Gastric varices are dilated submucosal veins in the stomach, which can be a life-threatening cause of bleeding in the upper gastrointestinal tract. They are most commonly found in patients with portal hypertension, or elevated pressure in the portal vein system, which may be a complication of cirrhosis. Gastric varices may also be found in patients with thrombosis of the splenic vein, into which the short gastric veins which drain the fundus of the stomach flow. The latter may be a complication of acute pancreatitis, pancreatic cancer, or other abdominal tumours, as well as hepatitis C. Gastric varices and associated bleeding are a potential complication of schistosomiasis resulting from portal hypertension.

Patients with bleeding gastric varices can present with bloody vomiting (hematemesis), dark, tarry stools (melena), or rectal bleeding. The bleeding may be brisk, and patients may soon develop shock. Treatment of gastric varices can include injection of the varices with cyanoacrylate glue, or a radiological procedure to decrease the pressure in the portal vein, termed transjugular intrahepatic portosystemic shunt or TIPS. Treatment with intravenous octreotide is also useful to shunt blood flow away from the stomach's circulation. More aggressive treatment including splenectomy (or surgical removal of the spleen) or liver transplantation may be required in some cases.

Dilated submucosal veins are the most prominent histologic feature of esophageal varices. The expansion of the submucosa leads to elevation of the mucosa above the surrounding tissue, which is apparent during endoscopy and is a key diagnostic feature. Evidence of recent variceal hemorrhage includes necrosis and ulceration of the mucosa. Evidence of past variceal hemorrhage includes inflammation and venous thrombosis.

Gastric varices can present in two major ways. First, patients with cirrhosis may be enrolled in screening gastroscopy programs to detect esophageal varices. These evaluations may detect gastric varices that are asymptomatic. When gastric varices are symptomatic, however, they usually present acutely and dramatically with upper gastrointestinal bleeding. The symptoms can include vomiting blood, melena (passing black, tarry stools); or passing maroon stools or frank blood in the stools. Many people with bleeding gastric varices present in shock due to the profound loss of blood.

Secondly, patients with acute pancreatitis may present with gastric varices as a complication of a blood clot in the splenic vein. The splenic vein sits over the pancreas anatomically and inflammation or cancers of the pancreas may result in a blot clot forming in the splenic vein. As the short gastric veins of the fundus of the stomach drain into the splenic vein, thrombosis of the splenic vein will result in increased pressure and engorgement of the short veins, leading to varices in the fundus of the stomach.

Laboratory testing usually shows low red blood cell count and often a low platelet count. If cirrhosis is present, there may be coagulopathy manifested by a prolonged INR; both of these may worsen the bleeding from gastric varices.

In very rare cases, gastric varices are caused by splenic vein occlusion as a result of the mass effect of slow-growing pancreatic neuroendocrine tumors.

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

In ideal circumstances, patients with known varices should receive treatment to reduce their risk of bleeding. The non-selective β-blockers (e.g., propranolol, timolol or nadolol) and nitrates (e.g., isosorbide mononitrate (IMN) have been evaluated for secondary prophylaxis. Non-selective β-blockers (but not cardioselective β-blockers like atenolol) are preferred because they decrease both cardiac output by β blockade and splanchnic blood flow by blocking vasodilating β receptors at splanchnic vasculature. The effectiveness of this treatment has been shown by a number of different studies.

However, non-selective β-blockers do not prevent the "formation" of esophageal varices.

When medical contraindications to beta-blockers exist, such as significant reactive airway disease, then treatment with prophylactic endoscopic variceal ligation is often performed.

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.

Intestinal varices are dilated submucosal veins in the intestine.

One treatment includes a transjugular intrahepatic portosystemic shunt.

Congestion of the mucosa in other parts of the gastrointestinal tract can also be seen in portal hypertension. When the condition involves the colon, it is termed "portal hypertensive colopathy".

Anorectal varices are the dilation of collateral submucosal vessels due to backflow in the veins of the rectum. Typically this occurs due to portal hypertension which shunts venous blood from the portal system through the portosystemic anastomosis present at this site into the systemic venous system. This can also occur in the oesophagus, causing oesophageal varices, and at the level of the umbilicus, causing caput medusae. Between 44% and 78% of patients with portal hypertension get anorectal varices.

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.

Unlike oesophageal varices, rectal varices are less prone to bleeding, are less serious when a bleed does occur, and are easier to treat because of the more accessible location.

Typically, treatment consists of addressing the underlying portal hypertension. Some treatments include portosystemic shunting, ligation, and under-running suturing. Insertion of a transjugular intrahepatic portosystemic shunt (TIPS) has been shown to alleviate varices caused by portal hypertension. Successful treatment of portal hypertension that subsequently reduces anorectal varices provides a confirmation of the initial diagnosis, allowing for a distinction between varices and hemorrhoids, which would not have been alleviated by reduction of portal hypertension.

Ileus is a cause of colic in horses due to functional obstruction of the intestines. It most commonly seen in horses postoperatively, especially following colic surgery. Horses experiencing ileus are at risk for gastric rupture due to rapid reflux build-up, and require intense medical management with frequent nasogastric intubation. Ileus may increase adhesion formation, because intestinal segments have more prolonged contact and intestinal distention causes serosal injury and ischemia. It is usually treated with aggressive fluid support, prokinetics, and anti-inflammatories.

Portal hypertensive gastropathy can also be treated with endoscopic treatment delivered through a fibre-optic camera into the stomach. Argon plasma coagulation and electrocautery have both been used to stop bleeding from ectatic vessels, and to attempt to obliterate the vessels, but have limited utility if the disease is diffuse.

Transjugular intrahepatic portosystemic shunt procedures, or TIPS involve decompressing the portal vein by shunting a portal venule to a lower pressure systemic venule, under guidance with fluoroscopy. Since it treats the root cause of portal hypertension gastropathy, it has been putatively used for the condition. The literature reports suggest both regression of portal hypertensive gastropathy on endoscopic images and improvement in bleeding after TIPS.

Finally, cryotherapy involves the use of pressurized carbon dioxide administered through the endoscope to freeze and destroy tissue in a focal area. It is being studied for the treatment of portal hypertensive gastropathy.

A varix (pl. varices) is an abnormally dilated vessel with a tortuous course. Varices usually occur in the venous system, but may also occur in arterial or lymphatic vessels.

Examples of varices include:

- Varicose veins, large tortuous veins usually found on legs

- Sublingual varices

- Esophageal varices, commonly stemming from cirrhosis of the liver, also known as oesophageal varicose

- Gastric varices, commonly stemming from cirrhosis of the liver

- Intestinal varices

- Scrotal varices

- Vulvar varices

- Pelvic varices

- Vesical varices, varicose veins associated with the urinary bladder

- Rectal varices, which can be similar to external haemorrhoids

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.

Esophageal diseases can derive from congenital conditions, or they can be acquired later in life.

Many people experience a burning sensation in their chest occasionally, caused by stomach acids refluxing into the esophagus, normally called heartburn. Extended exposure to heartburn may erode the lining of the esophagus, leading potentially to Barrett's esophagus which is associated with an increased risk of adenocarcinoma most commonly found in the distal one-third of the esophagus.

Some people also experience a sensation known as globus esophagus, where it feels as if a ball is lodged in the lower part of the esophagus.

The following are additional diseases and conditions that affect the esophagus:

- Achalasia

- Acute esophageal necrosis

- Barrett's esophagus

- Boerhaave syndrome

- Caustic injury to the esophagus

- Chagas disease

- Diffuse esophageal spasm

- Esophageal atresia and Tracheoesophageal fistula

- Esophageal cancer

- Esophageal dysphagia

- Esophageal varices

- Esophageal web

- Esophagitis

- GERD

- Hiatus hernia

- Jackhammer esophagus (hypercontractile peristalsis)

- Killian–Jamieson diverticulum

- Mallory-Weiss syndrome

- Neurogenic dysphagia

- Nutcracker esophagus

- Schatzki's ring

- Zenker's Diverticulum

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").

Paralysis of the intestine is often termed paralytic ileus, in which the intestinal paralysis need not be complete, but it must be sufficient to prohibit the passage of food through the intestine and lead to intestinal blockage. Paralytic ileus is a common side effect of some types of surgery, commonly called postsurgical ileus. It can also result from certain drugs and from various injuries and illnesses, such as acute pancreatitis. Paralytic ileus causes constipation and bloating. On listening to the abdomen with a stethoscope, no bowel sounds are heard because the bowel is inactive.

A temporary paralysis of a portion of the intestines occurs typically after abdominal surgery. Since the intestinal content of this portion is unable to move forward, food or drink should be avoided until peristaltic sound is heard, by auscultation (use of a stethoscope) of the area where this portion lies. Intestinal atony or paralysis may be caused by inhibitory neural reflexes, inflammation or other implication of neurohumoral peptides.

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.

Specific causes of colic are best managed with certain drugs. These include:

- Spasmolytic agents, most commonly Buscopan, especially in the case of gas colic.

- Pro-motility agents: metoclopramide, lidocaine, bethanechol, and erythromycin are used in cases of ileus.

- Anti-inflammatories are often used in the case of enteritis or colitis.

- Anti-microbials may be administered if an infectious agent is suspected to be the underlying cause of colic.

- Phenylephrine: used in cases of nephrosplenic entrapment to contract the spleen, and is followed by light exercise to try to shift the displaced colon back into its normal position.

- Psyllium may be given via nasogastric tube to treat sand colic.

- Anthelminthics for parasitic causes of colic.

Horses are withheld feed when colic signs are referable to gastrointestinal disease. In long-standing cases, parenteral nutrition may be instituted. Once clinical signs improve, the horse will slowly be re-fed (introduced back to its normal diet), while being carefully monitored for pain.

An increasing number of people are now surviving cancer, with improved treatments producing cure of the malignancy (cancer survivors). There are now over 14 million such people in the US, and this figure is expected to increase to 18 million by 2022. More than half are survivors of abdominal or pelvic cancers, with about 300,000 people receiving abdominal and pelvic radiation each year. It has been estimated there are 1.6 million people in the US with post-radiation intestinal dysfunction, a greater number than those with inflammatory bowel disease such as Crohn's disease or ulcerative colitis.

Proximal enteritis usually is managed medically. This includes nasogastric intubation every 1–2 hours to relieve gastric pressure secondary to reflux, which often produces to 2–10 L, as well as aggressive fluid support to maintain hydration and correct electrolyte imbalances. Maintaining hydration in these patients can be very challenging. In some cases, fluid support may actually increase reflux production, due to the decreased intravascular oncotic pressure from low total protein and albumin levels, leading to loss of much of these IV fluids into the intestinal lumen. These horses will often display dependent edema (edema that collects in locations based on gravity). Colloids such as plasma or Hetastarch may be needed to improve intravascular oncotic pressure, although they can be cost prohibitive for many owners. Reflux levels are monitored closely to help evaluate fluid losses, and horses recovering from DPJ show improved hydration with decreased reflux production and improved attitude.

Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used for pain relief, reduction of inflammation, and for their anti-endotoxin effects, but care must be taken since they may produce gastrointestinal ulceration and damage the kidneys. Due to a suspected link to "Clostridial" infection, anti-microbials are often administered, usually penicillin or metronidazole. Aminoglycosides should be used with extreme caution due to the risk of nephrotoxicosis (damage to the kidney). The mucosa of the intestines is damaged with DPJ, often resulting in absorption of endotoxin and risking laminitis, so therapy to combat and treat endotoxemia is often employed. This includes treatment with drugs that counteract endotoxin such as Polymyxin B and Bio-Sponge, fluid support, and laminitis prevention such as icing of the feet. Prokinetic drugs such as lidocaine, erythromycin, metoclopramide, and bethanechol are often used to treat the ileus associated with the disease.

Horses are withheld food until reflux returns to less than 1–2 L of production every 4 hours, and gut sounds return, often requiring 3–7 days of therapy. Parenteral nutrition is often provided to horses that are withheld feed for greater than 3–4 days. It is suspected to improve healing and shorten the duration of the illness, since horses often become cachexic due to the protein losing enteropathy associated with this disease.

Surgery may need to be performed to rule out colic with similar presenting signs such as obstruction or strangulation, and in cases that are long-standing (> 7 days) to perform a resection and anastomosis of the diseased bowel. However, some horses have recovered with long-term medical support (up to 20 days).

In primary chronic intestinal pseudo-obstruction (the majority of chronic cases), the condition may be caused by an injury to the smooth muscle (myopathic) or the nervous system (neuropathic) of the gastrointestinal tract.

In some cases there appears to be a genetic association. One form has been associated with DXYS154.

Secondary chronic intestinal pseudo-obstruction can occur as a consequence of a number of other conditions, including Kawasaki disease, Parkinson's disease, Chagas' disease, Hirschsprung's disease, intestinal hypoganglionosis, collagen vascular diseases, mitochondrial disease, endocrine disorders and use of certain medications. The term may be used synonymously with enteric neuropathy if a neurological cause is suspected.