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Colorectal polyp

A colorectal polyp is a polyp occurring on the lining of the colon or rectum. Untreated colorectal polyps can develop into colorectal cancer.

Signs and symptoms
Colorectal polyps are not usually associated with symptoms. and fatigue arising from blood loss. Another symptom may be an increased mucus production especially those involving villous adenomas. Copious production of mucus causes loss of potassium that can occasionally result in symptomatic hypokalemia. Occasionally, if a polyp is big enough to cause a bowel obstruction, there may be nausea, vomiting and severe constipation. ==Structure==
Structure
Polyps are either pedunculated (attached to the intestinal wall by a stalk) or sessile (grow directly from the wall). In addition to the gross appearance categorization, they are further divided by their histologic appearance as tubular adenomas which are tubular glands, villous adenomas which are long finger-like projections on the surface, and tubulovillous adenomas which have features of both. ==Genetics==
Genetics
Hereditary syndromes causing increased colorectal polyp formation include: • Familial adenomatous polyposis (FAP) • Hereditary nonpolyposis colorectal cancerPeutz–Jeghers syndromeJuvenile polyposis syndrome Several genes have been associated with polyposis, such as GREM1, MSH3, MLH3, NTHL1, RNF43 and RPS20. Familial adenomatous polyposis Familial adenomatous polyposis (FAP) is a form of hereditary cancer syndrome involving mutations in one of two genes. FAP and attenuated FAP (originally called hereditary flat adenoma syndrome) are caused by APC gene defects on chromosome 5 while autosomal recessive FAP (or MUTYH-associated polyposis) is caused by defects in the MUTYH gene on chromosome 1.. The syndrome was first described in 1863 by Virchow on a 15-year-old boy with multiple polyps in his colon. The syndrome involves development of multiple polyps at an early age and those left untreated will all eventually develop cancer. The gene is expressed 100% in those with the mutation and it is autosomal dominant. 10–20% of patients have negative family history and acquire the syndrome from spontaneous germline mutation. The average age of newly diagnosed patient is 29 and the average age of newly discovered colorectal cancer is 39. It is recommended that those affected undergo colorectal cancer screening at younger age with treatment and prevention are surgical with removal of affected tissues. Hereditary nonpolyposis colorectal cancer (Lynch syndrome) Hereditary nonpolyposis colorectal cancer (HNPCC, also known as Lynch syndrome) is a hereditary colorectal cancer syndrome. It is the most common hereditary form of colorectal cancer in the United States and accounts for about 3% of all cases of cancer. It was first recognized by Alder S. Warthin in 1885 at the University of Michigan. It was later further studied by Henry Lynch who recognized an autosomal dominant transmission pattern with those affected having relatively early onset of cancer (mean age 44 years), greater occurrence of proximal lesions, mostly mucinous or poorly differentiated adenocarcinoma, greater number of synchronous and metachronous cancer cells, and good outcome after surgical intervention. The Amsterdam Criteria were initially used to define Lynch syndrome before the underlying genetic mechanism had been worked out. The Criteria required that the patient has three family members all first-degree relatives with colorectal cancer that involves at least two generations with at least one affected person being younger than 50 years of age when the diagnosis was made. The Amsterdam Criteria is too restrictive and was later expanded to include cancers of endometrial, ovarian, gastric, pancreatic, small intestinal, ureteral, and renal pelvic origin. The increased risk of cancer seen in patients with by the syndrome is associated with dysfunction of DNA repair mechanism. Molecular biologists have linked the syndrome to specific genes such as hMSH2, hMSH1, hMSH6, and hPMS2. Peutz–Jeghers syndrome Peutz–Jeghers syndrome is an autosomal dominant syndrome that presents with hamartomatous polyps, which are disorganized growth of tissues of the intestinal tract, and hyperpigmentation of the interlining of the mouth, lips and fingers. The syndrome was first noted in 1896 by Hutchinson, and later separately described by Peutz, and then again in 1940 by Jeghers. The syndrome is associated with malfunction of serine-threonine kinase 11 or STK 11 gene, and has a 2–10% increase in risk of developing cancer of the intestinal tract. The syndrome also causes increased risk of extraintestinal cancer such as that involving breast, ovary, cervix, fallopian tubes, thyroid, lung, gallbladder, bile ducts, pancreas, and testicles. The polyps often bleeds and may cause obstruction that would require surgery. Any polyp larger than 1.5 cm needs removal and patients should be monitored closely and screen every two years for malignancy. Juvenile polyposis syndrome Juvenile polyposis syndrome is an autosomal dominant syndrome characterized by increased risk of cancer of intestinal tract and extraintestinal cancer. It often presents with bleeding and obstruction of the intestinal tract along with low serum albumin due to protein loss in the intestine. The syndrome is linked to malfunction of SMAD4 a tumor suppression gene that is seen in 50% of cases. Individuals with multiple juvenile polyps have at least 10% chance of developing malignancy and should undergo abdominal colectomy with ileorectal anastomosis, and close monitoring via endoscopy of rectum. For individuals with few juvenile polyps, patients should undergo endoscopic polypectomy. ==Types==
Types
Colorectal polyps can broadly be classified as follows: • hyperplastic, • neoplastic (adenomatous and malignant), • hamartomatous and, • inflammatory. Comparison table Hyperplastic polyp Most hyperplastic polyps are found in the distal colon and rectum. They have no malignant potential, while hyperplastic polyps do not. They grow at the normal rate of the host tissue and rarely cause problems such as compression. A common example of a hamartomatous lesion is a strawberry naevus. Hamartomatous polyps are often found by chance; occurring in syndromes such as Peutz–Jegher syndrome or juvenile polyposis syndrome. Peutz–Jeghers syndrome is associated with polyps of the GI tract and also increased pigmentation around the lips, genitalia, buccal mucosa, feet, and hands. People are often diagnosed with Peutz–Jegher after presenting at around the age of nine with an intussusception. The polyps themselves carry little malignant potential but because of potential coexisting adenomas there is a 15% chance of colonic malignancy. Juvenile polyps are hamartomatous polyps that often become evident before twenty years of age, but can also be seen in adults. They are usually solitary polyps found in the rectum which most commonly present with rectal bleeding. Juvenile polyposis syndrome is characterised by the presence of more than five polyps in the colon or rectum, or numerous juvenile polyps throughout the gastrointestinal tract, or any number of juvenile polyps in any person with a family history of juvenile polyposis. People with juvenile polyposis have an increased risk of colon cancer. Inflammatory polyp These are polyps that are associated with inflammatory conditions such as ulcerative colitis and Crohn's disease. == Prevention ==
Prevention
Diet and lifestyle are believed to play a large role in whether colorectal polyps form. Studies show there to be a protective link between consumption of cooked green vegetables, brown rice, legumes, and dried fruit and decreased incidence of colorectal polyps. ==Diagnosis==
Diagnosis
Colorectal polyps can be detected using a faecal occult blood test, flexible sigmoidoscopy, colonoscopy, virtual colonoscopy, digital rectal examination, barium enema or a pill camera. • 1–2 cm=10% risk of cancer NICE classification In colonoscopy, colorectal polyps can be classified by NICE (Narrow-band imaging International Colorectal Endoscopic): ==Treatment==
Treatment
Polyps can be removed during a colonoscopy or sigmoidoscopy using a wire loop that cuts the stalk of the polyp and cauterises it to prevent bleeding. Minimally invasive surgery is indicated for polyps that are too large or in unfavorable locations, such as the appendix, that cannot be removed endoscopically. These techniques may be employed as an alternative to the more invasive colectomy. ==Follow-up==
Follow-up
By United States guidelines, the following follow-up is recommended: ==References==
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