Pathological processes involving the STOMACH.
An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the ESOPHAGUS and the beginning of the DUODENUM.
Tumors or cancer of the STOMACH.
Lining of the STOMACH, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. The surface cells produce MUCUS that protects the stomach from attack by digestive acid and enzymes. When the epithelium invaginates into the LAMINA PROPRIA at various region of the stomach (CARDIA; GASTRIC FUNDUS; and PYLORUS), different tubular gastric glands are formed. These glands consist of cells that secrete mucus, enzymes, HYDROCHLORIC ACID, or hormones.
Ulceration of the GASTRIC MUCOSA due to contact with GASTRIC JUICE. It is often associated with HELICOBACTER PYLORI infection or consumption of nonsteroidal anti-inflammatory drugs (NSAIDS).
The region between the sharp indentation at the lower third of the STOMACH (incisura angularis) and the junction of the PYLORUS with the DUODENUM. Pyloric antral glands contain mucus-secreting cells and gastrin-secreting endocrine cells (G CELLS).
Bursting of the STOMACH.
The superior portion of the body of the stomach above the level of the cardiac notch.
Twisting of the STOMACH that may result in gastric ISCHEMIA and GASTRIC OUTLET OBSTRUCTION. It is often associated with DIAPHRAGMATIC HERNIA.
Excision of the whole (total gastrectomy) or part (subtotal gastrectomy, partial gastrectomy, gastric resection) of the stomach. (Dorland, 28th ed)
A group of organs stretching from the MOUTH to the ANUS, serving to breakdown foods, assimilate nutrients, and eliminate waste. In humans, the digestive system includes the GASTROINTESTINAL TRACT and the accessory glands (LIVER; BILIARY TRACT; PANCREAS).

Helicobacter pylori can be induced to assume the morphology of Helicobacter heilmannii. (1/688)

Cultures of Helicobacter pylori obtained from the American Type Culture Collection (strain 43504) were grown as isolated colonies or lawns on blood agar plates and in broth culture with constant shaking. Examination of bacterial growth with Gram-stained fixed preparation and differential interference contrast microscopy on wet preparations revealed that bacteria grown on blood agar plates had a morphology consistent with that normally reported for H. pylori whereas bacteria from broth cultures had the morphologic appearance of Helicobacter heilmannii. Bacteria harvested from blood agar plates assumed an H. heilmannii-like morphology when transferred to broth cultures, and bacteria from broth cultures grew with morphology typical of H. pylori when grown on blood agar plates. Analysis by PCR of bacteria isolated from blood agar plates and broth cultures indicated that a single strain of bacteria (H. pylori) was responsible for both morphologies.  (+info)

Spontaneous gastrointestinal perforation in patients with lymphoma receiving chemotherapy and steroids. Report of three cases. (2/688)

Spontaneous gastrointestinal perforations in three patients with lymphoma were considered to be treatment-related conditions. All three were diagnosed as having malignant lymphoma by histological examination, and treated with chemotherapy and steroids. Four to 14 days after the start of chemotherapy, they complained of abdominal pain and plain roentgenograms revealed pneumoperitoneum. The interval between the onset of peritonitis and operation was almost 24 h. Emergency operations were carried out; one patient with a jejunal perforation underwent resection of the jejunum, another with a gastric perforation received a simple closure with omental patch, and the third with a gastric perforation underwent gastrectomy. Two patients recovered from the surgery, while the gastrectomy patient died due to sepsis. The favorable outcome of the surgical intervention is attributed to early diagnosis, prompt exploration, and selective operative procedures. We recommended a simple closure with omental patch for gastroduodenal perforation. Resection and primary anastomosis are possible only in the small bowel.  (+info)

Prevention of nonsteroidal anti-inflammatory drug-induced gastropathy: clinical and economic implications of a single-tablet formulation of diclofenac/misoprostol. (3/688)

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used to manage arthritis. While controlling symptoms and improving quality of life, NSAID use is associated with gastroduodenal injury and a 2%-4% annual risk for symptomatic gastroduodenal ulceration, hemorrhage, and perforation. This requires clinicians to balance the efficacy of NSAIDs against the potential risk of serious gastrointestinal events. Identification and stratification of risk can help guide the optimal approach for arthritis management of individual patients or large populations such as managed care organizations. NSAID-induced gastroenteropathy carries considerable economic consequences; 46% of arthritis costs are related to managing serious adverse events. It is reasonable to assume that these costs may not be incurred if high-risk patients are recognized and optimally managed. Newer therapies with proven safety margins present an attractive option, especially for patients at higher risk. The single-tablet formulations of diclofenac and misoprostol (Arthrotec) offer an alternative in managing NSAID patients because of their inherent safety profile. Studies with diclofenac/misoprostol indicate its effectiveness in treating signs and symptoms of arthritis and in reducing the incidence of NSAID-induced gastroenteropathy. As such, this agent may provide improved medical and economic outcomes. This review discusses the clinical aspects of NSAID-induced gastroenteropathy, including available preventive therapies. Approaches to assessing patients' risk for developing complications, and the relationship of medical risk and economic outcomes, are also examined. Although not all patients require preventive therapy, patients with heightened risk may benefit clinically and economically from gastroprotective NSAIDs. Additional research or modeling may provide further insight into the economic implications of managing and preventing NSAID-induced gastroenteropathy.  (+info)

A case of gastric pseudoterranoviasis in a 43-year-old man in Korea. (4/688)

A case of Pseudoterranova decipiens infection was found in a 43-year-old man by gastroendoscopic examination on August 20, 1996. On August 6, 1996, he visited a local clinic, complaining of epigastric pain two days after eating raw marine fishes. Although the symptoms were relieved soon, endoscopic examination was done for differential diagnosis. A white, live nematode larva was removed from the fundus of the stomach. The larva was 38.3 x 1.0 mm in size and had a cecum reaching to the mid-level of the ventriculus. A lot of transverse striations were regularly arranged on the cuticle of its body surface, but the boring tooth and mucron were not observed at both ends of the worm. The worm was identified as the 4th stage larva of P. decipiens.  (+info)

Analysis of Helicobacter pylori vacA and cagA genotypes and serum antibody profile in benign and malignant gastroduodenal diseases. (5/688)

BACKGROUND: Helicobacter pylori species comprise different strains, cytotoxic and non-cytotoxic, which can be identified on the basis of their genomic pattern. AIMS: (1) To evaluate the polymorphism of the vacA gene and to ascertain whether the cagA gene is present in patients with gastric adenocarcinoma. (2) To study the anti-H pylori antibody profile using western blotting. PATIENTS: Twenty one patients with gastric adenocarcinoma and 71 with H pylori associated benign disease (nine gastric ulcer, 29 duodenal ulcer, 25 antral gastritis, and eight duodenitis). METHODS: The polymerase chain reaction was used to verify the presence or absence of cagA and to study the polymorphism of vacA in gastric mucosal samples obtained during endoscopy for patients with benign diseases and at surgery for patients with gastric adenocarcinoma. Fasting sera were used to assess anti-H pylori antibodies against different H pylori antigens by western blotting. RESULTS: CagA gene and the allele s1 of vacA were significantly less frequent in patients with antral gastritis (60% and 60%) compared with patients with gastric adenocarcinoma (94% and 100%) and with other non-malignant gastroduodenal diseases (93% and 87%) (chi 2 = 16.01, p < 0.001; and chi 2 = 13.97, p < 0.01). In patients with gastric adenocarcinoma, antibodies against a 74 kDa H pylori antigen were less frequently found than in patients with benign diseases. CONCLUSIONS: H pylori infection caused by cagA positive/vacA s1 strains is a frequent finding in patients with gastric adenocarcinoma. Prospective studies are needed to confirm whether the low incidence of positive serological response to the 74 kDa H pylori antigen in patients with gastric adenocarcinoma is important.  (+info)

Bovine colostrum is a health food supplement which prevents NSAID induced gut damage. (6/688)

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) are effective for arthritis but cause gastrointestinal injury. Bovine colostrum is a rich source of growth factors and is marketed as a health food supplement. AIMS: To examine whether spray dried, defatted colostrum or milk preparations could reduce gastrointestinal injury caused by indomethacin. METHODS: Effects of test solutions, administered orally, were examined using an indomethacin restraint rat model of gastric damage and an indomethacin mouse model of small intestinal injury. Effects on migration of the human colonic carcinoma cell line HT-29 and rat small intestinal cell line RIE-1 were assessed using a wounded monolayer assay system (used as an in vitro model of wound repair) and effects on proliferation determined using [3H]thymidine incorporation. RESULTS: Pretreatment with 0.5 or 1 ml colostral preparation reduced gastric injury by 30% and 60% respectively in rats. A milk preparation was much less efficacious. Recombinant transforming growth factor beta added at a dose similar to that found in the colostrum preparation (12.5 ng/rat), reduced injury by about 60%. Addition of colostrum to drinking water (10% vol/vol) prevented villus shortening in the mouse model of small intestinal injury. Addition of milk preparation was ineffective. Colostrum increased proliferation and cell migration of RIE-1 and HT-29 cells. These effects were mainly due to constituents of the colostrum with molecular weights greater than 30 kDa. CONCLUSIONS: Bovine colostrum could provide a novel, inexpensive approach for the prevention and treatment of the injurious effects of NSAIDs on the gut and may also be of value for the treatment of other ulcerative conditions of the bowel.  (+info)

Gastric antral vascular ectasia in cirrhotic patients: absence of relation with portal hypertension. (7/688)

BACKGROUND: Portal hypertensive gastropathy and gastric antral vascular ectasia (GAVE) are increasingly recognised as separate entities. The pathogenic role of portal hypertension for the development of GAVE is still controversial. AIMS: To evaluate the effects of portal decompression on chronic bleeding related to GAVE in cirrhotic patients. METHODS: Eight patients with cirrhosis and chronic blood loss related to GAVE were included. GAVE was defined endoscopically and histologically. RESULTS: All patients had severe portal hypertension (mean portocaval gradient (PCG) 26 mm Hg) and chronic low grade bleeding. Seven patients underwent transjugular intrahepatic portosystemic shunt (TIPS) and one had an end to side portacaval shunt. Rebleeding occurred in seven patients. In these, TIPS was found to be occluded after 15 days in one patient; in the other six, the shunt was patent and the PCG was below 12 mm Hg in five. In the responder, PCG was 16 mm Hg. Antrectomy was performed in four non-responders; surgery was uneventful, and they did not rebleed after surgery, but two died 11 and 30 days postoperatively from multiorgan failure. In one patient, TIPS did not control GAVE related bleeding despite a notable decrease in PCG. This patient underwent liver transplantation 14 months after TIPS; two months after transplantation, bleeding had stopped and the endoscopic appearance of the antrum had normalised. CONCLUSIONS: Results suggest that GAVE is not directly related to portal hypertension, but is influenced by the presence of liver dysfunction. Antrectomy is a therapeutic option when chronic bleeding becomes a significant problem but carries a risk of postoperative mortality.  (+info)

Plaunotol prevents indomethacin-induced gastric mucosal injury in rats by inhibiting neutrophil activation. (8/688)

BACKGROUND: Activated neutrophils play a critical role in indomethacin-induced gastric mucosal injury. AIM: To investigate the effect of plaunotol, an anti-ulcer agent, on neutrophil activation in vitro and its effect on gastric mucosal injury and gastric accumulation of neutrophils in rats given indomethacin. METHODS: Human monocytes and neutrophils were isolated from the peripheral blood of healthy volunteers. We examined the effect of plaunotol on neutrophil elastase release, production of O2-, intracellular calcium concentration and expression of adhesion molecules CD11b and CD18 in activated neutrophils in vitro. The effect of plaunotol on TNF-alpha production by monocytes stimulated with endotoxin also was investigated in vitro. The effect of plaunotol (100 mg/kg, p.o.) on gastric mucosal injury and neutrophil accumulation was investigated in male Wistar rats given indomethacin (30 mg/kg, p.o.). RESULTS: Plaunotol inhibited the fMLP-induced release of neutrophil elastase from activated neutrophils, as well as the opsonized zymosan-induced production of O2- by neutrophils. Plaunotol significantly inhibited increased levels of intracellular calcium, a second messenger of neutrophil activation, in vitro. The fMLP-induced increases in CD11b and CD18 expression were also inhibited by plaunotol in vitro. Plaunotol inhibited monocytic production of TNF-alpha, a potent activator of neutrophils. Both gastric mucosal injury and gastric neutrophil infiltration in rats given indomethacin were significantly inhibited by the oral administration of plaunotol. CONCLUSIONS: Plaunotol inhibits indomethacin-induced gastric mucosal injury, at least in part by inhibiting neutrophil activation.  (+info)

Stomach diseases refer to a range of conditions that affect the stomach, a muscular sac located in the upper part of the abdomen and is responsible for storing and digesting food. These diseases can cause various symptoms such as abdominal pain, nausea, vomiting, heartburn, indigestion, loss of appetite, and bloating. Some common stomach diseases include:

1. Gastritis: Inflammation of the stomach lining that can cause pain, irritation, and ulcers.
2. Gastroesophageal reflux disease (GERD): A condition where stomach acid flows back into the esophagus, causing heartburn and damage to the esophageal lining.
3. Peptic ulcers: Open sores that develop on the lining of the stomach or duodenum, often caused by bacterial infections or long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs).
4. Stomach cancer: Abnormal growth of cancerous cells in the stomach, which can spread to other parts of the body if left untreated.
5. Gastroparesis: A condition where the stomach muscles are weakened or paralyzed, leading to difficulty digesting food and emptying the stomach.
6. Functional dyspepsia: A chronic disorder characterized by symptoms such as pain, bloating, and fullness in the upper abdomen, without any identifiable cause.
7. Eosinophilic esophagitis: A condition where eosinophils, a type of white blood cell, accumulate in the esophagus, causing inflammation and difficulty swallowing.
8. Stomal stenosis: Narrowing of the opening between the stomach and small intestine, often caused by scar tissue or surgical complications.
9. Hiatal hernia: A condition where a portion of the stomach protrudes through the diaphragm into the chest cavity, causing symptoms such as heartburn and difficulty swallowing.

These are just a few examples of stomach diseases, and there are many other conditions that can affect the stomach. Proper diagnosis and treatment are essential for managing these conditions and preventing complications.

In anatomical terms, the stomach is a muscular, J-shaped organ located in the upper left portion of the abdomen. It is part of the gastrointestinal tract and plays a crucial role in digestion. The stomach's primary functions include storing food, mixing it with digestive enzymes and hydrochloric acid to break down proteins, and slowly emptying the partially digested food into the small intestine for further absorption of nutrients.

The stomach is divided into several regions, including the cardia (the area nearest the esophagus), the fundus (the upper portion on the left side), the body (the main central part), and the pylorus (the narrowed region leading to the small intestine). The inner lining of the stomach, called the mucosa, is protected by a layer of mucus that prevents the digestive juices from damaging the stomach tissue itself.

In medical contexts, various conditions can affect the stomach, such as gastritis (inflammation of the stomach lining), peptic ulcers (sores in the stomach or duodenum), gastroesophageal reflux disease (GERD), and stomach cancer. Symptoms related to the stomach may include abdominal pain, bloating, nausea, vomiting, heartburn, and difficulty swallowing.

Stomach neoplasms refer to abnormal growths in the stomach that can be benign or malignant. They include a wide range of conditions such as:

1. Gastric adenomas: These are benign tumors that develop from glandular cells in the stomach lining.
2. Gastrointestinal stromal tumors (GISTs): These are rare tumors that can be found in the stomach and other parts of the digestive tract. They originate from the stem cells in the wall of the digestive tract.
3. Leiomyomas: These are benign tumors that develop from smooth muscle cells in the stomach wall.
4. Lipomas: These are benign tumors that develop from fat cells in the stomach wall.
5. Neuroendocrine tumors (NETs): These are tumors that develop from the neuroendocrine cells in the stomach lining. They can be benign or malignant.
6. Gastric carcinomas: These are malignant tumors that develop from the glandular cells in the stomach lining. They are the most common type of stomach neoplasm and include adenocarcinomas, signet ring cell carcinomas, and others.
7. Lymphomas: These are malignant tumors that develop from the immune cells in the stomach wall.

Stomach neoplasms can cause various symptoms such as abdominal pain, nausea, vomiting, weight loss, and difficulty swallowing. The diagnosis of stomach neoplasms usually involves a combination of imaging tests, endoscopy, and biopsy. Treatment options depend on the type and stage of the neoplasm and may include surgery, chemotherapy, radiation therapy, or targeted therapy.

Gastric mucosa refers to the innermost lining of the stomach, which is in contact with the gastric lumen. It is a specialized mucous membrane that consists of epithelial cells, lamina propria, and a thin layer of smooth muscle. The surface epithelium is primarily made up of mucus-secreting cells (goblet cells) and parietal cells, which secrete hydrochloric acid and intrinsic factor, and chief cells, which produce pepsinogen.

The gastric mucosa has several important functions, including protection against self-digestion by the stomach's own digestive enzymes and hydrochloric acid. The mucus layer secreted by the epithelial cells forms a physical barrier that prevents the acidic contents of the stomach from damaging the underlying tissues. Additionally, the bicarbonate ions secreted by the surface epithelial cells help neutralize the acidity in the immediate vicinity of the mucosa.

The gastric mucosa is also responsible for the initial digestion of food through the action of hydrochloric acid and pepsin, an enzyme that breaks down proteins into smaller peptides. The intrinsic factor secreted by parietal cells plays a crucial role in the absorption of vitamin B12 in the small intestine.

The gastric mucosa is constantly exposed to potential damage from various factors, including acid, pepsin, and other digestive enzymes, as well as mechanical stress due to muscle contractions during digestion. To maintain its integrity, the gastric mucosa has a remarkable capacity for self-repair and regeneration. However, chronic exposure to noxious stimuli or certain medical conditions can lead to inflammation, erosions, ulcers, or even cancer of the gastric mucosa.

A stomach ulcer, also known as a gastric ulcer, is a sore that forms in the lining of the stomach. It's caused by a breakdown in the mucous layer that protects the stomach from digestive juices, allowing acid to come into contact with the stomach lining and cause an ulcer. The most common causes are bacterial infection (usually by Helicobacter pylori) and long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs). Stomach ulcers may cause symptoms such as abdominal pain, bloating, heartburn, and nausea. If left untreated, they can lead to more serious complications like internal bleeding, perforation, or obstruction.

The pyloric antrum is the distal part of the stomach, which is the last portion that precedes the pylorus and the beginning of the duodenum. It is a thickened, muscular area responsible for grinding and mixing food with gastric juices during digestion. The pyloric antrum also helps regulate the passage of chyme (partially digested food) into the small intestine through the pyloric sphincter, which controls the opening and closing of the pylorus. This region is crucial in the gastrointestinal tract's motor functions and overall digestive process.

A stomach rupture, also known as gastrointestinal perforation, is a serious and potentially life-threatening condition that occurs when there is a hole or tear in the lining of the stomach. This can allow the contents of the stomach to leak into the abdominal cavity, causing inflammation and infection (peritonitis).

Stomach rupture can be caused by several factors, including trauma, severe gastritis or ulcers, tumors, or certain medical procedures. Symptoms may include sudden and severe abdominal pain, nausea, vomiting, fever, and decreased bowel sounds. If left untreated, stomach rupture can lead to sepsis, organ failure, and even death. Treatment typically involves surgery to repair the perforation and antibiotics to treat any resulting infection.

The gastric fundus is the upper, rounded portion of the stomach that lies above the level of the cardiac orifice and extends up to the left dome-shaped part of the diaphragm. It is the part of the stomach where food and liquids are first stored after entering through the esophagus. The gastric fundus contains parietal cells, which secrete hydrochloric acid, and chief cells, which produce pepsinogen, a precursor to the digestive enzyme pepsin. It is also the site where the hormone ghrelin is produced, which stimulates appetite.

Stomach volvulus is a medical condition that involves the twisting or rotation of the stomach around its axis, leading to obstruction of the inflow and outflow of the stomach. This can result in strangulation of the blood supply to the stomach wall, potentially causing ischemia, necrosis, and perforation if not promptly treated. It is a surgical emergency that requires immediate medical attention. The condition can be congenital or acquired, with the acquired form being more common and often associated with underlying conditions such as gastric distention, laxity of gastrocolic ligaments, or previous abdominal surgery.

A Gastrectomy is a surgical procedure involving the removal of all or part of the stomach. This procedure can be total (complete resection of the stomach), partial (removal of a portion of the stomach), or sleeve (removal of a portion of the stomach to create a narrow sleeve-shaped pouch).

Gastrectomies are typically performed to treat conditions such as gastric cancer, benign tumors, severe peptic ulcers, and in some cases, for weight loss in individuals with morbid obesity. The type of gastrectomy performed depends on the patient's medical condition and the extent of the disease.

Following a gastrectomy, patients may require adjustments to their diet and lifestyle, as well as potential supplementation of vitamins and minerals that would normally be absorbed in the stomach. In some cases, further reconstructive surgery might be necessary to reestablish gastrointestinal continuity.

The digestive system is a complex group of organs and glands that process food. It converts the food we eat into nutrients, which the body uses for energy, growth, and cell repair. The digestive system also eliminates waste from the body. It is made up of the gastrointestinal tract (GI tract) and other organs that help the body break down and absorb food.

The GI tract includes the mouth, esophagus, stomach, small intestine, large intestine, and anus. Other organs that are part of the digestive system include the liver, pancreas, gallbladder, and salivary glands.

The process of digestion begins in the mouth, where food is chewed and mixed with saliva. The food then travels down the esophagus and into the stomach, where it is broken down further by stomach acids. The digested food then moves into the small intestine, where nutrients are absorbed into the bloodstream. The remaining waste material passes into the large intestine, where it is stored until it is eliminated through the anus.

The liver, pancreas, and gallbladder play important roles in the digestive process as well. The liver produces bile, a substance that helps break down fats in the small intestine. The pancreas produces enzymes that help digest proteins, carbohydrates, and fats. The gallbladder stores bile until it is needed in the small intestine.

Overall, the digestive system is responsible for breaking down food, absorbing nutrients, and eliminating waste. It plays a critical role in maintaining our health and well-being.

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