Intestinal atresia is a malformation where there is a narrowing or absence of a portion of the intestine. This defect can either occur in the small or large intestine.

The most common cause of non-duodenal intestinal atresia is a vascular accident in utero that leads to decreased intestinal perfusion and ischemia of the respective segment of bowel. This leads to narrowing, or in the most severe cases, complete obliteration of the intestinal lumen.

In the case that the superior mesenteric artery, or another major intestinal artery, is occluded, large segments of bowel can be entirely underdeveloped. Classically, the affected area of bowel assumes a spiral configuration and is described to have an "apple peel" like appearance; this is accompanied by lack of a dorsal mesentery.

Ileal atresia can also result as a complication of meconium ileus.

Enteric duplication cysts, sometimes simply called duplication cysts, are rare congenital malformations of the gastrointestinal tract. They most frequently occur in the small intestine, particularly the ileum, but can occur anywhere along the gastrointestinal tract. They may be cystic or tubular in conformation.

The condition of having duplication cysts has been called intestinal duplication.

The condition is diagnosed most often in infancy and early childhood. It strikes about 2,000 infants (one in every 1,900) in the United States in the first year of life. Its incidence begins to rise at about one to five months of life, peaks at four to nine months of age, and then gradually declines at around 18 months.

Intussusception occurs more frequently in boys than in girls, with a ratio of approximately 3:1.

In adults, intussusception represents the cause of approximately 1% of bowel obstructions and is frequently associated with neoplasm, malignant or otherwise.

Causes of intussusception are not clearly established or understood. About 90% of cases of intussusception in children arise from an unknown cause. They can include infections, anatomical factors, and altered motility.

- Meckel's diverticulum

- Polyp

- Duplication

- Appendix

- Hyperplasia of Peyer's patches

- Idiopathic

An earlier version of the rotavirus vaccine that is no longer used was linked to intussusception, but the current versions are not clearly linked. Due to a potential risk, they are thus not recommended in babies who have had intussusception.

Laparotomy for other forms of volvulus, especially anal volvulus.

In a cecal volvulus, the cecum may be returned to a normal position and sutured in place, a procedure known as cecopexy. If identified early, before presumed intestinal wall ischemia has resulted in tissue breakdown and necrosis, the cecal volvulus can be detorsed laparoscopically.

Intestinal neuronal dysplasia (or neuronal intestinal dysplasia or NID) is an inherited disease of the intestine that affects one in 3000 children and adults. The intestine uses peristalsis to push its contents toward the anus; IND sufferers have a problem with the motor neurons that lead to the intestine, inhibiting this process and thus preventing digestion.

It can often be confused for Hirschsprung's disease, as both have similar symptoms.

There is no cure for short bowel syndrome except transplant. In newborn infants, the 4-year survival rate on parenteral nutrition is approximately 70%. In newborn infants with less than 10% of expected intestinal length, 5 year survival is approximately 20%. Some studies suggest that much of the mortality is due to a complication of the total parenteral nutrition (TPN), especially chronic liver disease. Much hope is vested in Omegaven, a type of lipid TPN feed, in which recent case reports suggest the risk of liver disease is much lower.

Although promising, small intestine transplant has a mixed success rate, with postoperative mortality rate of up to 30%. One-year and 4-year survival rate are 90% and 60%, respectively.

It can be grouped into NID A and NID B, with the "A" form affecting the sympathetic innervation, and the "B" version affecting the parasympathetic innervation.

In 2002 Martucciello G et al. published the first analysis of associated anomalies in IND population is an important clinical approach to investigate possible pathogenetic correlations. Two recessive syndromes were identified (3 families). The first was characterized by NID B, intestinal malrotation, and congenital short bowel, the second by NID B, short stature, mental retardation, and facial dysmorphism. In this study, gastrointestinal anomalies accounted for 67.4% of all associated disorders. These data suggest a strong correlation between IND and intestinal development.

Duplications are usually removed surgically, even if they are found incidentally (i.e. not causing symptoms or encountered on routine studies for other reasons), as there is a high incidence of complications resulting from untreated cases. Cysts are often technically easier to remove than tubular malformations since tubular structures usually share a blood supply with the associated gut.

Blind loop syndrome is a complication of surgical operations of the abdomen, as well as inflammatory bowel disease or scleroderma. Another cause is jejunoileal diverticula.

Colitis is inflammation of the colon. Acute cases are medical emergencies as the horse rapidly loses fluid, protein, and electrolytes into the gut, leading to severe dehydration which can result in hypovolemic shock and death. Horses generally present with signs of colic before developing profuse, watery, fetid diarrhea.

Both infectious and non-infectious causes for colitis exist. In the adult horse, "Salmonella", "Clostridium difficile", and "Neorickettsia risticii" (the causative agent of Potomac Horse Fever) are common causes of colitis. Antibiotics, which may lead to an altered and unhealthy microbiota, sand, grain overload, and toxins such as arsenic and cantharidin can also lead to colitis. Unfortunately, only 20–30% of acute colitis cases are able to be definitively diagnosed. NSAIDs can cause slower-onset of colitis, usually in the right dorsal colon (see Right dorsal colitis).

Treatment involves administration of large volumes of intravenous fluids, which can become very costly. Antibiotics are often given if deemed appropriate based on the presumed underlying cause and the horse's CBC results. Therapy to help prevent endotoxemia and improve blood protein levels (plasma or synthetic colloid administration) may also be used if budgetary constraints allow. Other therapies include probiotics and anti-inflammatory medication. Horses that are not eating well may also require parenteral nutrition. Horses usually require 3–6 days of treatment before clinical signs improve.

Due to the risk of endotoxemia, laminitis is a potential complication for horses suffering from colitis, and may become the primary cause for euthanasia. Horses are also at increased risk of thrombophlebitis.

The overgrowth of bacteria in the small intestine is prevented by various mechanical and chemical factors which include the constant peristaltic movement of contents along the length of the gastrointestinal tract and the antibacterial properties of gastric secretions, pancreatic secretions and bile.

It follows that a disruption of any of these factors could lead to bacterial overgrowth and indeed BLS has been found to occur in persons with anatomical anomalies that result in stagnation. BLS has also been associated with achlorhydria, dysmotility, fistulae, and strictures. Chronic or high dose opioid therapy may contribute to BLS by reducing gastric motility.

Due to the disruption of digestive processes by the overgrowth of intestinal bacteria malabsorption of bile salts, fat and fat-soluble vitamins, protein and carbohydrates results in damage to the mucosal lining of the intestine by bacteria or via the production of toxic metabolites.

Short bowel syndrome in adults and children is usually caused by surgery. This surgery may be done for:

- Crohn's disease, an inflammatory disorder of the digestive tract

- Volvulus, a spontaneous twisting of the small intestine that cuts off the blood supply and leads to tissue death

- Tumors of the small intestine

- Injury or trauma to the small intestine

- Necrotizing enterocolitis (premature newborn)

- Bypass surgery to treat obesity

- Surgery to remove diseases or damaged portion of the small intestine

Some children are also born with an abnormally short small intestine, known as congenital short bowel.

Occasionally there can be an obstruction by large numbers of roundworms. This is most commonly seen in young horses as a result of a very heavy infestation of "Parascaris equorum" that can subsequently cause a blockage and rupture of the small intestine. Rarely, dead worms will be seen in reflux. Deworming heavily infected horses may cause a severe immune reaction to the dead worms, which can damage the intestinal wall and cause a fatal peritonitis. Veterinarians often treat horses with suspected heavy worm burdens with corticosteroids to reduce the inflammatory response to the dead worms. Blockages of the small intestine, particularly the ileum, can occur with "Parascaris equorum" and may well require colic surgery to remove them manually. Large roundworm infestations are often the result of a poor deworming program. Horses develop immunity to parascarids between 6 months age and one year and so this condition is rare in adult horses. Prognosis is fair unless the foal experiences hypovolemia and septic shock, with a survival rate of 33%.

Horses may develop pharyngitis, laryngitis, or esophagitis secondary to indwelling nasogastric tube. Other complications include thrombophlebitis, laminitis (which subsequently reduces survival rate), and weight loss. Horses are also at increased risk of hepatic injury.

Survival rates for DPJ are 25–94%. Horses that survive the incident rarely have reoccurrence.

Atresia is a condition in which an orifice or passage in the body is (usually abnormally) closed or absent.

Examples of atresia include:

- Biliary atresia, a condition in newborns in which the common bile duct between the liver and the small intestine is blocked or absent.

- Choanal atresia, blockage of the back of the nasal passage, usually by abnormal bony or soft tissue.

- Esophageal atresia, which affects the alimentary tract and causes the esophagus to end before connecting normally to the stomach.

- Imperforate anus, malformation of the opening between the rectum and anus.

- Intestinal atresia, malformation of the intestine, usually resulting from a vascular accident in utero.

- Microtia, absence of the ear canal or failure of the canal to be tubular or fully formed (can be related to Microtia, a congenital deformity of the pinna, or outer ear).

- Ovarian follicle atresia, the degeneration and subsequent resorption of one or more immature ovarian follicles.

- Potter sequence, congenital decreased size of the kidney leading to absolutely no functionality of the kidney, usually related to a single kidney.

- Pulmonary atresia, malformation of the pulmonary valve in which the valve orifice fails to develop.

- Renal agenesis, only having one kidney.

- Tricuspid atresia, a form of congenital heart disease whereby there is a complete absence of the tricuspid valve, and consequently an absence of the right atrioventricular connection.

- Vaginal atresia, a congenital occlusion of the vagina or subsequent adhesion of the walls of the vagina, resulting in its occlusion.

A Richter's hernia occurs when the antimesenteric wall of the intestine protrudes through a defect in the abdominal wall. This is discrete from other types of abdominal hernias in that only one intestinal wall protrudes through the defect, such that the lumen of the intestine is incompletely contained in the defect, while the rest remains in the peritoneal cavity. If such a herniation becomes necrotic and is subsequently reduced during hernia repair, perforation and peritonitis may result. A Richter's hernia can result in strangulation and necrosis in the absence of intestinal obstruction. It is a relatively rare but dangerous type of hernia.

Richter's hernia have also been noted in laparoscopic port-sites, usually when the fascia is not closed for ports larger than 10mm. A high index of suspicion is required in the post operative period as this sinister problem can closely mimic more benign complications like port-site haematomas.

Treatment is resection and anastomosis.

Mortality increases with delay in surgical intervention.

Treatment of accessory pancreas depends on the location and extent of the injured tissue. Surgery may be an option, or some physicians order prophylactic antibiotics.

These lesions usually present in neonates, although they may not come to clinical attention until adulthood (for cosmetic reasons). There is no gender predilection. They are present in approximately 3-6 per 1000 live births.

Risk factors for small intestine cancer include:

- Crohn's disease

- Celiac disease

- Radiation exposure

- Hereditary gastrointestinal cancer syndromes: familial adenomatous polyposis, hereditary nonpolyposis colorectal cancer, Peutz-Jeghers syndrome

- Males are 25% more likely to develop the disease

Benign tumours and conditions that may be mistaken for cancer of the small bowel:

- Hamartoma

- Tuberculosis

Little research is conducted on these cancers due to their relative rarity when compared to the more common colorectal cancers. APC-min mice which carry a gene deficiency corresponding to that of humans with FAP also go on to develop small intestinal tumors, though humans do not.

DPJ is most commonly seen in the Southeastern US, although cases have been reported throughout the United States and Canada, as well as sporadically in the United Kingdom and Europe. Horses in the Southeastern US tend to have a more severe form of the disease relative to other locations. Age, breed, and gender appear to have no effect on disease prevalence.

Cronkhite–Canada syndrome is a rare syndrome characterized by multiple polyps of the digestive tract. It is sporadic (i.e. it does not seem to be a hereditary disease), and it is currently considered acquired and idiopathic (i.e. cause remains unknown).

About two-thirds of patients are of Japanese descent and the male to female ratio is 2:1. It was characterized in 1955.