Gastritis

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Gastritis
proton pump inhibitors, antibiotics, sucralfate, bismuth subsalicylate,[1] antiemetics
Frequency~50% of people[4]
Deaths50,000 (2015)[5]

Gastritis is

autoimmune problems, low red blood cells due to not enough vitamin B12 may occur, a condition known as pernicious anemia.[3]

Common causes include infection with

autoimmune problems, radiation therapy and Crohn's disease.[1][8] Endoscopy, a type of X-ray known as an upper gastrointestinal series, blood tests, and stool tests may help with diagnosis.[1] The symptoms of gastritis may be a presentation of a myocardial infarction.[2] Other conditions with similar symptoms include inflammation of the pancreas, gallbladder problems, and peptic ulcer disease.[2]

Prevention is by avoiding things that cause the disease.

viscous lidocaine may help.[9] If gastritis is due to NSAIDs these may be stopped.[1] If H. pylori is present it may be treated with a combination of antibiotics such as amoxicillin and clarithromycin.[1] For those with pernicious anemia, vitamin B12 supplements are recommended either by mouth or by injection.[3] People are usually advised to avoid foods that bother them.[10]

Gastritis is believed to affect about half of people worldwide.

intestines known as duodenitis, resulted in 50,000 deaths in 2015.[5] H. pylori was first discovered in 1981 by Barry Marshall and Robin Warren.[12]

Signs and symptoms

A peptic ulcer may accompany gastritis. Endoscopic image.

Many people with gastritis experience no symptoms at all. However,

abdomen,[14]
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

There are two categories of gastritis depending on the cause of the disease. There is erosive gastritis, for which the common causes are stress, alcohol, some drugs, such as aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), and Crohn's disease. And, there is non-erosive gastritis, for which the most common cause is a Helicobacter pylori infection. [15][1]

Helicobacter pylori

ICD11.[6][7] More than 80% of individuals infected with the bacterium are asymptomatic and it has been postulated that it may play an important role in the natural stomach ecology.[17]

Critical illness

Gastritis may also develop after major surgery or traumatic injury ("Cushing ulcer"), 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.[citation needed]

Diet

Evidence does not support a role for specific foods, including spicy foods and coffee, in the development of

peptic ulcers.[18] People are usually advised to avoid foods that bother them.[10] There is little specific advice on diet published by authoritative sources. The National Health Service of the United Kingdom advises avoiding spicy, acidic or fried foods which may irritate the stomach.[19]

Pathophysiology

Acute

Early acute superficial gastritis: Marked neutrophilic infiltrates appear in the mucous neck region and lamina with a pit microabscess. This case was caused by Helicobacter pylori.

Acute erosive gastritis typically involves discrete foci of surface necrosis due to damage to mucosal defenses.

peptic ulcers forming.[21][22][23] Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach called prostaglandin. These drugs used in a short period are not typically dangerous. However, regular use can lead to gastritis.[24] Additionally, severe physiologic stress from sepsis, hypoxia, trauma, or surgery is also a common etiology for acute erosive gastritis, resulting in "stress ulcers". This form of gastritis can occur in more than 5% of hospitalized patients.[citation needed
]

Also, alcohol consumption does not cause chronic gastritis. It does, however, erode the mucosal lining of the stomach; low doses of alcohol stimulate hydrochloric acid secretion. High doses of alcohol do not stimulate secretion of acid.[25]

Chronic

Chronic gastritis refers to a wide range of problems of the gastric tissues.

kidney failure. Since 1992, chronic gastritis lesions are classified according to the Sydney system.[26]

Metaplasia

Mucous gland metaplasia, the reversible replacement of differentiated cells, occurs in the setting of severe damage of the gastric glands, which then waste away (atrophic gastritis) and are 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. With complete metaplasia, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits dysplasia.[20]

Diagnosis

Updated Sydney System for visual classification of gastritis on histopathology.

Often, a diagnosis can be made based on patients' description of their symptoms. Other methods which may be used to verify gastritis include:

The OLGA staging frame of chronic gastritis on histopathology. Atrophy is scored as the percentage of atrophic glands and scored on a four-tiered scale. No atrophy (0%) = score 0; mild atrophy (1–30%) = score 1; moderate atrophy (31–60%) = score 2; severe atrophy (>60%) = score 3. These scores (0–3) are used in the OLGA staging assessment in each 10 compartment:[28]

Corpus
No atrophy
(score 0)		 Mild atrophy
(score 1)		 Moderate atrophy
(score 2)		 Severe atrophy
(score 3)
Antrum
(including
incisura
angularis)
No atrophy (score 0) Stage 0 Stage I Stage II Stage II
Mild atrophy (score 1) Stage I Stage I Stage II Stage III
Moderate atrophy (score 2) Stage II Stage II Stage III Stage IV
Severe atrophy (score 3) Stage III Stage III Stage IV Stage IV

Treatment

proton-pump inhibitors that help reduce the amount of acid are often prescribed.[29][30]

Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine.

NSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is bismuth subsalicylate.[32]

Several regimens are used to treat H. pylori infection. Most use a combination of two

antibiotics
and a proton pump inhibitor. Sometimes bismuth is added to the regimen.

History

In 1,000 A.D,

subacute, and chronic gastritis. In 1870, Samuel Fenwick noted that pernicious anemia causes glandular atrophy in gastritis. German surgeon Georg Ernst Konjetzny noticed that both gastric ulcer and gastric cancer are the results of gastric inflammation. Shields Warren and Willam A. Meissner described the intestinal metaplasia of the stomach as a feature of chronic gastritis.[33]

See also

References

  1. ^ a b c d e f g h i j k l m n o p q r "Gastritis". The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). November 27, 2013. Archived from the original on 6 March 2015. Retrieved 1 March 2015.
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  7. ^ a b "ICD-11 for Mortality and Morbidity Statistics". icd.who.int. Retrieved 9 January 2024.
  8. ISBN 978-0-19-937333-8. Archived
    from the original on 2016-03-05.
  9. ISBN 978-1-4557-3394-1. Archived
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  10. ^
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  11. PMID 26063472
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  13. ^ a b "Gastritis Symptoms". eMedicineHealth. 2008. Archived from the original on 2008-12-06. Retrieved 2008-11-18.
  14. ^ "Gastritis". National Digestive Diseases Information Clearinghouse. National Institute of Diabetes and Digestive and Kidney Diseases. December 2004. Archived from the original on 2008-10-11. Retrieved 2008-10-06.
  15. ^ Vakil N (June 2021). "Gastritis - Digestive Disorders". MSD Manual Consumer Version. Merck & Co. Archived from the original on 13 August 2021. Retrieved 25 February 2022.
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  17. PMID 17016449. Archived
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  18. ISBN 978-1-60547-968-2. Archived
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  19. ^ "Gastritis: Things you can do to ease gastritis". National Health Service. 2019-05-20. Retrieved 2021-08-29.
  20. ^ a b c Vakil N (January 2007). "Gastritis". Merck Manual - Professional Version. Merck & Co. Archived from the original on 25 January 2009. Retrieved 11 January 2009.
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  23. S2CID 46147389
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  24. ^ a b Siegelbaum J (23 August 2019). "GI Health Resources > Gastritis". Jackson Siegelbaum Gastroenterology. Archived from the original on 15 June 2021. Retrieved 25 February 2022.
  25. S2CID 23245888
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  26. ^ Mayo Clinic Staff (April 13, 2007). "Gastritis". MayoClinic. Archived from the original on December 8, 2008. Retrieved 2008-11-18.
  27. ^ "Exams and Tests". eMedicinHealth. 2008. Archived from the original on 2008-12-11. Retrieved 2008-11-18.
  28. PMID 23983680.  This article incorporates text available under the CC BY 3.0
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  29. ^
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  30. S2CID 29732662
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  32. ^ "Gastritis". The Lecturio Medical Concept Library. Retrieved 22 July 2021.
  33. ISBN 978-953-51-0907-5
    . Retrieved 10 July 2018.

Further reading

External links

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