive tract with anomalies of ectodermal tissues • Currently considered idiopathic • MC in Japanese descents • male to female ratio is 2:1 • GI manifestation: • Polyps found in Stomach (MC) > large intestine > small intestine > esophagus (Least common) • Are non- malignant • Other manifestation: • anomalies of ectodermal tissues, such as alopecia, atrophy of the nails, or skin pigmentation
  • 21.
    6. Cowden Syndrome/Multiple Hamartoma Syn. • Rare, AD disorder • A/w mutations in PTEN, a tumor suppressor gene • characterized by multiple non-cancerous tumor-like growths called hamartomas, typically found in the skin, mucous membranes (mouth, nasal membranes, GI tract), thyroid gland, and breast tissue. • While the hamartomas are benign, people with Cowden Syndrome are at increased risk of certain forms of cancer, including breast cancer (30-50% risk) thyroid cancer (10% risk) endometrial, kidney cancers.
  • 22.
    • Benign ectodermaltumor— tricholemmoma —80% • Macrocephaly—40% • GI polyposis—35% and no risk of GI malignancy benign cutaneous neoplasm that shows differentiation toward cells of the outer root sheath
  • 23.
    • Benign Adenomatous polyps •Serrated polyp • Tubular adenoma • Tubulovillous adenoma • Villous adenoma • Malignant Adenomatous polyps • Carcinoma in situ • Invasive carcinoma • Polypoid carcinoma Neoplastic Mucosal Polyps • Syndromic Polyps • Familial Adenomatous Polyp (FAP) • Hereditary Nonpolyposis Colon Cancer (Lynch’s Syndrome)
  • 24.
    Introduction • Most colorectalcancers arise in preexisting adenomatous polyps. • Occur in up to 25% of the population older than 50 years of age. • More common on left side. • By definition, these lesions are dysplastic. • abnormalities in crypt architecture (such as irregular branching or crowded “back-to- back” glands) and cytologic detail (enlarged, pleomorphic, and hyperchromatic nuclei with multiple mitoses and pseudostratification) • Heredity plays a role not only in FAP and Lynch syndrome but also in the development of sporadic adenomas. • Several lines of evidence support the assumption that colorectal adenocarcinomas arise from adenomatous polyps.
  • 25.
    Histologic variants –according to glandular structure Histologic type Tubular adenomas Villous adenomas Tubulovillous adenomas Characteristics characterized by a complex network of branching adenomatous glands contain fronds or folds of mucosa that have overgrown their underlying stroma and project toward the colonic lumen both histologic types coexist % of total adenomatous polyps 65% - 85% (most common) 5%- 10% (least common) 10%- 25% Malignant potential 5% (have less atypia) 40% (have severe atypia) 22% Location Found anywhere in colon Found mostly in rectum Mostly in rectum Attachment Most often pedunculated Most often sessile
  • 27.
    • According tothe invasion and degree of dysplasia, polyps can be described as: Carcinoma in situ- when the basement membrane is intact Intramucosal carcinoma- Extension into the lamina propria Invasive carcinoma/ Malignant polyp- Invasion into the muscularis mucosae
  • 28.
    Haggitt’s Classification (depthof invasion) Level Depth of invasion Level 0 Carcinoma does not invade the muscularis mucosae (carcinoma-in-situ or intramucosal carcinoma). Level 1 Carcinoma invades through the muscularis mucosae into the submucosa but is limited to the head of the polyp Level 2 Carcinoma invades the level of the neck of the polyp (junction between the head and stalk). Level 3 Carcinoma invades any part of the stalk Level 4 Carcinoma invades into the submucosa of the bowel wall below the stalk of the polyp but above the muscularis propria. • By definition, all sessile polyps with invasive carcinoma are level 4 by Haggitt’s criteria.
  • 29.
    Pathogenesis and MolecularBiology • Neoplastic mucosal epithelium evolves through a series of progressive, cumulative molecular and cellular steps that lead to altered proliferation, cellular accumulation, and glandular disarray. • The adenoma–carcinoma sequence is the most accepted pathway taken by neoplasms that have “chromosomal instability.”
  • 30.
    • Genetic changesthat lead to the development of adenomas (and carcinomas) can be loosely organized into three major classes: 1. loss of tumor-suppressor gene activity 2. alterations in proto-oncogenes 3. abnormalities of genes involved in DNA repair
  • 31.
    Genetic change MechanismExample loss of tumor- suppressor gene activity Tumor-suppressor gene-  acts as the “gatekeeper” of colonic epithelial proliferation  inactivation of this gene will lead to net cellular proliferation and initiation of neoplasia in the colon APC on chromosome 5q is a tumor suppressor gene alterations in proto- oncogenes Cellular proto-oncogene-  play a role in signal transduction and the normal regulation of cell growth.  They function by being turned on when growth is stimulated and then turned off when sufficient growth has been achieved. Mutations of the K-ras oncogene • small adenomas- 9%, • adenomas greater than 1cm - 58% • more common in pedunculated than flat adenomas. abnormalities of genes involved in DNA repair Altered DNA mismatch repair-  creates an inability to repair DNA mismatches and results in a diffuse mutational signature in the tumor called microsatellite instability, or MSI.  This defect leads to the mutational inactivation of several key genes important for maintaining normal cellular behavior. The transforming growth factor- receptor II (TGF-RII) Mutation seen in 85% of MSI colorectal cancers
  • 32.
    Evidence for adenoma–carcinomasequence 1. The prevalence of adenomas and carcinomas is very similar – carcinoma patients are about five years older 2. The distribution of adenomas in the colon is the same as that of cancers (70% left sided) 3. When small cancers are studied, they almost always have adjacent adenomatous tissue 4. Adenomas are found in 1/3rd of specimens resected for colorectal cancer 5. Sporadic adenomas are identical to the adenomas of familial adenomatous polyposis, which is associated with a 100 per cent chance of colorectal adenocarcinoma unless treated 6. Larger adenomas are more likely to be dysplastic and to have higher grades of dysplasia than small adenomas. 7. Incidence of colorectal cancer falls within a screening programme that involves colonoscopy and polypectomy -L n B 26e
  • 33.
    • Neoplastic polposisare manifested most commonly in 2 forms- Familial Adenomatous Polpsosis (FAP) Adenomatous Polyposis Syndrome Hereditary Nonpolyposis Colon Cancer HNPCC (Lynch’s Syndrome)
  • 34.
    Adenomatous Polyposis Syndrome Familial AdenomatousPolpsosis (FAP) Hereditary Nonpolyposis Colon Cancer HNPCC (Lynch’s Syndrome)
  • 35.
    Familial Adenomatous Polpsosis(FAP) Hereditary Nonpolyposis Colon Cancer (Lynch’s Syndrome) Inheritance Autosomal dominant Autosomal dominant Prevalence Less common more common than FAP Clinically patients develop hundreds to thousands of adenomatous polyps shortly after puberty cancers arise in discrete adenomas, but polyposis (i.e., dozens or hundreds of polyps) does not occur Average age at which polps appear 15-20 years 20-30 years Average age at which colorectal cancer appears 30-40 years 40-50 years Genetic abnormality mutation in the APC gene, located on chromosome 5q mutations in mismatch repair genes, most commonly affected genes are MLH1 and MSH2 % of overall colorectal cancers accounts for only about 1% of all colorectal adenocarcinomas. 1%–3% of all colon cancers Life time risk of developing colon cancer 100% 80%
  • 36.
    Extracolonic Manifestations Familial AdenomatousPolpsosis (FAP) Hereditary Nonpolyposis Colon Cancer HNPCC (Lynch’s Syndrome) Extracolonic manifestation Endodermal- Adenomas and carcinomas of the  stomach (seen in 90% with FAP),  duodenum,  small intestine,  thyroid  biliary tree Ectodermal-  Epidermoid cysts,  Congenital hypertrophy of the retinal pigment epithelium (CHRPE)  Brain tumors (Turcot Syn.) Mesodermal-  Desmoid tumors,  Fibromas  Osteomas (Gardner Syn.) endometrial carcinoma (most common), ovarian, pancreas, stomach, small bowel, biliary, and urinary tract carcinomas Seen in up to 50 % of patients with FAP Can be used to screen affected families
  • 37.
    Skull film demonstratingosteomas of the calvarium Chest radiograph demonstrating multiple fibromas in FAP Congenital hypertrophy of the retinal pigment epithelium (CHRPE)
  • 38.
    Gardner Syndrome • Commonlya/w FAP—10%. • Presents with bone, skin, soft tissue and dental abnormalities. • Jaw osteomas are very common. • Other features are epidermoid cysts (50%), exostoses, fibromas, lipomas. • a/w desmoid tumors seen in the scar, abdomen, intraabdominal region and mesenteric fibromatosis. • Congenital hypertrophy of retinal pigment epithelium (CHRPE) —commonly seen. • Often associated with MEN IIb syndrome. mandible demonstrating protuberant mandibular osteomas Mandibular radiograph demonstrating a large osteoma of the mandible
  • 39.
    Clinical Features • Mostpatients do not have symptoms • Overt bleeding (hematochezia)- may occur with larger polyps, which may be evident when the polyps are located distally in the rectum. • Secretory diarrhea with accompanying hypokalemia and hypochlorhydria- common in villous type • Prolapse- common in tubular type • Very large colonic polyps may be associated with obstructive symptoms, such as lower abdominal cramping or alterations in bowel habits, but this is unusual.
  • 40.
    Screening policy ofFAP • Colonoscopy of blood relatives, including cousins, nephews and nieces, is mainstay of screening. • At-risk family members are offered genetic testing in their early teens. • Should be examined at the age of 10–12 years, repeated every year. • Most of those who are going to get polyps will have them at 20 years, and these require operation. • If there are no polyps at 20 years, continue with 5 yearly examination until age 50 years. • If there are still no polyps, there is probably no inherited gene.
  • 41.
    Screening modalities AdvantagesDisadvantages Fecal occult blood testing  Easy  noninvasive  Low cost  Good sensitivity with repeat testing  May not detect most polyps  Low specificity  Colonoscopy required for positive result  Poor compliance with serial testing Sigmoidoscopy  Examines colon most at risk  Very sensitive for polyp detection in left colon  Does not require full bowel preparation (enemas only)  Invasive  Uncomfortable  Slight risk of perforation or bleeding  May miss proximal lesions  Colonoscopy required if polyp identified Colonoscopy  Examines entire colon  Highly sensitive and specific  Therapeutic  Most invasive  Uncomfortable and requires sedation  Requires bowel preparation  Risk of perforation or bleeding  Costly Double-contrast barium enema  Examines entire colon  Good sensitivity for polyps >1 cm  Examines entire colon  Requires bowel preparation  Less sensitivity for polyps <1 cm  May miss lesions in the sigmoid colon  Colonoscopy required for positive result Computed tomography colonography (virtual colonoscopy)  Noninvasive  Sensitivity may be as good as colonoscopy  Requires bowel preparation  Insensitive for small polyps  Colonoscopy required for positive result
  • 42.
    Diagnosis • Stool foroccult blood • Colonoscopy, preferable to sigmoidoscopy • because 50% of individuals with advanced proximal neoplasms (adenoma 1 cm; adenoma with villous features or dysplasia; cancer) have no distal neoplasms. • Chromoendoscopy or high-resolution optical methods (e.g., narrow-band imaging, laser confocal endoscopy) to identify flat adenomas. Colonoscopic view of intestinal polyp
  • 43.
    • CT colonography,or “virtual” colonoscopy, involves the use of helical CT. • Has the potential advantage of being a rapid and safe method of providing full structural evaluation of the entire colon. • Sensitivity of CT colonography for adenomas greater than 10 mm was 90% • Availability of a genetic diagnosis has changed the approach to this disease. • A mutation in APC can be found in most (90%) of pts of FAP. • Upper GIscopy- as carcinoma of duodenum / periampullary is common in FAP
  • 44.
    Diagnosis of HNPCC-Amsterdam criteria 1. three affected relatives with histologically verified adenocarcinoma of the large bowel (one must be a first-degree relative of one of the others) 2. in two successive generations of a family 3. with one patient diagnosed before age 50 years 4. FAP excluded 5. tumors verified by pathological examination • Modified Amsterdam Criteria: • Same as the Amsterdam criteria, except that cancer must be associated with HNPCC (colon, endometrium, small bowel, ureter, renal pelvis) instead of specifically colon cancer
  • 45.
    Treatment of FAP •The aim of surgery is to prevent the development of colorectal cancer. • The surgical options are: 1. Colectomy with ileorectal anastomosis (IRA) • Advantages: avoids the temporary stoma avoids the potential compromise to sexual function that accompanies proctectomy. has a lower morbidity and mortality. • Disadvantages: rectum is left and requires regular surveillance Colectomy with ileorectal anastomosis (IRA)
  • 46.
    2. Restorative proctocolectomy(RPC) with an ileal pouch-anal anastomosis, the anastomosis may be defunctioned with a loop ileostomy; • Advantage: Safest bcoz of removing the whole colon and rectum (although a small cuff of rectal mucosa may be left behind with a stapled anastomosis). • Disadvantage: Requires temporary stoma formaton 3. Total proctectomy and end ileostomy normally reserved for patients with a low rectal cancer
  • 47.
    • It hasbeen found that adenomas can regress in FAP in response to treatment with sulindac (Clinoril). • Even large numbers of polyps regress in patients on 150 to 200 mg of sulindac twice per day • Unfortunately, the polyps reappear when the drug is stopped. • Development of cancer despite treatment with sulindac has been reported.
  • 48.
    Treatment of HNPCC •Once detected, adenomas should be completely removed. 1. Endoscopic Snare Polypectomy relatively safe and easily performed when adenomas are small or pedunculated. but is more difficult when polyps are large or sessile. Potential complications include bleeding and perforation of the polypectomy site. Data from the NPS (National Polyp Study) suggested a recurrence rate of 32% to 42% by 3 years after index polypectomy. Endoscopic Snare Polypectomy
  • 49.
    2. Segmental surgicalresection polypectomy is adequate treatment provided that a margin of more than 2 mm is present, the cancer is not poorly differentiated, and no vascular or lymphatic invasion is noted. When there is uncertainty about the polypectomy margin in the case of pathologically advanced lesions, surgical resection is advised. Carried when there is large sessile villous adenomas (2 cm) that have great potential for malignant degeneration.
  • 50.
    Sub-Mucosal Polyps • Submucosalmasses can expand to push the colonic mucosa into the bowel lumen and thus appear as polypoid lesions. • Many submucosal lesions are clinically asymptomatic and must be differentiated from neoplastic lesions. • Many submucosal lesions are not detected on endoscopic mucosal biopsy because standard biopsy forceps do not reach beyond the mucosa. • If a submucosal lesion is suspected, multiple biopsy specimens of the same site sometimes provide tissue for diagnosis.
  • 51.
    1. Lipomas • arebenign fatty tumors that occur throughout the gastrointestinal tract • most commonly found in the cecum near the ileocecal valve • appear endoscopically as soft, smooth polyps that are pliable and deformable. • The overlying mucosa is intact but may be light yellow in appearance. • These are benign lesions that have little clinical significance and are commonly seen in obese patients. Lipomatous infiltration of ileocecal valve seen at colonoscopy & Colectomy specimen showing a large submucosal lipoma cut in cross section.
  • 52.
    2. Pneumatosis cystoidesintestinalis • consists of multiple airfilled cysts within the submucosa. • Usually an incidental finding in patients with COPD, scleroderma, asymptomatic pneumoperitoneum secondary to recent surgery or instrumentation (in which air or colonic gas diffuses into the cysts) • These sometimes resolve with administration of oxygen. • A far more virulent form of pneumatosis is associated with fulminant mucosal inflammation, ischemia, or necrotizing enterocolitis in children. • These cysts are thought to result from mucosal invasion by gas-producing bacteria.
  • 53.
    3. Colitis cysticaprofunda • Intestinal wall is thickened by submucosal mucus-filled cysts with accumulation of fibroblasts in the lamina propria. • Presents as an ulcerating or mass lesion in the rectosigmoid • May result from the downward displacement of colonic glands during trauma or chronic inflammation followed by healing. • The appearance of aberrant submucosal glandular epithelium and acellular mucous lakes must be distinguished from a colloid carcinoma • Has no malignant potential.
  • 54.
    4. Lymphomatous polyposisof the colon • Isolated lymphoid nodules consisting of benign lymphoid tissue may appear as sessile smooth polyps of various sizes • predilection for the distal colon and rectum • usually asymptomatic. • Diffuse nodular lymphoid hyperplasia occurs in children as an incidental finding. • The nodules must be distinguished from primary or secondary lymphoma of the large intestine, which may present as mucosal nodularity. • Flow cytometry of the lymphocytes in the lesion will be helpful; • benign polyposis is polyclonal, • lymphomas are monoclonal and may overexpress cyclin D. Lymphomatous polyposis of the colon
  • 55.
    5. Carcinoid tumorsof rectum • Isolated, small, yellow-gray submucosal nodules. • Often incidental findings during sigmoidoscopy. • Most are smaller than 1 cm- have little malignant potential. • Lesions larger than 2 cm- more likely to be malignant but seldom give rise to metastases. • Should be treated aggressively with complete excision. • Are usually asymptomatic but may present with hematochezia. • Rectal carcinoid tumors are not associated with the carcinoid syndrome. • Carcinoid tumors in the proximal colon may be locally invasive or metastasize to the liver, liberating vasoactive peptides into the systemic circulation and producing the carcinoid syndrome.

Editor's Notes

  • #37 Turcots- AR Brain tumors- Cerebellar medulloblastoma and glioblastomas