In adults, most common causes are hemorrhoids and diverticulosis, both of which are relatively benign; however, it can also be caused by colorectal cancer, which is potentially fatal. In a newborn infant, haematochezia may be the result of swallowed maternal blood at the time of delivery, but can also be an initial symptom of necrotizing enterocolitis, a serious condition affecting premature infants. In babies, haematochezia in conjunction with abdominal pain is associated with intussusception. In adolescents and young adults, inflammatory bowel disease, particularly ulcerative colitis, is a serious cause of haematochezia that must be considered and excluded.

Hematochezia can be due to upper gastrointestinal bleeding. However, as the blood from such a bleed is usually chemically modified by action of acid and enzymes, it presents more commonly as black "tarry" feces known as melena. Haematochezia from an upper gastrointestinal source is an ominous sign, as it suggests a very significant bleed which is more likely to be life-threatening.

Beeturia can cause red colored feces after eating beets because of insufficient metabolism of a red pigment, and is a differential sign that may be mistaken as hematochezia.

Consumption of dragon fruit or pitaya may also cause red discoloration of the stool and sometimes the urine (pseudohematuria). This too, is a differential sign that is sometimes mistaken for hematochezia.

In infants, the Apt test can be used to distinguish fetal hemoglobin from maternal blood.

Other common causes of blood in the stool include:

- Colorectal cancer

- Crohns disease

- Ulcerative colitis

- Other types of inflammatory bowel disease, inflammatory bowel syndrome, or ulceration

- Rectal or anal hemorrhoids or anal fissures, particularly if they rupture or are otherwise irritated

- "Shigella" or shiga toxin producing "E. coli" food poisoning

- Necrotizing enterocolitis

- Diverticulosis

- Salmonellosis

- Upper gastrointestinal bleeding

- Peptic ulcer disease

- Esophageal varices

- Gastric cancer

- Intense exercise, especially a high-impact activity like running in hot weather.

Safety regulations from US accreditor the Joint Commission may have unintentionally decreased digital rectal examination and FOBT in hospital settings such as Emergency Departments.

Conditions such as ulcerative colitis or certain types of relapsing infectious diarrhea can vary in severity over time, and FOBT may assist in assessing the severity of the disease. Medications associated with gastrointestinal bleeding such as Bortezomib are sometimes monitored by FOBT.

Hematochezia is the passage of fresh blood through the anus, usually in or with stools (contrast with melena). Hematochezia is commonly associated with lower gastrointestinal bleeding, but may also occur from a brisk upper gastrointestinal bleed. The difference between hematochezia and rectorrhagia is that, in the latter, rectal bleeding is not associated with defecation; instead, it is associated with expulsion of fresh bright red blood without stools. The phrase bright red blood per rectum (BRBPR) is associated with hematochezia and rectorrhagia. It is also important to differentiate from hematopapyrus - blood on the toilet paper noticed when wiping. The term is from Greek αἷμα ("blood") and χέζειν ("to defaecate").

Diseases causing inflammation in the GI tract can lead to blood in the stool. Inflammation can occur anywhere along the GI tract in Crohn's disease, or in the colon if a person has ulcerative colitis.

- Crohns disease

- Ulcerative colitis

This list of diagnoses include diseases in which the wall of the bowel is compromised by disease.

- Peptic ulcer disease—divided into either duodenal or gastric ulcers, most common common causes include:

- Non steroidal anti-inflammatory drug (NSAID)—the use of these medications results in a structural change in the wall of the gut, namely ulcers, and potential blood in the stool.

- "H. pylori" infection—this bacterial infection can erode the wall of the stomach or duodenum, leading to a structural change in the stomach wall and bleeding in the stool.

- Chronic disease

- Diverticulitis and diverticulosis result from an out pouching of the colonic mucosa, or gut wall, leading to a break down of weak gut wall and an increased susceptibility to infection due to the bacteria in the GI tract, thus the potential for vascular compromise, the collection of bacteria in the area of perforation (abscess), the abnormal formation of communication between another part of the hollow GI tract (fistula), or blockage of the bowel (obstruction).

- Meckel's diverticulum is a congenital remnant of the omphalo-mesenteric duct that connected the fetal yolk sac to the intestines which is normal closed off and destroyed during the process of development. If a portion, or all of this duct remains a diverticulum or fistula can result, leading to the potential for a source of bleeding.

The literature, from 1953 through 2010, often cited that the cause of gastric antral vascular ectasia is unknown. The causal connection between cirrhosis and GAVE has not been proven. A connective tissue disease has been suspected in some cases.

Autoimmunity may have something to do with it, as 25% of all sclerosis patients who had a certain anti-RNA marker have GAVE. RNA autoimmunity has been suspected as a cause or marker since at least 1996. Gastrin levels may indicate a hormonal connection.

Most patients who are eventually diagnosed with watermelon stomach come to a physician complaining of anemia and blood loss. Sometimes, a patient may come to the physician because he or she notices blood in the stools—either melena (black and tarry stools) and/or hematochezia (red bloody stools).

Treatment of hemosuccus pancreaticus depends on the source of the hemorrhage. If the bleeding is identified on angiography to be coming from a vessel that is small enough to occlude, embolization through angiography may stop the bleeding. Both coils in the end-artery and stents across the area of bleeding have been used to control the hemorrhage. However, the bleeding may be refractory to the embolization, which would necessitate surgery to remove the pancreas at the source of hemorrhage. Also, the cause of bleeding may be too diffuse to be treated with embolization (such as with pancreatitis or with pancreatic cancer). This may also require surgical therapy, and usually a distal pancreatectomy, or removal of the part of the pancreas from the area of bleeding to the tail, is required.

When the fecal stream is diverted as part of a colostomy, a condition called diversion colitis may develop in the section of bowel that no longer is in contact with stool. The mucosal lining is nourished by short-chain fatty acids, which are produced as a result of bacterial fermentation in the gut. Long-term lack of exposure to this nutrients can cause inflammation of the colon (colitis). Symptoms include rectal bleeding, mucous discharge, tenesmus and abdominal pain.

Hemosuccus pancreaticus, also known as pseudohematobilia or Wirsungorrhage is a rare cause of hemorrhage in the gastrointestinal tract. It is caused by a bleeding source in the pancreas, pancreatic duct, or structures adjacent to the pancreas, such as the splenic artery, that bleed into the pancreatic duct, which is connected with the bowel at the duodenum, the first part of the small intestine. Patients with hemosuccus may develop symptoms of gastrointestinal hemorrhage, such as blood in the stools, maroon stools, or melena, which is a dark, tarry stool caused by digestion of red blood cells. They may also develop abdominal pain. It is associated with pancreatitis, pancreatic cancer and aneurysms of the splenic artery. Hemosuccus may be identified with endoscopy (esophagogastroduodenoscopy), where fresh blood may be seen from the pancreatic duct. Alternatively, angiography may be used to inject the celiac axis to determine the blood vessel that is bleeding. This may also be used to treat hemosuccus, as embolization of the end vessel may terminate the hemorrhage. However, a distal pancreatectomy—surgery to removal of the tail of the pancreas—may be required to stop the hemorrhage.

Anal warts are irregular, verrucous lesions caused by human papilloma virus. Anal warts are usually transmitted by unprotected, anoreceptive intercourse. Anal warts may be asymptomatic, or may cause rectal discharge, anal wetness, rectal bleeding, and pruritus ani. Lesions can also occur within the anal canal, where they are more likely to create symptoms.

It is difficult to determine how common hemorrhoids are as many people with the condition do not see a healthcare provider. However, symptomatic hemorrhoids are thought to affect at least 50% of the US population at some time during their lives, and around 5% of the population is affected at any given time. Both sexes experience about the same incidence of the condition, with rates peaking between 45 and 65 years. They are more common in Caucasians and those of higher socioeconomic status.

Long-term outcomes are generally good, though some people may have recurrent symptomatic episodes. Only a small proportion of persons end up needing surgery.

The lifetime risk for a person with Meckel's diverticulum to develop certain complications is about 4–6%. Gastrointestinal bleeding, peritonitis or intestinal obstruction may occur in 15–30% of symptomatic patients (Table 1). Only 6.4% of all complications requires surgical treatment; and untreated Meckel's diverticulum has a mortality rate of 2.5–15%.

Table 1 – Complications of Meckel's Diverticulum:

Meckel's diverticulum occurs in about 2% of the population. Prevalence in males is 3–5 times higher than in females. Only 2% of cases are symptomatic, which usually presents among children at the age of 2.

Most cases of Meckel's diverticulum are diagnosed when complications manifest or incidentally in unrelated conditions such as laparotomy, laparoscopy or contrast study of the small intestine. Classic presentation in adults includes intestinal obstruction and inflammation of the diverticulum (diverticulitis). Painless rectal bleeding most commonly occurs in toddlers.

Inflammation in the ileal diverticulum has symptoms that mimic appendicitis, therefore its diagnosis is of clinical importance. Detailed knowledge of the pathophysiological properties is essential in dealing with the life-threatening complications of Meckel's diverticulum.

The exact cause of symptomatic hemorrhoids is unknown. A number of factors are believed to play a role, including irregular bowel habits (constipation or diarrhea), lack of exercise, nutritional factors (low-fiber diets), increased intra-abdominal pressure (prolonged straining, ascites, an intra-abdominal mass, or pregnancy), genetics, an absence of valves within the hemorrhoidal veins, and aging. Other factors believed to increase risk include obesity, prolonged sitting, a chronic cough, and pelvic floor dysfunction. Squatting while defecating may also increase the risk of severe hemorrhoids. Evidence for these associations, however, is poor.

During pregnancy, pressure from the fetus on the abdomen and hormonal changes cause the hemorrhoidal vessels to enlarge. The birth of the baby also leads to increased intra-abdominal pressures. Pregnant women rarely need surgical treatment, as symptoms usually resolve after delivery.

Hypoprothrombinemia can be the result of a genetic defect, may be acquired as the result of another disease process, or may be an adverse effect of medication. For example, 5-10% of patients with systemic lupus erythematosus exhibit acquired hypoprothrombinemia due to the presence of autoantibodies which bind to prothrombin and remove it from the bloodstream (lupus anticoagulant-hypoprothrombinemia syndrome). The most common viral pathogen that is involved is Adenovirus, with a prevalence of 50% in postviral cases.

Inheritance:

Autosomal recessive condition in which both parents must carry the recessive gene in order to pass the disease on to offspring. If both parents have the autosomal recessive condition, the chance of mutation in offspring increases to 100%. An individual will be considered a carrier if one mutant copy of the gene is inherited, and will not illustrate any symptoms. The disease affects both men and women equally, and overall, is a very uncommon inherited or acquired disorder.

Non-inheritance and other factors:

There are two types of prothrombin deficiencies that occur depending on the mutation:

Type I (true deficiency), includes a missense or nonsense mutation, essentially decreasing prothrombin production. This is associated with bleeding from birth. Here, plasma levels of prothrombin are typically less than 10% of normal levels.

Type II, known as dysprothrombinemia, includes a missense mutation at specific Xa factor cleavage sites and serine protease prothrombin regions. Type II deficiency creates a dysfunctional protein with decreased activity and usually normal or low-normal antigen levels. A vitamin K-dependent clotting factor is seldom seen as a contributor to inherited prothrombin deficiencies, but lack of Vitamin K decreases the synthesis of prothrombin in liver cells.

Acquired underlying causes of this condition include severe liver disease, warfarin overdose, platelet disorders, and disseminated intravascular coagulation (DIC).

It may also be a rare adverse effect to Rocephin.

Hypoprothrombinemia is a rare blood disorder in which a deficiency in immunoreactive prothrombin (Factor II), produced in the liver, results in an impaired blood clotting reaction, leading to an increased physiological risk for spontaneous bleeding. This condition can be observed in the gastrointestinal system, cranial vault, and superficial integumentary system, effecting both the male and female population. Prothrombin is a critical protein that is involved in the process of hemostasis, as well as illustrating procoagulant activities. This condition is characterized as an autosomal recessive inheritance congenital coagulation disorder affecting 1 per 2,000,000 of the population, worldwide, but is also attributed as acquired.

Male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidemia, older age, familial disease and elevated creatinine concentrations are markers of a poor outcome. Frank hematuria has shown discordant results with most studies showing a better prognosis, perhaps related to the early diagnosis, except for one group which reported a poorer prognosis. Proteinuria and hypertension are the most powerful prognostic factors in this group.

There are certain other features on kidney biopsy such as interstitial scarring which are associated with a poor prognosis. ACE gene polymorphism has been recently shown to have an impact with the DD genotype associated more commonly with progression to kidney failure.

Men are affected three times as often as women. There is also marked geographic variation in the prevalence of IgA nephropathy throughout the world. It is the most common glomerular disease in the Far East and Southeast Asia, accounting for almost half of all the patients with glomerular disease. However, it accounts for only about 25% of the proportion in European and about 10% among North Americans, with African–Americans having a very low prevalence of about 2%. However, a confounding factor in this analysis is the existing policy of screening and use of kidney biopsy as an investigative tool. School children in Japan undergo routine urinalysis (as do army recruits in Singapore) and any suspicious abnormality is pursued with a kidney biopsy, which might partly explain the high observed incidence of IgA nephropathy in those countries.