Gastrinoma causes the following symptoms:

- Hypergastrinemia

- Ulcers of the duodenum, stomach, and small intestine.

- Severe diarrhea.

- Generalized cancer symptoms.

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.

Individuals with the disease present with upper abdominal pain (epigastric), at times accompanied by nausea, vomiting, loss of appetite, edema, and weight loss. A small amount of gastrointestinal bleeding may occur, which is typically due to superficial mucosal erosions; large volume bleeding is rare. 20% to 100% of patients, depending on time of presentation, develop a protein-losing gastropathy accompanied by low blood albumin and edema.

Symptoms and pathological features of Ménétrier disease in children are similar to those in adults, but disease in children is usually self-limited and often follows respiratory infection.

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.

A gastrinoma is a tumor in the pancreas or duodenum that secretes excess of gastrin leading to ulceration in the duodenum, stomach and the small intestine. There is hypersecretion of HCl acid into the duodenum, which causes the ulcers. Excessive HCl acid production also causes hyperperistalsis, and inhibits the activity of lipase, causing severe diarrhea.

It is frequently the source of the gastrin in Zollinger-Ellison syndrome.

It is usually found in the duodenum, although it may arise in the stomach or pancreas. Those occurring in the pancreas have a greater potential for malignancy. Most gastrinomas are found in the gastrinoma triangle; this is bound by the junction of cystic and common bile ducts, junction of the second and third parts of the duodenum, and the junction of the neck and body of the pancreas.

With Ménétrier disease, the stomach is characterized by large, tortuous gastric folds in the fundus and body of the stomach, with antrum generally spared, giving the mucosa a cobblestone or cerebriform (brain-like) appearance. Histologically, the most characteristic feature is massive foveolar hyperplasia (hyperplasia of surface and glandular mucous cells). The glands are elongated with a corkscrew-like appearance and cystic dilation is common. Inflammation is usually only modest, although some cases show marked intraepithelial lymphocytosis. Diffuse or patchy glandular atrophy, evident as hypoplasia of parietal and chief cells, is typical.

Although ICD-10 classifies it under "Other gastritis" (K29.6), and the lamina propria may contain mild chronic inflammatory infiltrate, Ménétrier disease is not considered a form of gastritis. It is rather considered as one of the two most well understood hypertrophic gastropathies; the other being Zollinger–Ellison syndrome.

Hyperchlorhydria, sometimes called chlorhydria, refers to the state in the stomach where gastric acid levels are higher than the reference range. The combining forms of the name ("" + ""), referring to chlorine and hydrogen, are the same as those in the name of hydrochloric acid, which is the active constituent of gastric acid.

In humans, the normal pH is around 1 to 3, which varies throughout the day. The highest basal secretion levels are in the late evening (around 12 A.M. to 3 A.M.). Hyperchlorhydria is usually defined as having a pH less than 2. It has no negative consequences unless other conditions are also present such as gastroesophageal reflux disease (GERD).

Irrespective of the cause, achlorhydria can result as known complications of bacterial overgrowth and intestinal metaplasia and symptoms are often consistent with those diseases:

- gastroesophageal reflux disease (source needed)

- abdominal discomfort

- early satiety

- weight loss

- diarrhea

- constipation

- abdominal bloating

- anemia

- stomach infection

- malabsorption of food.

- carcinoma of stomach.

Since acidic pH facilitates the absorption of iron, achlorhydric patients often develop iron deficiency anemia.

Acidic environment of stomach helps conversion of pepsinogen into pepsin which is most important to digest the protein into smaller component like complex protein into simple peptides and amino acids inside stomach which is later absorbs by gastro intestinal tract.

Bacterial overgrowth and B12 deficiency (pernicious anemia) can cause micronutrient deficiencies that result in various clinical neurological manifestations, including visual changes, paresthesias, ataxia, limb weakness, gait disturbance, memory defects, hallucinations and personality and mood changes.

Risk of particular infections, such as "Vibrio vulnificus" (commonly from seafood) is increased. Even without bacterial overgrowth, low stomach acid (high pH) can lead to nutritional deficiencies through decreased absorption of basic electrolytes (magnesium, zinc, etc.) and vitamins (including vitamin C, vitamin K, and the B complex of vitamins). Such deficiencies may be involved in the development of a wide range of pathologies, from fairly benign neuromuscular issues to life-threatening diseases.

Achlorhydria or hypochlorhydria refers to states where the production of hydrochloric acid in gastric secretions of the stomach and other digestive organs is absent or low, respectively. It is associated with various other medical problems.

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.

Atrophic gastritis (also known as Type A or Type B Gastritis more specifically) is a process of chronic inflammation of the stomach mucosa, leading to loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. As a result, the stomach's secretion of essential substances such as hydrochloric acid, pepsin, and intrinsic factor is impaired, leading to digestive problems. The most common are vitamin B deficiency which results in a megaloblastic anemia and malabsorbtion of iron, leading to iron deficiency anaemia. It can be caused by persistent infection with "Helicobacter pylori", or can be autoimmune in origin. Those with the autoimmune version of atrophic gastritis are statistically more likely to develop gastric carcinoma, Hashimoto's thyroiditis, and achlorhydria.

Type A gastritis primarily affects the body/fundus of the stomach, and is more common with pernicious anemia.

Type B gastritis primarily affects the antrum, and is more common with "H. pylori" infection.

The symptoms of early and late dumping syndrome are different and vary from person to person. Early dumping syndrome symptoms may include:

- nausea

- vomiting

- abdominal pain and cramping

- diarrhea

- feeling uncomfortably full or bloated after a meal

- sweating

- weakness

- dizziness

- flushing, or blushing of the face or skin

- rapid or irregular heartbeat

The symptoms of late dumping syndrome may include:

- hypoglycemia

- sweating

- weakness

- rapid or irregular heartbeat

- flushing

- dizziness

About 75 percent of people with dumping syndrome report symptoms of early dumping syndrome and about 25 percent report symptoms of late dumping syndrome. Some people have symptoms of both types of dumping syndrome.

In the stomach there is a slight balance between acid and the wall lining which is protected by mucus. When this mucus lining is disrupted for whatever reason, signs and symptoms of acidity result. This may result in upper abdominal pain, indigestion, loss of appetite, nausea, vomiting and heartburn. When the condition is allowed to progress, the pain may become continuous; blood may start to leak and be seen in the stools. If the bleeding is rapid and of adequate volume it may even result in vomiting of bright red blood (hematemesis). When the acidity is uncontrolled, it can even cause severe blood loss (anemia) or lead to perforation (hole) in the stomach which is a surgical emergency. In many individuals, the progressive bleeding from an ulcer mixes with the feces and presents as black stools. Presence of blood in stools is often the first sign that there is a problem in the stomach.

Patients with atrophic gastritis are also at increased risk for the development of gastric adenocarcinoma. The optimal endoscopic surveillance strategy is not known but all nodules and polyps should be removed in these patients.

Dumping syndrome occurs when food, especially sugar, moves too fast from the stomach to the duodenum—the first part of the small intestine—in the upper gastrointestinal (GI) tract. This condition is also called rapid gastric emptying. It is mostly associated with conditions following gastric or esophageal surgery, though it can also arise secondary to diabetes or to the use of certain medications; it is caused by an absent or insufficiently functioning pyloric sphincter, the valve between the stomach and the duodenum.

Dumping syndrome has two forms, based on when symptoms occur. Early dumping syndrome occurs 10 to 30 minutes after a meal. It results from rapid movement of fluid into the intestine following a sudden addition of a large amount of food from the stomach. The small intestine expands rapidly due to the presence of hypertonic/hyperosmolar contents from the stomach, especially sweet foods. This causes symptoms due to the shift of fluid into the intestinal lumen, with plasma volume contraction and acute intestinal distention. Osmotic diarrhea, distension of the small bowel leading to crampy abdominal pain, and reduced blood volume can result.

Late dumping syndrome occurs 2 to 3 hours after a meal. It results from excessive movement of sugar into the intestine, which raises the body's blood glucose level and causes the pancreas to increase its release of the hormone insulin. The increased release of insulin causes a rapid drop in blood glucose levels, a condition known as alimentary hypoglycemia, or low blood sugar.

Disorders of the stomach are very common and induce a significant amount of morbidity and suffering in the population. Data from hospitals indicate that more than 25% of the population suffers from some type of chronic stomach disorder including abdominal pain and indigestion. These symptoms occur for long periods and cause prolonged suffering, time off work and a poor quality of life. Moreover, visits to doctors, expense of investigations and treatment result in many days lost from work and a colossal cost to the financial system.

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.

Depending on the nature of the disease process causing malabsorption and its extent, gastrointestinal symptoms may range from severe to subtle or may even be totally absent. Diarrhea, weight loss, flatulence, abdominal bloating, abdominal cramps, and pain may be present. Although diarrhea is a common complaint, the character and frequency of stools may vary considerably ranging from over 10 watery stools per day to less than one voluminous putty-like stool, the latter causing some patients to complain of constipation. On the other hand, stool mass is invariably increased in patients with steatorrhea and generalized malabsorption above the normal with 150–200 g/day. Not only do unabsorbed nutrients contribute to stool mass but mucosal fluid and electrolyte secretion is also increased in diseases associated with mucosal inflammation such as coeliac disease. In addition, unabsorbed fatty acids, converted to hydroxy-fatty acids by colonic flora, as well as unabsorbed bile acids both impair absorption and induce secretion of water and electrolytes by the colon adding to stool mass. Weight loss is common among patients with significant intestinal malabsorption but must be evaluated in the context of caloric intake. Some patients compensate for fecal wastage of unabsorbed nutrients by significantly increasing their oral intake. Eliciting a careful dietary history from patients with suspected malabsorption is therefore crucial. Excessive flatus and abdominal bloating may reflect excessive gas production due to fermentation of unabsorbed carbohydrate, especially among patients with primary or secondary disaccharidase deficiency. Malabsorption of dietary nutrients and excessive fluid secretion by inflamed small intestine also contribute to abdominal distention and bloating. Prevalence, severity, and character of abdominal pain vary considerably among the various disease processes associated with intestinal malabsorption. For example, pain is common in patients with chronic pancreatitis or pancreatic cancer and Crohn disease, but it is absent in many patients with coeliac disease or postgastrectomy malabsorption.

Substantial numbers of patients with intestinal malabsorption present initially with symptoms or laboratory abnormalities that point to other organ systems in the absence of or overshadowing symptoms referable to the gastrointestinal tract. For example, there is increasing epidemiologic evidence that more patients with coeliac disease present with anemia and osteopenia in the absence of significant classic gastrointestinal symptoms. Microcytic, macrocytic, or dimorphic anemia may reflect impaired iron, folate, or vitamin B12 absorption. Purpura, subconjunctival hemorrhage, or even frank bleeding may reflect hypoprothrombinemia secondary to vitamin K malabsorption. Osteopenia is common, especially in the presence of steatorrhea. Impaired calcium and vitamin D absorption and chelation of calcium by unabsorbed fatty acids resulting in fecal loss of calcium may all contribute. If calcium deficiency is prolonged, secondary hyperparathyroidism may develop. Prolonged malnutrition may induce amenorrhea, infertility, and impotence. Edema and even ascites may reflect hypoproteinemia associated with protein losing enteropathy caused by lymphatic obstruction or extensive mucosal inflammation. Dermatitis and peripheral neuropathy may be caused by malabsorption of specific vitamins or micronutrients and essential fatty acids.

The most common symptoms of gastroparesis are the following:

- Chronic nausea (93%)

- Vomiting (especially of undigested food) (68–84%)

- Abdominal pain (46–90%)

- A feeling of fullness after eating just a few bites (60–86%)

Other symptoms include the following:

- Abdominal bloating

- Body aches (myalgia)

- Erratic blood glucose levels

- Gastroesophageal reflux (GERD)

- Heartburn

- Lack of appetite

- Morning nausea

- Muscle weakness

- Night sweats

- Palpitations

- Spasms of the stomach wall

- Constipation or infrequent bowel movements

- Weight loss and malnutrition

Morning nausea may also indicate gastroparesis. Vomiting may not occur in all cases, as sufferers may adjust their diets to include only small amounts of food.

Many people with gastritis experience no symptoms at all. However, upper central abdominal pain is the most common symptom; the pain may be dull, vague, burning, aching, gnawing, sore, or sharp. Pain is usually located in the upper central portion of the abdomen, but it may occur anywhere from the upper left portion of the abdomen around to the back.

Other signs and symptoms may include the following:

- Nausea

- Vomiting (if present, may be clear, green or yellow, blood-streaked, or completely bloody, depending on the severity of the stomach inflammation)

- Belching (if present, usually does not relieve the pain much)

- Bloating

- Early satiety

- Loss of appetite

- Unexplained weight loss

Most patients with fundic gland polyps (FGPs) do not have any symptoms, and the diagnosis is made on gastroscopy done for other reasons. Retrospective analysis of patients with sporadic FGPs shows that a high percentage do have symptoms, but that this is more likely to be related to the underlying disease responsible for the polyposis. These symptoms include:

- epigastric pain

- nausea

- vomiting

- weight loss

The polyps on endoscopy are usually tiny, numerous and sessile, and usually scattered throughout the fundus of the stomach, where parietal cells are more numerous. They have the same colour as the gastric mucosa, and never have a stalk.

When the polyps are biopsied, the pathology typically shows shortened gastric pits, and both superficial and deep cystic lesions in the fundic glands, lined by all three types of cells of acid-producing mucosa: mucous, parietal and chief cells. As sometimes parietal cell hyperplasia may develop deep dilations of gland, one should be really strict in the diagnosis of FGPs (i.e. the presence of deep and superficial dilations). Infrequently, the two lesions may coexist. Foci of dysplasia can sometimes be seen.

Common causes include "Helicobacter pylori" and NSAIDs. Less common causes include alcohol, cocaine, severe illness and Crohn disease, among others.

Primary complications of gastroparesis include:

- Fluctuations in blood glucose due to unpredictable digestion times (in diabetic patients)

- General malnutrition due to the symptoms of the disease (which frequently include vomiting and reduced appetite) as well as the dietary changes necessary to manage it

- Severe fatigue and weight loss due to calorie deficit

- Intestinal obstruction due to the formation of bezoars (solid masses of undigested food)

- Bacterial infection due to overgrowth in undigested food

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).