Hemolysis can be due to hereditary and acquired disorders.

The etiology of premature erythrocyte destruction is diverse and can be due to conditions such as intrinsic membrane defects, abnormal hemoglobins, erythrocyte enzymatic defects, immune destruction of erythrocytes, mechanical injury, and hypersplenism. Hemolysis may be an extravascular or an intravascular phenomenon. Autoimmune hemolytic anemia and hereditary spherocytosis are examples of extravascular hemolysis because the red blood cells are destroyed in the spleen and other reticuloendothelial tissues.[1] Intravascular hemolysis occurs in hemolytic anemia due to prosthetic cardiac valves, G-6-PD deficiency, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, following transfusion of ABO incompatible blood, and paroxysmal nocturnal hemoglobinuria (PNH). Hemolysis may also be intramedullary when fragile RBC precursors are destroyed in the bone marrow prior to release into the circulation. Intramedullary hemolysis occurs in pernicious anemia and thalassemia major. Hemolysis is associated with a release of RBC lactate dehydrogenase (LDH). Hemoglobin released from damaged RBC leads to an increase in indirect bilirubin and urobilinogen. A patient with mild hemolysis may have normal hemoglobin levels if increased RBC production matches the rate of RBC destruction. However, patients with mild hemolysis may develop marked anemia if their bone marrow erythrocyte production is transiently shut off by viral (parvovirus B-19) or other infections. This scenario would be an aplastic crisis since the bone marrow can no longer compensate for ongoing hemolysis. Skull and skeletal deformities can occur in childhood due to a marked increase in hematopoiesis and resultant bone marrow expansion in disorders such as thalassemia.

Colon cancer is believed to arise from polyps, which are protrusions that extend from the mucosal surface of the colonic wall. Colon polyps may be nonneoplastic or neoplastic, based on their histopathology. Nonneoplastic polyps include hyperplastic, hamartomatous, inflammatory, and lymphoid polyps. Neoplastic polyps, which are generally called adenomas, can be further subdivided into benign or malignant adenomas. The malignant type is called a polypoid carcinoma, whereas villous adenomas, tubulovillous adenomas, and tubular adenomas are benign adenomas that have the potential to become malignant. Tubular adenomas represent 75% of all neoplastic polyps and are the least likely to progress to a malignant state. Villous adenomas are the most likely to progress to becoming cancerous, while tubulovillous adenomas have an intermediate potential for becoming cancerous.[4] Several factors predict the probability that an adenoma will develop into cancer. These include the size of the polyp, the relative proportion of its villous components, and the presence of significant cytologic abnormalities. Overall, fewer than 1% of all polyps progress to cancer. However, from 5% to 40% of adenomas are estimated to progress to cancer.[4] Generally, the smaller the polyp, the lower the likelihood of cancer. Polyps less than 1 cm have a very low incidence of cancer, whereas for those between 1 cm and 10 cm in size, the incidence rises to about 10%. Larger polyps are associated with carcinoma up to 45% of the time. The process in which normal mucosa is converted into an adenoma then cancer is gradual, occurring over approximately 5 to 10 years.

Colorectal cancer develops in the colon (the first 45 feet [0.60.9 meter] of the large intestine) or the rectum (the last few inches of the large intestine). Colorectal cancer affects the lower part of the digestive tract. It occurs most often in people over 50 but may develop in younger adults with a family history of colorectal cancer. Most colorectal cancers develop out of polyps, tissue growths that arise out of the tissue that lines the large intestine. Most polyps are benign, but some undergo changes in their genetic makeup that cause them to eventually become cancerous. Colorectal cancer usually develops over a period of several years. In many cases the patient has no symptoms but is diagnosed as the result of screening for the disease. About half of patients go to their doctor because they have abdominal pain; a third notice a change in bowel habits; and 15 percent have an obstruction (blockage) in their intestines. In some cases these patients may notice that their bowel movements are unusually thin in shape. As a rule, the larger the cancer and the closer it is to the anus, the more likely the patient is to have noticeable changes in bowel habits. Colorectal cancer is the fourth most common cancer in the United States. According to the American Cancer Society (ACS), about 112,000 people are diagnosed with colon cancer annually; about 41,000 new cases of rectal cancer are diagnosed each year; and about 57,000 persons die each year from colorectal cancer. According to the World Health Organization (WHO) there are about 940,000 new cases of and 500,000 deaths from colorectal cancer reported worldwide each year. Colorectal cancer is most common in older adults; the average age at the time of diagnosis is 72. Colon cancer in teenagers or young adults is unusual. Rates are equal for men and women. African Americans appear to have higher rates of colon cancer than members of other racial groups in the United States, but the reasons are unclear. The lifetime risk of developing colon cancer in the United States is about 7 percent. Researchers at the National Cancer Institute have identified several factors that increase a persons risk of colon cancer: Age over 50. A family history of colorectal cancer. Parents, siblings, or children of a person diagnosed with colon cancer have an increased risk of developing it, particularly if the relative was diagnosed at a young age. Having either of two specific genes that increase the risk of colon cancer. These genes are associated with 3 percent of all colon cancers, and can lead to colon cancer by age forty. They can be detected by genetic testing. In women, a personal history of breast cancer. A history of ulcerative colitis or Crohns disease. A history of polyps in the colon or rectum. Polyps are growths that develop along the inner wall of the colon or rectum, most often in people over fifty. Most are benign (not cancerous), but some may develop into cancerous tumors. A diet high in fat and low in fiber. A history of heavy smoking or alcohol consumption. Obesity and diabetes. Gigantism and other disorders involving growth hormone. Previous radiation treatment for cancers elsewhere in the abdomen. Causes and Symptoms of Colorectal Cancer The cause of most cases of colorectal cancer is the change in normally benign intestinal polyps to cancerous tumors. There are several different types of intestinal polyps, but only two carry a risk of developing into cancers. These two types can be removed during screening tests for colorectal cancer. The triggers that cause some polyps to become cancerous are not completely understood. In addition to changes in bowel habits, abdominal cramping, and signs of intestinal blockage, patients with colorectal cancer may have the following symptoms: General tiredness, unexplained weight loss, and lack of appetite Bleeding from the rectum or blood or mucus on the stools Anemia Pain when passing a bowel movement Nausea and vomiting A feeling that the bowel hasnt completely emptied following a bowel movement