Crohn's disease is an inflammatory bowel disease that can affect any part of the digestive tract, even the stomach, although it's a rare presentation. Its main feature is inflammatory ulcers that can affect the total thickness of the stomach wall and can bleed but rarely perforate.

Symptoms include abdominal pain, loss of appetite, and weight loss. Diarrhea is also a symptom that can develop, so checking stools for the appearance of blood is important. It is possible for symptoms of Crohn's disease to remain with a person for weeks or go away on their own. Reporting the symptoms to a doctor is recommended to prevent further complications.

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.

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.

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.

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.

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 small and large intestines may be affected by infectious, autoimmune, and physiological states. Inflammation of the intestines is called enterocolitis, which may lead to diarrhoea.

Acute conditions affecting the bowels include infectious diarrhoea and mesenteric ischaemia. Causes of constipation may include faecal impaction and bowel obstruction, which may in turn be caused by ileus, intussusception, volvulus. Inflammatory bowel disease is a condition of unknown aetiology, classified as either Crohn's disease or ulcerative colitis, that can affect the intestines and other parts of the gastrointestinal tract. Other causes of illness include intestinal pseudoobstruction, and necrotizing enterocolitis.

Diseases of the intestine may cause vomiting, diarrhoea or constipation, and altered stool, such as with blood in stool. Colonoscopy may be used to examine the large intestine, and a person's stool may be sent for culture and microscopy. Infectious disease may be treated with targeted antibiotics, and inflammatory bowel disease with immunosuppression. Surgery may also be used to treat some causes of bowel obstruction.

The normal thickness of the small intestinal wall is 3–5 mm, and 1–5 mm in the large intestine. Focal, irregular and asymmetrical gastrointestinal wall thickening on CT scan suggests a malignancy. Segmental or diffuse gastrointestinal wall thickening is most often due to ischemic, inflammatory or infectious disease.

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.

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.

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.

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.

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.

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.

Most of the symptoms of BLS are non specific but nevertheless warrant the utmost attention. These include:

- Loss of appetite

- Nausea

- Flatulence

- Diarrhea

- Fullness after a meal

- Fatty stools (steatorrhea)

- Unintentional weight loss

- Generalised weakness

As a result of the concomitant vitamin and mineral deficiencies that occur as a result of the malabsorption associated with BLS patients with advanced cases should be investigated for:

- Vitamin B12 deficiency

- Folate deficiency

- Iron deficiency

- Vitamin E deficiency

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.

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.

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

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.

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.

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.

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

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.

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 atresia is the complete occlusion of the pyloric outlet of the stomach and is an extremely rare event.