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Gastritis is the of the . It may occur as a short episode or have a long duration. There may be no symptoms, but the most common symptom is upper . Other symptoms include and , bloating, , loss of appetite and .

(2026). 9781451160970, Lippincott Williams & Wilkins. .
Complications may include , , and . Autoimmune atrophic gastritis may lead to issues including pernicious anemia.

Common causes include infection with Helicobacter pylori and use of nonsteroidal anti-inflammatory drugs (). Other causes include , , , severe illness, problems, radiation therapy and Crohn's disease.

(2026). 9780199373338, Oxford University Press. .
, a type of known as an upper gastrointestinal series, blood tests, and stool tests may help with diagnosis. Other conditions with similar symptoms include , , and peptic ulcer disease.

Prevention involves avoidance of things which irritate the gut and which trigger symptoms, including alcohol, nonsteroidal anti-inflammatory drugs (NSAIDs), tobacco, and certain foods.This is an example. It is also recommended to treat for any underlying H. pylori infection before starting NSAID treatment in order to prevent irritation and gastroduodenal ulcers. Treatment includes medications such as , H2 blockers, and proton pump inhibitors. During an acute flare-up, drinking viscous lidocaine may help.

(2026). 9781455733941, Elsevier Health Sciences.
If gastritis is caused by NSAID use (e.g. aspirin, ibuprofen, naproxen), usage may be ceased. If H. pylori is present, it may be treated with a combination of such as and . For those with pernicious anemia, vitamin B12 supplements are recommended by injection.

Gastritis is believed to be present in 30% to 50% of people worldwide, but most cases are asymptomatic. In 2013 there were approximately 90 million new cases of the condition. The risk of developing gastritis increases as one ages.

(2026). 9780323083737, Elsevier Health Sciences. .
Gastritis, along with a similar condition in the first part of the called , resulted in 50,000 deaths in 2015. H. pylori was first discovered in 1981 by and .


Classification
There are multiple classification systems which may be used to categorise gastritis cases. The Updated Sydney System (USS) of 1994 is commonly used for classification, based primarily on the morphological features of the disease seen in endoscopic biopsies. The Kyoto system (from the 2015 Kyoto Consensus Conference) classifies gastritis based primarily on the cause and duration of symptoms, resulting in the 3 types acute, chronic, and special. Gastritis may also be classified based on the kind of mucosal injury, resulting in the 2 types erosive and non-erosive.

The Operative Link for Gastritis Assessment (OLGA) staging system may also be used to classify cases of gastritis. The OLGA system was devised in an attempt to evaluate complication risk, in particular the development of gastritis into intestinal metaplasia or . The degree of atrophy and metaplasia at two main sites is scored on a four-tiered scale.

Stage II
Stage III
Stage IV
Stage IV


Signs and symptoms
Many people with gastritis experience no symptoms at all. However, upper central 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 , 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:


Causes

Infection
Helicobacter pylori infection is the most common cause of gastritis; when contracted this way, it may be termed H. pylori gastritis. H. pylori is a kind of bacteria which colonizes the gut of more than half of the world's population. While the bacteria is present in over half of the world's population, infection does not necessarily cause symptoms and thus most cases are asymptomatic. It has been suggested that H. pylori plays an important role in the natural stomach ecology.

While H. pylori is the most common infectious cause of gastritis, there are other pathogens which can cause the disease. Uncommon causes include those of the genera and . Rare bacterial causes include Helicobacter heilmannii, , and those of the genera , , , Proteus, , , and . Rare fungal causes include those of the genus and those which can cause . Rare parasitic causes include Ascaris lumbricoides and those of the parasitic genera , , and .


Drugs
Gastritis can result from usage of some drugs, the most common being usage of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen. Other drugs include , , when administered at toxic levels, (a kind of polystyrene sulfonate), , and those associated with and for cancer. Drugs used for COVID-19 treatment have also been found to cause gastritis; and are associated with chronic gastritis, while lopinavir/ritonavir is associated with the acute form.


Stress, injury, and illness
Gastritis (usually acute gastritis) may develop after acute stress, shock, and direct . Specific conditions include , (specifically in the stomach), , and food poisoning. Gastritis may also develop after major surgery or traumatic injury (), burns (Curling ulcer), or severe infections. Gastritis may also occur in those who have had weight loss surgery resulting in the banding or reconstruction of the digestive tract.

Gastritis is also associated with , in which bile and/or pancreatic enzymes flow up into the stomach; when bile travels further upwards into the esophagus, it is called gastric reflux. Excessive refluxed bile in the stomach causes irritation and inflammation to the stomach lining, leading to the development of gastric ulcers and/or gastritis; when contracted this way, it may be termed bile reflux gastritis.


Autoimmune (atrophic)
Autoimmune atrophic gastritis is a chronic form of gastritis caused by the destruction of gastric parietal cells due to an . These cells in the stomach produce necessary for the absorption of vitamin B12, and their destruction can result in vitamin B12 deficiency. Later stages of autoimmune atrophic gastritis may develop into pernicious anemia or megaloblastic anemia.


Diet
Evidence does not support a role for specific foods, including spicy foods and coffee, in the development of .
(2026). 9781605479682, Wolters Kluwer Health/Lippincott Williams & Wilkins. .
People are, however, usually advised to avoid foods that trigger symptoms.
(2026). 9780199585823, Oxford University Press, USA. .
There is little specific advice on diet published by authoritative sources. The National Health Service of the advises avoiding spicy, acidic or fried foods which may irritate the stomach.

It is generally advised to avoid alcohol consumption for the prevention and mitigation of gastrointestinal injury. Some sources describe alcohol as a potential cause of gastritis, while others describe it instead as a potential contributor to the erosion of the stomach's mucosal lining when ingested in large doses.


Diagnosis
Gastritis should be investigated when a patient reports abdominal discomfort, pain, and/or nausea. Diagnosis relies primarily on the findings of an upper endoscopy with , but also involves taking a comprehensive patient history. While history and other tests can help provide insights, histopathological examination of gastric biopsies are the gold standard, and allow one to identify the distribution, severity, and etiology of the disease.

Other tests which may be ordered to diagnose or rule out gastritis include:


Treatment
are a common treatment for mild to medium gastritis. When antacids do not provide enough relief, medications such as H2 blockers and proton-pump inhibitors that help reduce the amount of acid are often prescribed.

Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. They include the medications and . If are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is bismuth subsalicylate.

Several regimens are used to treat H. pylori infection. Most use a combination of two and a proton pump inhibitor. Sometimes bismuth is added to the regimen.


History
Gastric cancer was first described in 1000 A.D. by Persian physician . In 1728, German physician Georg Ernst Stahl coined the term "gastritis". Italian anatomical pathologist Giovanni Battista Morgagni further described the characteristics of gastric inflammation, including the characteristics of erosive or ulcerative gastritis and erosive gastritis. Between 1808 and 1831, French physician François-Joseph-Victor Broussais gathered information from autopsies of dead French soldiers. He described chronic gastritis as "gastritide" and erroneously believed that gastritis was the cause of , , and . In 1854, Charles Handfield Jones and described the microscopic changes of the stomach's inner lining in gastritis. In 1855, Baron Carl von Rokitansky first described hypertrophic gastritis. In 1859, British physician first described acute, subacute, and chronic gastritis. In 1870, Samuel Fenwick noted that pernicious anemia causes glandular in gastritis. German surgeon Georg Ernst Konjetzny noticed that both gastric ulcers and gastric cancer are the results of gastric inflammation. and Willam A. Meissner described the intestinal metaplasia of the stomach as a feature of chronic gastritis.
(2013). 9789535109075, University of Pécs.


Pathophysiology

Acute
Acute erosive gastritis typically involves discrete foci of surface necrosis due to damage to mucosal defenses. NSAIDs inhibit cyclooxygenase-1, or COX-1, an enzyme responsible for the biosynthesis of in the stomach, increasing the likelihood of forming. NSAIDs also inhibit synthesis, a hormone with a protective effect on the stomach's mucosal lining. While short-term NSAID use causes no problems, long-term use can lead to gastritis or other complications.


Metaplasia
is the transformation of differentiated cells from one type into another type. metaplasia can occur after severe damage to the gastric glands causes them to waste away (atrophic gastritis) and be progressively replaced by mucous glands. Gastric ulcers may develop; it is unclear if they are the causes or the consequences.

Intestinal metaplasia typically begins in response to chronic mucosal injury in the antrum and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics. Intestinal metaplasia is classified histologically as complete or incomplete. In the complete type, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In the incomplete type, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits .


See also


Further reading

External links
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