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.

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.

Esophageal varices (sometimes spelled oesophageal varices) are extremely dilated sub-mucosal veins in the lower third of the esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding. Esophageal varices are typically diagnosed through an esophagogastroduodenoscopy.

Most patients with portal hypertensive gastropathy have either a stable or improving course in the appearance of the gastropathy on endoscopy. However, according to retrospective data, roughly one in seven patients with portal hypertensive gastropathy will develop bleeding (either acute or chronic) attributable to the gastropathy. Patients with chronic bleeding will usually come to the attention of the medical system because of anemia.

The diagnosis of portal hypertensive gastropathy is usually made on endoscopy. The usual appearance of portal hypertensive gastropathy on endoscopy is a mosaic-like or reticular pattern in the mucosa. Red spots may or may not be present. The pattern is usually seen throughout the stomach. A similar pattern can be seen with a related condition called gastric antral vascular ectasia (GAVE), or watermelon stomach. However, in GAVE, the ectatic blood vessels are more commonly found in the antrum or lower part of the stomach.

Intestinal varices are dilated submucosal veins in the intestine.

One treatment includes a transjugular intrahepatic portosystemic shunt.

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.

The main symptom is vomiting, which typically occurs after meals of undigested food, devoid of any bile. A history of previous peptic ulcers and loss of weight is not uncommon. In advanced cases, signs to look for on physical examination are wasting and dehydration. Visible peristalsis from left to right may be present. Succussion splash is a splash-like sound heard over the stomach in the left upper quadrant of the abdomen on shaking the patient, with or without the stethoscope. Bowel sound may be increased due to excessive peristaltic action of stomach. Fullness in left hypochondrium may also be present.

Portal hypertensive gastropathy refers to changes in the mucosa of the stomach in patients with portal hypertension; by far the most common cause of this is cirrhosis of the liver. These changes in the mucosa include friability of the mucosa and the presence of ectatic blood vessels at the surface. Patients with portal hypertensive gastropathy may experience bleeding from the stomach, which may uncommonly manifest itself in vomiting blood or melena; however, portal hypertension may cause several other more common sources of upper gastrointestinal bleeding, such as esophageal varices and gastric varices. On endoscopic evaluation of the stomach, this condition shows a characteristic mosaic or "snake-skin" appearance to the mucosa of the stomach.

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").

The terms rectal varices and haemorrhoids are often used interchangeably, but this is not correct. Haemorrhoids occur due to prolapse of the rectal venous plexus and are no more common in patients with portal hypertension than those without. Rectal varices, however, are only found in patients with portal hypertension and are common in conditions such as cirrhosis.

Hemosuccus pancreaticus is a rare entity, and estimates of its rate are based on small case series. It is the least frequent cause of upper gastrointestinal bleeding (1/1500) and is most often caused by chronic pancreatitis, pancreatic pseudocysts, or pancreatic tumors. As a result, the diagnosis may easily be overlooked. The usual presentation of hemosuccus is the development of symptoms of upper or lower gastrointestinal bleeding, such as melena (or dark, black tarry stools), maroon stools, or hematochezia, which is frank rectal bleeding. The source of hemorrhage is usually not determined by standard endoscopic techniques, and the symptoms of the condition are usually grouped as a cause of obscure overt gastrointestinal hemorrhage. Over one-half of patients with hemosuccus also develop abdominal pain, usually located in the epigastrium, or uppermost part of the abdomen. The pain is described as being "crescendo-decrescendo" in nature, meaning that it increases and decreases in intensity slowly with time. This is thought to be due to transient blockage of the pancreatic duct from the source of bleeding, or from clots. If the source of the bleeding also involves obstruction of the common bile duct (such as with some tumours of the head of the pancreas), the patient may develop jaundice, or "silver stools", an uncommon finding of acholic stools mixed with blood.

Bleeding of the lower GI tract will typically appear as hematochezia and can vary in degree of seriousness. Slow bleeding from the ascending portion of the colon can result in partial digestion of the blood and the appearance of melena in the stool.

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.

The upper GI tract is defined as the organs involved in digestion above the ligament of Treitz and comprises the esophagus, stomach, and duodenum. Upper gastrointestinal bleeding is typically characterized by melena (black stool). Bright red blood may be seen with active, rapid bleeding.

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

Gastric outlet obstruction (GOO) is a medical condition where there is an obstruction at the level of the pylorus, which is the outlet of the stomach. Individuals with gastric outlet obstruction will often have recurrent vomiting of food that has accumulated in the stomach, but which cannot pass into the small intestine due to the obstruction. The stomach often dilates to accommodate food intake and secretions. Causes of gastric outlet obstruction include both benign causes (such as peptic ulcer disease affecting the area around the pylorus), as well as malignant causes, such as gastric cancer.

Causation related to ulcers may involve severe pain which the patient may interpret as a heart condition/attack.

Treatment of the condition depends upon the underlying cause; it can involve antibiotic treatment when Helicobacter pylori is related to an ulcer, endoscopic therapies (such as dilation of the obstruction with balloons or the placement of self expandable metallic stents), other medical therapies, or surgery to resolve the obstruction.

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.

Signs and symptoms may include a sudden pain in the epigastrium to the right of the midline indicating the perforation of a duodenal ulcer. In a gastric ulcer perforation creates a history of burning pain in epigastrium, with flatulence and dyspepsia.

In intestinal perforation, pain starts from the site of perforation and spreads across the abdomen.

Gastrointestinal perforation results in severe abdominal pain intensified by movement, nausea, vomiting and hematemesis. Later symptoms include fever and or chills. In any case, the abdomen becomes rigid with tenderness and rebound tenderness. After some time the abdomen becomes silent and heart sounds can be heard all over. Patient stops passing flatus and motion, abdomen is distended.

The symptoms of esophageal rupture may include sudden onset of chest pain.

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.

Underlying causes include gastric ulcers, duodenal ulcers, appendicitis, gastrointestinal cancer, diverticulitis, inflammatory bowel disease, superior mesenteric artery syndrome, trauma and ascariasis. Typhoid fever, non-steroidal anti-inflammatory drugs, ingestion of corrosives may also be responsible.

Most damage to the pyloric valve occurs as a complication of gastric surgery. Other causes of biliary reflux may be:

- Peptic ulcer

- Gallbladder surgery (cholecystectomy)

A significant fraction of cases are idiopathic, with no identified specific etiology.

Fecal occult blood (FOB) refers to blood in the feces that is not visibly apparent (unlike other types of blood in stool such as melena or hematochezia). A fecal occult blood test (FOBT) checks for hidden (occult) blood in the stool (feces).

Other tests look for globin, DNA, or other blood factors including transferrin, while conventional stool guaiac tests look for heme.

Gastrointestinal (GI) complaints and low intensity GI bleeding frequently occur in marathon runners. Strenuous exercise, particularly in elite athlete runners and less frequently in other exercise activities, can cause acute incapacitating gastrointestinal symptoms including heartburn, nausea, vomiting, abdominal pain, diarrhea and gastrointestinal bleeding. Approximately one third of endurance runners experience transient but exercise limiting symptoms, and repetitive gastrointestinal bleeding occasionally causes iron deficiency and anaemia. Runners can sometimes experience significant symptoms including hematemesis. Exercise is associated with extensive changes in gastrointestinal (GI) tract physiology, including diversion of blood flow from the GI tract to muscle and lungs, decreased GI absorption and small intestinal motility, increased colonic transit, neuroimmunoendocrine changes in hormones and peptides such as vasoactive intestinal peptide, secretin and peptide-histidine-methionine. Substantial changes occur in stress hormones including cortisol, in circulating concentrations and metabolic behavior of various leucocytes, and in immunoglobulin levels and major histocompatibility complex expression. Symptoms can be exacerbated by dehydration or by pre-exercise ingestion of certain foods and hypertonic liquids, and lessened by adequate training.

Ingestion of 800 mg of cimetidine 2 hr before running a marathon did not significantly affect the frequency of gastrointestinal symptoms or occult gastrointestinal bleeding. Conversely, 800 mg of cimetidine 1 hr before the start and again at 50 miles of a 100-mile running race substantially decreased GI symptoms and postrace guaiac test positivity but did not affect race performance.

Biliary reflux, bile reflux or duodenogastric reflux is a condition that occurs when bile flows upward (refluxes) from the duodenum into the stomach and esophagus.

Biliary reflux can be confused with acid reflux, also known as gastroesophageal reflux disease (GERD). While bile reflux involves fluid from the small intestine flowing into the stomach and esophagus, acid reflux is backflow of stomach acid into the esophagus. These conditions are often related, and differentiating between the two can be difficult.

Bile is a digestive fluid made by the liver, stored in the gallbladder, and discharged into duodenum after food is ingested to aid in the digestion of fat. Normally, the pyloric sphincter prevents bile from entering the stomach. When the pyloric sphincter is damaged or fails to work correctly, bile can enter the stomach and then be transported into the esophagus as in gastric reflux. The presence of small amounts of bile in the stomach is relatively common and usually asymptomatic, but excessive refluxed bile causes irritation and inflammation.

Dieulafoy's lesions are characterized by a single large tortuous small artery in the submucosa which does not undergo normal branching or a branch with caliber of 1–5 mm (more than 10 times the normal diameter of mucosal capillaries). The lesion bleeds into the gastrointestinal tract through a minute defect in the mucosa which is not a primary ulcer of the mucosa but an erosion likely caused in the submucosal surface by protrusion of the pulsatile arteriole.

Approximately 75% of Dieulafoy's lesions occur in the upper part of the stomach within 6 cm of the gastroesophageal junction, most commonly in the lesser curvature. Extragastric lesions have historically been thought to be uncommon but have been identified more frequently in recent years, likely due to increased awareness of the condition. The duodenum is the most common location (14%) followed by the colon (5%), surgical anastamoses (5%), the jejunum (1%) and the esophagus (1%). The pathology in these extragastric locations is essentially the same as that of the more common gastric lesion.

In contrast to peptic ulcer disease, a history of alcohol abuse or NSAID use is usually absent in DL.

Dieulafoy's lesions occur twice as often in men as women and patients typically have multiple comorbidities, including hypertension, cardiovascular disease, chronic kidney disease, and diabetes.