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).

GAVE is characterized by dilated capillaries in the lamina propria with fibrin thrombi. The main histomorphologic differential diagnosis is portal hypertension, which is often apparent from clinical findings.

Research in 2010 has shown that anti-RNA polymerase III antibodies may be used as a risk marker for GAVE in systemic sclerosis patients.

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.

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.

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.

Pancreatic diseases that affect digestion refers to disorders affecting the exocrine pancreas, which is a part of the pancreas involved in digestion.

One of the most common conditions of the exocrine pancreas is acute pancreatitis, which in the majority of cases relates to gallstones that have impacted in the pancreatic part of the biliary tree, or due to acute or chronic alcohol abuse or as a side-effect of ERCP. Other forms of pancreatitis include chronic and hereditary forms. Chronic pancreatitis may predispose to pancreatic cancer and is strongly linked to alcohol use. Other rarer diseases affecting the pancreas may include pancreatic pseudocysts, exocrine pancreatic insufficiency, and pancreatic fistulas.

Pancreatic disease may present with or without symptoms. When symptoms occur, such as in acute pancreatitis, a person may suffer from acute-onset, severe mid-abdominal pain, nausea and vomiting. In severe cases, pancreatitis may lead to rapid blood loss and systemic inflammatory response syndrome. When the pancreas is unable to secrete digestive enzymes, such as with a pancreatic cancer occluding the pancreatic duct, result in jaundice. Pancreatic disease might be investigated using abdominal x-rays, MRCP or ERCP, CT scans, and through blood tests such as measurement of the amylase and lipase enzymes.

The small intestine consists of the duodenum, jejunum and ileum. Inflammation of the small intestine is called enteritis, which if localised to just part is called duodenitis, jejunitis and ileitis, respectively. Peptic ulcers are also common in the duodenum.

Chronic diseases of malabsorption may affect the small intestine, including the autoimmune coeliac disease, infective Tropical sprue, and congenital or surgical short bowel syndrome. Other rarer diseases affecting the small intestine include Curling's ulcer, blind loop syndrome, Milroy disease and Whipple's disease. Tumours of the small intestine include gastrointestinal stromal tumours, lipomas, hamartomas and carcinoid syndromes.

Diseases of the small intestine may present with symptoms such as diarrhoea, malnutrition, fatigue and weight loss. Investigations pursued may include blood tests to monitor nutrition, such as iron levels, folate and calcium, endoscopy and biopsy of the duodenum, and barium swallow. Treatments may include renutrition, and antibiotics for infections.

A Cushing ulcer, named after Harvey Cushing, is a gastric ulcer associated with elevated intracranial pressure. It is also called von Rokitansky-Cushing syndrome. Apart from in the stomach, ulcers may also develop in the proximal duodenum and distal esophagus.

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.

Zollinger–Ellison syndrome (ZES) is a disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers. Symptoms include abdominal pain and diarrhea.

The syndrome is caused by a gastrinoma, a neuroendocrine tumor that secretes a hormone called gastrin. The tumor causes excessive production of gastric acid, which leads to the growth of gastric mucosa and proliferation of parietal and ECL cells.

ZES may occur on its own or as part of an autosomal dominant syndrome called multiple endocrine neoplasia type 1 (MEN 1). The primary tumor is usually located in the pancreas, duodenum or abdominal lymph nodes, but ectopic locations (e.g., heart, ovary, gallbladder, liver, and kidney) have also been described.

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.

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.

Patients with Zollinger–Ellison syndrome may experience abdominal pain and diarrhea. The diagnosis is also suspected in patients who have severe ulceration of the stomach and small bowel, especially if they fail to respond to treatment.

- Chronic diarrhea, including steatorrhea (fatty stools)

- Pain in the esophagus, especially between and after meals at night

- Nausea

- Wheezing

- Vomiting blood

- Malnourishment

- Loss of appetite

Gastrinomas may occur as single tumors or as multiple small tumors. About one-half to two-thirds of single gastrinomas are malignant tumors that most commonly spread to the liver and to lymph nodes near the pancreas and small bowel.

Nearly 25 percent of patients with gastrinomas have multiple tumors as part of a condition called multiple endocrine neoplasia type 1 (MEN 1). MEN I patients have tumors in their pituitary gland and parathyroid glands, in addition to tumors of the pancreas.

The diagnosis is suspected based on polyhydramnios in uteru, bilious vomiting, failure to pass meconium in the first day of life, and abdominal distension. The presentations of NBO may vary. It may be subtle and easily overlooked on physical examination or can involve massive abdominal distension, respiratory distress and cardiovascular collapse. Unlike older children, neonates with unrecognized intestinal obstruction deteriorate rapidly.

Curling's ulcer (stress ulcer) or a Curling ulcer is an acute gastric erosion resulting as a complication from severe burns when reduced plasma volume leads to ischemia and cell necrosis (sloughing) of the gastric mucosa. The condition was first described in 1823 and named for a doctor, Thomas Blizard Curling, who observed ten such patients in 1842.

These stress ulcers (actually shallow multiple erosions) were once a common complication of serious burns, presenting in over 10% of cases, and especially common in child burn victims. They result in perforation and hemorrhage more often than other forms of intestinal ulceration and had correspondingly high mortality rates (at least 80%).

A similar condition involving elevated intracranial pressure is known as Cushing's ulcer.

The majority of people with a Meckel's diverticulum are asymptomatic. An asymptomatic Meckel's diverticulum is called a "silent" Meckel's diverticulum. If symptoms do occur, they typically appear before the age of two years.

The most common presenting symptom is painless rectal bleeding such as melaena-like black offensive stools, followed by intestinal obstruction, volvulus and intussusception. Occasionally, Meckel's diverticulitis may present with all the features of acute appendicitis. Also, severe pain in the epigastric region is experienced by the patient along with bloating in the epigastric and umbilical regions. At times, the symptoms are so painful that they may cause sleepless nights with acute pain felt in the foregut region, specifically in the epigastric and umbilical regions.

In some cases, bleeding occurs without warning and may stop spontaneously. The symptoms can be extremely painful, often mistaken as just stomach pain resulting from not eating or constipation.

Rarely, a Meckel's diverticulum containing ectopic pancreatic tissue can present with abdominal pain and increased serum amylase levels, mimicking acute pancreatitis.

The causes are divided into benign or malignant.

- Benign

- Peptic ulcer disease

- Infections, such as tuberculosis; and infiltrative diseases, such as amyloidosis.

- A rare cause of gastric outlet obstruction is blockage with a gallstone, also termed "Bouveret's syndrome".

- In children congenital pyloric stenosis / congenital hypertrophic pyloric stenosis may be a cause.

- A pancreatic pseudocyst can cause gastric compression.

- Pyloric mucosal diaphragm could be a rare cause.

- Malignant

- Tumours of the stomach, including adenocarcinoma (and its linitis plastica variant), lymphoma, and gastrointestinal stromal tumours

Signs and symptoms of a peptic ulcer can include one or more of the following:

- abdominal pain, classically epigastric strongly correlated to mealtimes. In case of duodenal ulcers the pain appears about three hours after taking a meal;

- bloating and abdominal fullness;

- waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus - although this is more associated with gastroesophageal reflux disease);

- nausea and copious vomiting;

- loss of appetite and weight loss;

- hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.

- melena (tarry, foul-smelling feces due to presence of oxidized iron from hemoglobin);

- rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis, extreme, stabbing pain, and requires immediate surgery.

A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include NSAIDs (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase, and most glucocorticoids (e.g. dexamethasone and prednisolone).

In people over the age of 45 with more than two weeks of the above symptoms, the odds for peptic ulceration are high enough to warrant rapid investigation by esophagogastroduodenoscopy.

The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, as gastric acid production is increased as food enters the stomach. Symptoms of duodenal ulcers would initially be relieved by a meal, as the pyloric sphincter closes to concentrate the stomach contents, therefore acid is not reaching the duodenum. Duodenal ulcer pain would manifest mostly 2–3 hours after the meal, when the stomach begins to release digested food and acid into the duodenum.

Also, the symptoms of peptic ulcers may vary with the location of the ulcer and the person's age. Furthermore, typical ulcers tend to heal and recur and as a result the pain may occur for few days and weeks and then wane or disappear. Usually, children and the elderly do not develop any symptoms unless complications have arisen.

Burning or gnawing feeling in the stomach area lasting between 30 minutes and 3 hours commonly accompanies ulcers. This pain can be misinterpreted as hunger, indigestion or heartburn. Pain is usually caused by the ulcer but it may be aggravated by the stomach acid when it comes into contact with the ulcerated area. The pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it may last from few minutes to several hours and it may be worse when the stomach is empty. Also, sometimes the pain may flare at night and it can commonly be temporarily relieved by eating foods that buffer stomach acid or by taking anti-acid medication. However, peptic ulcer disease symptoms may be different for every sufferer.

While emergency surgery was once the only treatment, combination therapies including enteral feeding with powerful antacids such as H-receptor antagonists or, more recently, proton pump inhibitors such as omeprazole have made Curling's ulcer a rare complication.

The first symptoms typically include fever, intermittent abdominal pain, and hepatomegaly. Occasionally, jaundice occurs.

Morbidity is common and is caused by complications of cholangitis, sepsis, choledocholithiasis, and cholangiocarcinoma. These morbid conditions often prompt the diagnosis. Portal hypertension may be present, resulting in other conditions including splenomegaly, hematemesis, and melena. These problems can severely affect the patient's quality of life. In a 10-year period between 1995 and 2005, only 10 patients were surgically treated for Caroli disease, with an average patient age of 45.8 years.

After reviewing 46 cases of Caroli disease before 1990, 21.7% of the cases were the result of an intraheptic cyst or nonobstructive biliary tree dilation, 34.7% were linked with congenital hepatic fibrosis, 13% were isolated choledochal cystic dilation, and the remaining 24.6% had a combination of all three.

The mechanism of development of Cushing ulcers is thought to be due to direct stimulation of vagal nuclei as a result of increased intracranial pressure. Alternatively, it may also be a direct result of Cushing reaction. Efferent fibers of the vagus nerve then release acetylcholine onto gastric parietal cell M receptors, causing insertion of hydrogen potassium ATPase vesicles into the apical plasma membrane. The end result is increased secretion of gastric acid with eventual ulceration of the gastric mucosa.

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

With early intervention, morbidity and mortality of cases of intestinal obstruction is low. The outcome is in part dependent upon congenital comorbidities and delays in diagnosis and management.

Signs and symptoms include early satiety, nausea, vomiting, extreme "stabbing" postprandial abdominal pain (due to both the duodenal compression and the compensatory reversed peristalsis), abdominal distention/distortion, burping (eructation), external hypersensitivity or tenderness of the abdominal area, reflux, and heartburn. In infants, feeding difficulties and poor weight gain are also frequent symptoms.

In some cases of SMA syndrome, severe malnutrition accompanying spontaneous wasting may occur. This, in turn, increases the duodenal compression, which worsens the underlying cause, creating a cycle of worsening symptoms.

"Food fear" is a common development among patients with the chronic form of SMA syndrome. For many, symptoms are partially relieved when in the left lateral decubitus or knee-to-chest position, or in the prone (face down) position. A Hayes maneuver (pressure applied below the umbilicus in cephalad and dorsal direction) elevates the root of the SMA, also slightly easing the constriction. Symptoms can be aggravated when leaning to the right or taking a supine (face up) position.