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.

Inflammation of the diverticulum can mimic symptoms of appendicitis, i.e., periumbilical tenderness and intermittent crampy abdominal pain. Perforation of the inflamed diverticulum can result in peritonitis. Diverticulitis can also cause adhesions, leading to intestinal obstruction.

Diverticulitis may result from:

- Association with the mesodiverticular band attaching to the diverticulum tip where torsion has occurred, causing inflammation and ischaemia.

- Peptic ulceration resulting from ectopic gastric mucosa of the diverticulum

- Following perforation by trauma or ingested foreign material e.g. stalk of vegetable, seeds or fish/chicken bone that become lodged in Meckel's diverticulum.

- Luminal obstruction due to tumors, enterolith, foreign body, causing stasis or bacterial infection.

- Association with acute appendicitis

Intestinal atresias are often discovered before birth: either during a routine sonogram which shows a dilated intestinal segment due to the blockage, or by the development of polyhydramnios (the buildup of too much amniotic fluid in the uterus). These abnormalities are indications that the fetus may have a bowel obstruction which a more detailed ultrasound study can confirm.

Some fetuses with bowel obstruction have abnormal chromosomes. An amniocentesis is recommended because it can determine not only the sex of the baby, but whether or not there is a problem with the chromosomes.

Symptoms: Vomiting, abdominal pain and severe or complete constipation.

- The vitelline vessels remnant that connects the diverticulum to the umbilicus may form a fibrous or twisting band (volvulus), trapping the small intestine and causing obstruction. Localised periumbilical pain may be experienced in the right lower quadrant (like appendicitis).

- "Incarceration": when a Meckel's diverticulum is constricted in an inguinal hernia, forming a Littré hernia that obstructs the intestine.

- Chronic diverticulitis causing stricture

- Strangulation of the diverticulum in the obturator foramen.

- Tumors e.g. carcinoma: direct spread of an adenocarcinoma arising in the diverticulum may lead to obstruction

- Lithiasis, stones that are formed in Meckel's diverticulum can:

1. Extrude into the terminal ileum, leading to obstruction

2. Induce local inflammation and intussusception.

- The diverticulum itself or tumour within it may cause intussusception. For example, from the ileum to the colon, causing obstruction. Symptoms of this include "currant jelly" stools and a palpable lump in the lower abdomen. This occurs when the diverticulum inverts into the lumen of the ileum, due to either:

1. An "active" peristaltic mechanism of the diverticulum that attempts to remove irritating factors

2. A "passive" process such as the transit of food

Regardless of cause, volvulus causes symptoms by two mechanisms:

- Bowel obstruction manifested as abdominal distension and bilious vomiting.

- Ischemia (loss of blood flow) to the affected portion of intestine.

Depending on the location of the volvulus, symptoms may vary. For example, in patients with a cecal volvulus, the predominant symptoms may be those of a small bowel obstruction (nausea, vomiting and lack of stool or flatus), because the obstructing point is close to the ileocecal valve and small intestine. In patients with a sigmoid volvulus, although abdominal pain may be present, symptoms of constipation may be more prominent.

Volvulus causes severe pain and progressive injury to the intestinal wall, with accumulation of gas and fluid in the portion of the bowel obstructed. Ultimately, this can result in necrosis of the affected intestinal wall, acidosis, and death. This is known as a closed loop obstruction because there exists an isolated ("closed") loop of bowel. Acute volvulus often requires immediate surgical intervention to untwist the affected segment of bowel and possibly resect any unsalvageable portion.

Volvulus occurs most frequently in middle-aged and elderly men. Volvulus can also arise as a rare complication in persons with redundant colon, a normal anatomic variation resulting in extra colonic loops.

Sigmoid volvulus is the most-common form of volvulus of the gastrointestinal tract. and is responsible for 8% of all intestinal obstructions. Sigmoid volvulus is particularly common in elderly persons and constipated patients. Patients experience abdominal pain, distension, and absolute constipation.

Cecal volvulus is slightly less common than sigmoid volvulus and is associated with symptoms of abdominal pain and small bowel obstruction.

Volvulus can also occur in patients with Duchenne muscular dystrophy due to the smooth muscle dysfunction.

Umbilical cord ulceration and intestinal atresia is a rare congenital disease that leads to intestinal atresia, umbilical cord ulceration and severe intrauterine haemorrhage. Only 15 cases have so far been reported, though newer studies are beginning to conclude that this disease has a higher incidence rate than has been previously reported. A particular study has given intestinal atresia and umbilical cord ulceration a clear link after 5 such cases were reported at the time of publication.

Midgut volvulus occurs in people (usually babies) that are predisposed because of congenital intestinal malrotation. Segmental volvulus occurs in people of any age, usually with a predisposition because of abnormal intestinal contents (e.g. meconium ileus) or adhesions. Volvulus of the cecum, transverse colon, or sigmoid colon occurs, usually in adults, with only minor predisposing factors such as redundant (excess, inadequately supported) intestinal tissue and constipation.

The causes of umbilical hernia are congenital and acquired malformation, but an apparent third cause is really a cause of a different type, a paraumbilical hernia.

A hernia is present at the site of the umbilicus (commonly called a navel or belly button) in newborns; although sometimes quite large, these hernias tend to resolve without any treatment by around the age of 2–3 years. Obstruction and strangulation of the hernia is rare because the underlying defect in the abdominal wall is larger than in an inguinal hernia of the newborn. The size of the base of the herniated tissue is inversely correlated with risk of strangulation (i.e., a narrow base is more likely to strangulate).

Babies are prone to this malformation because of the process during fetal development by which the abdominal organs form outside the abdominal cavity, later returning into it through an opening which will become the umbilicus.

Hernias may be asymptomatic and present only as a bulge of the umbilicus. Symptoms may develop when the contracting abdominal wall causes pressure on the hernia contents. This results in abdominal pain or discomfort. These symptoms may be worsened by the patient lifting or straining.

Symptoms of ileus include, but are not limited to:

- moderate, diffuse abdominal discomfort

- constipation

- abdominal distension

- nausea/vomiting, especially after meals

- vomiting of bilious fluid

- lack of bowel movement and/or flatulence

- excessive belching

Signs and symptoms of DIOS include a sudden onset of crampy abdominal pain, vomiting, and a palpable mass (often in the right lower quadrant) in the abdomen. The characteristic abdominal pain is typically located in the center or right lower quadrant of the abdomen. X-rays of the abdomen may reveal stool in the colon and air-fluid levels in the small intestines.

DIOS is sometimes classified by the degree of obstruction as incomplete or complete DIOS.

Decreased propulsive ability may be broadly classified as caused either by bowel obstruction or intestinal atony or paralysis. However, instances with symptoms and signs of a bowel obstruction occur, but with the absence of a mechanical obstruction, mainly in acute colonic pseudo-obstruction, Ogilvie's syndrome.

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.

The symptoms of short bowel syndrome can include:

- Abdominal pain

- Diarrhea and steatorrhea (oily, bulky stool, which can be malodorous)

- Fluid depletion

- Weight loss and malnutrition

- Fatigue

Persons with short bowel syndrome may have complications caused by malabsorption of vitamins and minerals, such as deficiencies in vitamins A, D, E, K, B (folic acid), and B, calcium, magnesium, iron, and zinc. These may appear as anemia, hyperkeratosis (scaling of the skin), easy bruising, muscle spasms, poor blood clotting, and bone pain.

Intestinal failure is decreased intestinal function such that nutrients, water, and electrolytes are not sufficiently absorbed. Short bowel syndrome is when there is less than of working bowel and is the most common cause of intestinal failure.

Clinical features of intestinal pseudo-obstruction can include abdominal pain, nausea, severe distension, vomiting, dysphagia, diarrhea and constipation, depending upon the part of the gastrointestinal tract involved. In addition, in the moments in which abdominal colic occurs, an abdominal x-ray shows intestinal air fluid level. All of these features are also similar in true mechanical obstruction of the bowel.

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.

On rare occasions, a piece of small intestine (or rarely colon) can become trapped through the epiploic foramen into the omental bursa. The blood supply to this piece of intestine is immediately occluded and surgery is the only available treatment. This type of colic has been associated with cribbers, possibly due to changes in abdominal pressure, and in older horses, possibly because the foramen enlarges as the right lobe of the liver atrophies with age, although it has been seen in horses as young as 4 months old. Horses usually present with colic signs referable to small intestinal obstruction. During surgery, the foramen can not be enlarged due to the risk of rupture of the vena cava or aorta, which would result in fatal hemorrhage. Survival is 74–79%, and survival is consistently correlated with abdominocentesis findings prior to surgery.

Intestinal pseudo-obstruction is a clinical syndrome caused by severe impairment in the ability of the intestines to push food through. It is characterized by the signs and symptoms of intestinal obstruction without any lesion in the intestinal lumen. Clinical features can include abdominal pain, nausea, severe distension, vomiting, dysphagia, diarrhea and constipation, depending upon the part of the gastrointestinal tract involved. The condition can begin at any age and it can be a primary condition (idiopathic or inherited) or caused by another disease (secondary).

It can be chronic or acute.

Uterine tears often occur a few days post parturition. They can lead to peritonitis and require surgical intervention to fix. Uterine torsions can occur in the third trimester, and while some cases may be corrected if the horse in anesthetized and rolled, others require surgical correction.

Fecal vomiting, also called feculent vomiting and stercoraceous vomiting is a kind of vomiting wherein the material vomited is of fecal origin. It is a common symptom of gastrojejunocolic fistula and intestinal obstruction in the ileum. Fecal vomiting is often accompanied by an odor of feces on the breath and other gastrointestinal symptoms, including abdominal pain, abdominal distension, dehydration, and diarrhea. In severe cases of bowel obstruction or constipation (such as those related to Clozapine-treatment) fecal vomiting has been identified as a cause of death.

Fecal vomiting occurs when the bowel is obstructed for some reason, and intestinal contents cannot move normally. Peristaltic waves occur in an attempt to decompress the intestine, and the strong contractions of the intestinal muscles push the contents backwards through the pyloric sphincter into the stomach, where they are then vomited.

Fecal vomiting can also occur in cats.

Fecal vomiting does not include vomiting of the proximal small intestine contents, which commonly occurs during vomiting.

The blockage of cerebrospinal fluid (CSF) flow may also cause a syrinx to form, eventually leading to syringomyelia. Central cord symptoms such as hand weakness, dissociated sensory loss, and, in severe cases, paralysis may occur.

Intestinal Connective tissue abnormality may cause Intestinal Desmosis The absence of the tendinous plexus layer was first described in 1998 by Meier-Ruge. Desmosis is implicated in disturbed gut motility.

Normal peristalsis depends upon the interaction between muscles, nerve cells and tendinous connective tissue. A malfunction of any of these leads to intestinal motility disorders.

Desmosis may be congenital (aplastic form) or acquired (atrophic form).

The "aplastic" form is rare. Typical clinical findings are hypoperistalsis, and pseudo-obstruction. These are found in premature infants, associated with low birth weight. The "atrophic" form is more frequent. Inflammation of the muscularis propria releases enzymes including collagenases which destroy the connective tissue of the bowel wall. Primarily newborns and small children are affected, although this manifestation can also be found in adults. The most common location is the colon with a necrotizing enterocolitis as well as Crohn Disease and diverticulitis. If the taenia are also affected, the disease is defined as complete atrophic desmosis, all other forms without involvement of the taenia are referred to as incomplete. Clinically, patients demonstrate chronic constipation.

As proposed by Giuseppe Martucciello, microscopic diagnosis requires laparoscopic intestinal full-thickness biopsies from colon. Histological findings are absence of the tendinous plexus layer and connective tissue fibers in longitudinal and circular muscle layer.

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.