Many people who have chronic gastritis do not experience any noticeable symptoms. Those who do, claim to experience one or several of the following: upper abdominal pain, indigestion, bloating, nausea, vomiting, belching, loss of appetite, and weight loss. Stomach bleeding or black stool has been reported in extreme cases.

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

This is the most common form of chronic gastritis. Involvement tends to occur in either an antral-predominant or multifocal atrophic pattern. "H. pylori" infection is also associated with development of peptic ulcer disease, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphomas.

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

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.

A gastric peptic ulcer is a mucosal perforation which penetrates the muscularis mucosae and lamina propria, usually produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: fibrinoid necrosis, inflammatory exudate, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.

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.

Diseases that affect the large intestine may affect it in whole or in part. Appendicitis is one such disease, caused by inflammation of the appendix. Generalised inflammation of the large intestine is referred to as colitis, which when caused be the bacteria "Clostridium difficile" is referred to as pseudomembranous colitis. Diverticulitis is a common cause of abdominal pain resulting from outpouchings that particularly affects the colon. Functional colonic diseases refer to disorders without a known cause, and include irritable bowel syndrome and intestinal pseudoobstruction. Constipation may result from lifestyle factors, impaction of a rigid stool in the rectum, or in neonates, Hirschprung's disease.

Diseases affecting the large intestine may cause blood to be passed with stool, may cause constipation, or may result in abdominal pain or a fever. Tests that specifically examine the function of the large intestine include barium swallows, abdominal x-rays, and colonoscopy.

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.

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.

In about 50-70% of patients with dyspepsia, no definite organic cause can be determined. In this case, dyspepsia is referred to as non-ulcer dyspepsia and its diagnosis is established by the presence of epigastralgia for at least 6 months, in the absence of any other cause explaining the symptoms.

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.

When dyspepsia can be attributed to a specific cause, the majority of cases concern gastroesophageal reflux disease (GERD) and peptic ulcer disease. Less common causes include gastritis, gastric cancer, esophageal cancer, coeliac disease, food allergy, inflammatory bowel disease, chronic intestinal ischemia and gastroparesis.

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.

The most common symptoms of GERD in adults are an acidic taste in the mouth, regurgitation, and heartburn. Less common symptoms include pain with swallowing/sore throat, increased salivation (also known as water brash), nausea, chest pain, and coughing.

GERD sometimes causes injury of the esophagus. These injuries may include one or more of the following:

- Reflux esophagitis – inflammation of esophageal epithelium which can cause ulcers near the junction of the stomach and esophagus

- Esophageal strictures – the persistent narrowing of the esophagus caused by reflux-induced inflammation

- Barrett's esophagus – intestinal metaplasia (changes of the epithelial cells from squamous to intestinal columnar epithelium) of the distal esophagus

- Esophageal adenocarcinoma – a form of cancer

Some researchers have proposed that recurrent ear infections, and idiopathic pulmonary fibrosis might be tied, in some cases, to GERD; however, a causative role has not been established. GERD does not appear to be linked to chronic sinusitis.

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.

Reactive gastropathy is morphologically distinct entity that can be separated from gastritis, which by definition has a significant inflammatory component.

As a reactive gastropathy may mimic a (true) gastritis symptomatically and visually in an endoscopic examination, it may incorrectly be referred to as a gastritis. Even aware of the underlying etiology of the pathologic process, e.g. NSAID use, the label "chemical gastritis" is applied to a chemical gastropathy.

Barrett's esophagus refers to an abnormal change (metaplasia) in the cells of the lower portion of the esophagus. It is characterized by the replacement of the normal stratified squamous epithelium lining of the esophagus by simple columnar epithelium with goblet cells (which are usually found lower in the gastrointestinal tract). The medical significance of Barrett's esophagus is its strong association (0.1 per 1 cm Prague C>M> total segment length per patient-year) with esophageal adenocarcinoma, a very often deadly cancer, because of which it is considered to be a premalignant condition.

The main cause of Barrett's esophagus is thought to be an adaptation to chronic acid exposure from reflux esophagitis. The incidence of esophageal adenocarcinoma has increased substantially in the Western world in recent years. The condition is found in 5–15% of patients who seek medical care for heartburn (gastroesophageal reflux disease), although a large subgroup of patients with Barrett's esophagus do not have symptoms. Diagnosis requires endoscopy (more specifically, esophagogastroduodenoscopy, a procedure in which a fibreoptic cable is inserted through the mouth to examine the esophagus, stomach, and duodenum) and biopsy. The cells of Barrett's esophagus, after biopsy, are classified into four general categories: nondysplastic, low-grade dysplasia, high-grade dysplasia, and frank carcinoma. High-grade dysplasia and early stages of adenocarcinoma can be treated by endoscopic resection and new endoscopic therapies such as radiofrequency ablation, whereas advanced stages (submucosal) are generally advised to undergo surgical treatment. Nondysplastic and low-grade patients are generally advised to undergo annual observation with endoscopy, with radiofrequency ablation as a therapeutic option. In high-grade dysplasia, the risk of developing cancer might be at 10% per patient-year or greater.

The condition is named after the Australian-born British thoracic surgeon Norman Barrett (1903–1979), who described it in 1950.

Those with the eating disorder bulimia are more likely to develop Barrett’s esophagus because bulimia can cause severe acid reflux, and because purging also floods the esophagus with acid.

The change from normal to premalignant cells that indicate Barrett's esophagus does not cause any particular symptoms. Barrett's esophagus, however, is associated with these symptoms:

- frequent and longstanding heartburn

- trouble swallowing (dysphagia)

- vomiting blood (hematemesis)

- pain under the sternum where the esophagus meets the stomach

- unintentional weight loss because eating is painful (odynophagia)

The risk of developing Barrett's esophagus is increased by central obesity (vs. peripheral obesity). The exact mechanism is unclear. The difference in distribution of fat among men (more central) and women (more peripheral) may explain the increased risk in males.

Among the causes of chronic pancreatitis are the following:

The relationship between etiologic factors, genetic predisposition, and the pace of disease progression requires further clarification, though recent research indicates smoking may be a high-risk factor to develop chronic pancreatitis. In a small group of patients chronic pancreatitis has been shown to be hereditary. Almost all patients with cystic fibrosis have established chronic pancreatitis, usually from birth. Cystic fibrosis gene mutations have also been identified in patients with chronic pancreatitis but in whom there were no other manifestations of cystic fibrosis. Obstruction of the pancreatic duct because of either a benign or malignant process may result in chronic pancreatitis.

GERD may be difficult to detect in infants and children, since they cannot describe what they are feeling and indicators must be observed. Symptoms may vary from typical adult symptoms. GERD in children may cause repeated vomiting, effortless spitting up, coughing, and other respiratory problems, such as wheezing. Inconsolable crying, refusing food, crying for food and then pulling off the bottle or breast only to cry for it again, failure to gain adequate weight, bad breath, and burping are also common. Children may have one symptom or many; no single symptom is universal in all children with GERD.

Of the estimated 4 million babies born in the US each year, up to 35% of them may have difficulties with reflux in the first few months of their lives, known as 'spitting up'. One theory for this is the "fourth trimester theory" which notes most animals are born with significant mobility, but humans are relatively helpless at birth, and suggests there may have once been a fourth trimester, but children began to be born earlier, evolutionarily, to accommodate the development of larger heads and brains and allow them to pass through the birth canal and this leaves them with partially undeveloped digestive systems.

Most children will outgrow their reflux by their first birthday. However, a small but significant number of them will not outgrow the condition. This is particularly true when a family history of GERD is present.

Chronic pancreatitis is a long-standing inflammation of the pancreas that alters the organ's normal structure and functions. It can present as episodes of acute inflammation in a previously injured pancreas, or as chronic damage with persistent pain or malabsorption. It is a disease process characterized by irreversible damage to the pancreas as distinct from reversible changes in acute pancreatitis.

Signs and symptoms of enteritis are highly variable and vary based on the specific cause and other factors such as individual variance and stage of disease.

Symptoms may include abdominal pain, cramping, diarrhoea, dehydration, fever, nausea, vomiting and weight loss.

Enteritis is inflammation of the small intestine. It is most commonly caused by food or drink contaminated with pathogenic microbes. but may have other causes such as NSAIDs, cocaine, radiation therapy as well as autoimmune conditions like Crohn's disease and coeliac disease. Symptoms include abdominal pain, cramping, diarrhoea, dehydration, and fever. Related diseases include inflammation of the stomach (gastritis) and large intestine (colitis).

Duodenitis, jejunitis and ileitis are subtypes of enteritis which are only localised to a specific part of the small intestine. Inflammation of both the stomach and small intestine is referred to as gastroenteritis. Inflammation of related organs of the gastrointestinal system are:

- gastritis

- gastroenteritis

- colitis

- enterocolitis