(A) The causes of the disease 1, dietary factors The incidence of colorectal polyps is significantly higher in those who eat a high-fat, high-protein, low-fiber diet for a long time. 2.Bile metabolism disorder After gastrojejunostomy and cholecystectomy for gastroduodenal ulcer, the flow and discharge time of bile are changed, and the content of bile acid in the large intestine is increased. Genetic factors Among colorectal cancer patients, about 10% of them have a family history of cancer. Similarly, when someone in the family has adenomatous polyps, the possibility of colorectal polyps in other members is significantly higher, especially familial polyposis has obvious family heritability. 4, intestinal inflammatory diseases chronic inflammatory lesions of the colonic mucosa is the main cause of inflammatory polyps, most often seen in chronic ulcerative colitis, Crohn’s disease and amebic dysentery, intestinal schistosomiasis and intestinal tuberculosis, etc., also seen in the anastomotic site after colon surgery. 5, genetic abnormalities The occurrence of familial polyps may be related to the loss of function and absence of an allelic oncogene called APC (adenomatous polyposis coli) in the long arm of chromosome 5. Under normal circumstances, the allele needs to function simultaneously to inhibit tumor growth, and when the gene is absent or mutated, the inhibitory effect on tumor disappears, resulting in colorectal adenomatous polyposis and carcinogenesis. 6, colonic polyps (1) adenoma: the incidence is 25% to 41%. This indicates that environmental and lifestyle changes are related. Adenomas occur more often in men than in women, and increase with age. From the autopsy data, the incidence of adenoma is 17% before the age of 50, 35% between 50 and 59, 56% between 60 and 69, and 63% for those over 70. It is generally believed that colorectal cancer originates from adenomatous polyps, and its cancer rate is 1.4% to 9.2%. Removal can reduce the risk of colorectal cancer. Mature classification: pathologically divided into 3 categories: a. tubular adenoma b. villous adenoma c. tubular villous adenoma ② characteristics of adenoma size, number and anatomical distribution: 38% of adenomas are ≤0.5cm, 36% are 0.6-1cm, and 26% are ≥1cm; 60% are solitary, 40% are multiple, and the number of multiple increases with age. Choroidal adenoma 60%>2cm, 86% are mild atypical hyperplasia, 6% are severe. ③ Adenoma and carcinoma: The concept of adenoma to carcinoma has been accepted. Worldwide, the prevalence of adenoma to carcinoma increases when immigrants migrate to areas with high incidence of colorectal cancer, and the rate of carcinoma is positively correlated with age and size of adenoma, which is obvious in the left hemicolectomy. 1.3% of adenomas smaller than 1 cm were malignant, only 9.5% of adenomas between 1 and 2 cm were malignant, and 46% of adenomas larger than 2 cm were malignant; ② only 4.8% of tubular adenomas were malignant, and 40.7% of villous; ③ 5.9% of mild typical hyperplasia were malignant, while 18% and 34.5% of moderate and severe ones were malignant respectively. The incidence of adenoma in the sigmoid colon was 31% in the proximal colon during the same period. Of these, 8% were progressive adenomas or carcinomas. D. Cancer time: Adenoma is a long chronic process, at least 5 years, average 10-15 years, which is also consistent with the slow growth of benign adenoma. E. Number of adenomas and cancer: 29.7% for single adenomas, 51.7%-76.9% for 2-5 adenomas, and 80% for 6-48 adenomas. Domestic reports of cancerous adenomas from multiple adenomas accounted for 71.4%. Most of the adenomas seen clinically are less than 2 cm in size, so there is no need to emphasize too much on the issue of carcinoma when considering their management. For adenomas with carcinoma in situ, local excision is sufficient for regular follow-up, and there is no need for extended surgery. For patients with adenomas, regular follow-up after excision is still necessary to pay attention to the occurrence of new adenomas. Other common polyps: (1) Juvenile polyps and polyposis: Juvenile polyps, also known as congenital polyps, retention polyps or juvenile adenomas, are common in young children, but can also be seen in adults, mostly under 10 years of age, more than 70% are solitary, but can also be multiple (usually 3 or 4), 60% occur within 10 cm from the anorectum. (2) Juvenile polyposis coli (JPC), multiple polyps have the same histomorphology as single juvenile polyps, but are familial. Single polyps are mostly benign and have no tendency to become malignant. In the case of multiple polyps, they can occur in all segments of the gastrointestinal tract and can be 25 to 40 or more. There are familial juvenile gastric polypomas limited to the stomach or familial juvenile colonic polypomas limited to the colon. Familial genereralized juvenile polyposis (FGJP) is an autosomal dominant disorder that can be combined with extragastric malformations. Although juvenile polyps are benign in form, they have a high chance of malignancy because they are frequent and can be combined with adenomas. The treatment is removal of polyps and regular lifelong screening should be started after the age of 10 years for this group of family members. (3) Inflammatory polyps: Inflammatory polyps with obvious infection, non-neoplastic, with ulceration and degeneration, including Crohn’s disease or ulcerative colitis, etc. Inflammatory polyps can be grouped into 2 categories: (1) multiple or single polyps consisting of inflammatory interstitial or granulation tissue and proliferating epithelium; (2) pseudopolyps related to mucosal inflammatory diseases, such as ulcerative colitis, Crohn’s disease, schistosomiasis granuloma, etc., which show polyps around the lesions of these diseases, or inflammatory polyps that occur at the edge of the line nodes or ulcers at the site of intestinal surgical anastomosis. There is a positive correlation between ulcerative colitis and colorectal carcinogenesis, and pathomorphology can be seen in the proliferating epithelium and cancer with migration, combined with experimental studies, the inflammatory lesions have a promotional effect on colorectal carcinogenesis. (4) Metaplastic (hyperplastic) polyps: Smaller semicircular polyps with protruding mucosal surface resembling dewlap, without tip. (5) mucosal hypertrophy (mucosal hyperplasia): endoscopic examination of the mucosa can be seen in small protrusions, that is, mucosal polyps, less than 0.5 cm. for the normal mucosa is submucosal tissue topping up, accounting for 18% of small polyps removed, no clinical significance. 7, colorectal polyposis The difference between colorectal polyposis and colorectal polyps is the difference in the number of polyps or adenomas. According to Morson’s criteria more than 100 are polyps (adenomatous) disease, including neoplastic and abiotic. However, in polyposis, malignant changes and other tumor features often occur in non-neoplastic cases. (1) Familial adenomatous polyposis (FAP): It is an autosomal dominant disease, in which the colorectum is often covered with polypoid adenomas (Figure 4), and if left untreated, about 3/4 of them become cancerous before the age of 35, and almost all of them develop into cancer after the age of 50. Since no polyps are found in infancy, this disease is not a congenital disease, but it is definitely related to family inheritance. It can be inherited by both men and women, but no intergenerational inheritance is found, i.e., it is limited to those who have the disease to pass on to the next generation. (2) Gardner syndrome: First reported by Gardner and Richard in 1953, Gardner syndrome is an inherited disease and is less common than familial polyposis. It is characterized clinically by the following conditions in addition to colorectal polyposis: ① adenomas: in addition to multiple adenomas in the colorectum, adenomas can also be seen in the stomach and small intestine, and adenomas can occur later or even at the age of 30 to 40 years. (ii) Osteomatosis: benign osteoma or exophytic bone warts, mostly in the craniofacial skeleton, especially in the maxilla. Soft tissue skin tumors: often multiple, located in the skin or subcutaneous, such as epidermoid cysts, fibromas, neurofibromas, especially located in the abdominal surgery scar, in addition to abdominal surgery fashion can be seen mesenteric fibromas. (3) Pemphigoid polyposis (Pentz-Jeghers syndrome): Pemphigoid polyposis is a rare familial disease, also known as Peutz-Jeghers syndrome, which was first described by Peutz in 1921 and systematically summarized by Jeghets et al. in 1943. It is a malformation tumor that can occur anywhere in the gastrointestinal tract. It is considered to be non-neoplastic but can become cancerous. Pathologically, polyps are composed of normal mucosal glands, similar to tubular adenomas, which include mucosal muscular layer extending in a dendritic pattern between the glandular ducts, so that mesenchymal stroma can be seen and smooth muscle fibers are its pathological features (Figure 5). (4) Cronkhit Canada syndrome: first reported by Cronkhit and Canada in 1955, it is a coexistence of skin pigmentation and juvenile polyps with pigmentation on the palmar side of the fingertips and the dorsum of the hand and nail atrophy, a juvenile polypoma combined with ectodermal changes, the former with typical lamina propria hyperplasia, inflammatory cells filling the enlarged and displaced glandular cavity, moderate morphology There is not enough evidence to suggest the possibility of gastrointestinal malignancy.