Gastric mucosa in the context of "Surface mucous cell"

A flagellum (/fləˈdʒɛləm/; pl.: flagella) (Latin for 'whip' or 'scourge') is a hair-like appendage that protrudes from certain plant and animal sperm cells, from fungal spores (zoospores), and from a wide range of microorganisms to provide motility. Many protists with flagella are known as flagellates.

A microorganism may have from one to many flagella. A gram-negative bacterium Helicobacter pylori, for example, uses its flagella to propel itself through the stomach to reach the mucous lining where it may colonise the epithelium and potentially cause gastritis, and ulcers – a risk factor for stomach cancer. In some swarming bacteria, the flagellum can also function as a sensory organelle, being sensitive to wetness outside the cell.

Peptic ulcer disease refers to damage of the inner part of the stomach's gastric mucosa (lining of the stomach), the first part of the small intestine, or sometimes the lower esophagus. An ulcer in the stomach is called a gastric ulcer, while one in the first part of the intestines is a duodenal ulcer. The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain, and upper abdominal pain that improves with eating. With a gastric ulcer, the pain may worsen with eating. The pain is often described as a burning or dull ache. Other symptoms include belching, vomiting, weight loss, or poor appetite. About a third of older people with peptic ulcers have no symptoms. Complications may include bleeding, perforation, and blockage of the stomach. Bleeding occurs in as many as 15% of cases.

Common causes include infection with Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). Other, less common causes include tobacco smoking, stress as a result of other serious health conditions, Behçet's disease, Zollinger–Ellison syndrome, Crohn's disease, and liver cirrhosis. Older people are more sensitive to the ulcer-causing effects of NSAIDs. The diagnosis is typically suspected due to the presenting symptoms with confirmation by either endoscopy or barium swallow. H. pylori can be diagnosed by testing the blood for antibodies, a urea breath test, testing the stool for signs of the bacteria, or a biopsy of the stomach. Other conditions that produce similar symptoms include stomach cancer, coronary heart disease, and inflammation of the stomach lining or gallbladder inflammation.

Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, flagellated, helical bacterium. Mutants can have a rod or curved rod shape that exhibits less virulence. Its helical body (from which the genus name Helicobacter derives) is thought to have evolved to penetrate the mucous lining of the stomach, helped by its flagella, and thereby establish infection. While many earlier reports of an association between bacteria and the ulcers had existed, such as the works of John Lykoudis, it was only in 1983 when the bacterium was formally described for the first time in the English-language Western literature as the causal agent of gastric ulcers by Australian physician-scientists Barry Marshall and Robin Warren. In 2005, the pair was awarded the Nobel Prize in Physiology or Medicine for their discovery.

Infection of the stomach with H. pylori does not necessarily cause illness: over half of the global population is infected, but most individuals are asymptomatic. Persistent colonization with more virulent strains can induce a number of gastric and non-gastric disorders. Gastric disorders due to infection begin with gastritis, or inflammation of the stomach lining. When infection is persistent, the prolonged inflammation will become chronic gastritis. Initially, this will be non-atrophic gastritis, but the damage caused to the stomach lining can bring about the development of atrophic gastritis and ulcers within the stomach itself or the duodenum (the nearest part of the intestine). At this stage, the risk of developing gastric cancer is high. However, the development of a duodenal ulcer confers a comparatively lower risk of cancer. Helicobacter pylori are class 1 carcinogenic bacteria, and potential cancers include gastric MALT lymphoma and gastric cancer. Infection with H. pylori is responsible for an estimated 89% of all gastric cancers and is linked to the development of 5.5% of all cases cancers worldwide. H. pylori is the only bacterium known to cause cancer.

Stomach cancer, also known as gastric cancer, is a malignant tumor of the stomach. It is a cancer that develops in the lining of the stomach, caused by abnormal cell growth. Most cases of stomach cancers are gastric carcinomas, which can be divided into several subtypes, including gastric adenocarcinomas. Lymphomas and mesenchymal tumors may also develop in the stomach. Early symptoms may include heartburn, upper abdominal pain, nausea, and loss of appetite. Later signs and symptoms may include weight loss, yellowing of the skin and whites of the eyes, vomiting, difficulty swallowing, and blood in the stool, among others. The cancer may spread from the stomach to other parts of the body, particularly the liver, lungs, bones, lining of the abdomen, and lymph nodes.

The bacterium Helicobacter pylori accounts for more than 60% of cases of stomach cancer. Certain strains of H. pylori have greater risks than others. Smoking, dietary factors such as pickled vegetables and obesity are other risk factors. About 10% of cases run in families, and between 1% and 3% of cases are due to genetic syndromes inherited such as hereditary diffuse gastric cancer. Most of the time, stomach cancer develops in stages over the years. Diagnosis is usually by biopsy done during endoscopy. This is followed by medical imaging to determine if the cancer has spread to other parts of the body. Japan and South Korea, two countries that have high rates of the disease, screen for stomach cancer.

Gastric glands are glands in the lining of the stomach that play an essential role in the process of digestion. Their secretions make up the digestive gastric juice. The gastric glands open into gastric pits in the mucosa. The gastric mucosa is covered in surface mucous cells that produce the mucus necessary to protect the stomach's epithelial lining from gastric acid secreted by parietal cells in the glands, and from pepsin, a secreted digestive enzyme. Surface mucous cells follow the indentations and partly line the gastric pits. Other mucus secreting cells are found in the necks of the glands. These are mucous neck cells that produce a different kind of mucus.

There are two types of gastric gland, the exocrine fundic or oxyntic gland, and the endocrine pyloric gland. The major type of gastric gland is the fundic gland that is present in the fundus and the body of the stomach making up about 80 per cent of the stomach area. These glands are often referred to simply as the gastric glands. The fundic gland contains the parietal cells that produce hydrochloric acid and intrinsic factor, and chief cells that produce pepsinogen and gastric lipase.

Gastric varices are dilated submucosal veins in the lining of 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 that 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 (surgical removal of the spleen) or liver transplantation, may be required in some cases.