Atrophic gastritis

Atrophic gastritis
Atrophic gastritis
Classification and external resources
Specialty	gastroenterology
ICD-10	K29.4
ICD-9-CM	535.1
DiseasesDB	29503
eMedicine	med/851
MeSH	D005757

Atrophic gastritis (also known as Type A or Type B Gastritis more specifically) is a process of chronic inflammation of the stomach mucosa, leading to loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. As a result, the stomach's secretion of essential substances such as hydrochloric acid, pepsin, and intrinsic factor is impaired, leading to digestive problems. The most common are vitamin B₁₂ deficiency which results in a megaloblastic anemia and malabsorbtion of iron, leading to iron deficiency anaemia.^[1] It can be caused by persistent infection with Helicobacter pylori, or can be autoimmune in origin. Those with the autoimmune version of atrophic gastritis are statistically more likely to develop gastric carcinoma, Hashimoto's thyroiditis, and achlorhydria.

Type A gastritis primarily affects the body/fundus of the stomach, and is more common with pernicious anemia.

Type B gastritis primarily affects the antrum, and is more common with H. pylori infection.

Pathophysiology

Atrophic gastritis. Low zoom.

Autoimmune Metaplastic Atrophic Gastritis (AMAG) is an inherited form of atrophic gastritis characterized by an immune response directed toward parietal cells and intrinsic factor.^[2] The presence of serum antibodies to parietal cells and to intrinsic factor are characteristic findings. The autoimmune response subsequently leads to the destruction of parietal cells, which leads to profound hypochlorhydria (and elevated gastrin levels). The inadequate production of intrinsic factor also leads to vitamin B₁₂ malabsorption and pernicious anemia. AMAG is typically confined to the gastric body and fundus.

Hypochlorhydria induces G Cell (Gastrin producing) hyperplasia, which leads to hypergastrinemia. Gastrin exerts a trophic effect on enterochromaffin-like cells (ECL cells are responsible for histamine secretion) and is hypothesized to be one mechanism to explain the malignant transformation of ECL cells into carcinoid tumors in AMAG.

Associated conditions

Patients with atrophic gastritis are also at increased risk for the development of gastric adenocarcinoma.^[3] The optimal endoscopic surveillance strategy is not known but all nodules and polyps should be removed in these patients.

Classification

Atrophic gastritis is classified depending on the level of progress as "close type" or "open type". This classification was advocated by Takemoto and Kimura of Tokyo University at 1966.

Causes

Recent research has shown that AMAG is a result of the immune system attacking the parietal cells.

Environmental Metaplastic Atrophic Gastritis (EMAG) is due to environmental factors, such as diet and H. pylori infection. EMAG is typically confined to the body of the stomach. Patients with EMAG are also at increased risk of gastric carcinoma.

References

↑ Gut 2003;52:496-501 doi:10.1136/gut.52.4.496
↑ "Autoimmune Metaplastic Atrophic Gastritis: Gastritis and Peptic Ulcer Disease: Merck Manual Professional".
↑ Giannakis M, Chen SL, Karam SM, Engstrand L, Gordon JI (March 2008). "Helicobacter pylori evolution during progression from chronic atrophic gastritis to gastric cancer and its impact on gastric stem cells". Proc. Natl. Acad. Sci. U.S.A. 105 (11): 4358–63. doi:10.1073/pnas.0800668105. PMC 2393758. PMID 18332421.

Diseases of the digestive system (primarily K20–K93, 530–579)

Upper GI tract

Esophagus	Esophagitis Candidal Eosinophilic Herpetiform Rupture Boerhaave syndrome Mallory-Weiss syndrome UES Zenker's diverticulum LES Barrett's esophagus Esophageal motility disorder Nutcracker esophagus Achalasia Diffuse esophageal spasm Gastroesophageal reflux disease (GERD) Laryngopharyngeal reflux (LPR) Esophageal stricture Megaesophagus

Stomach	Gastritis Atrophic Ménétrier's disease Gastroenteritis Peptic (gastric) ulcer Cushing ulcer Dieulafoy's lesion Dyspepsia Pyloric stenosis Achlorhydria Gastroparesis Gastroptosis Portal hypertensive gastropathy Gastric antral vascular ectasia Gastric dumping syndrome Gastric volvulus

Lower GI tract:
Intestinal/
Enteropathy

Small intestine (Duodenum/Jejunum/Ileum)	Enteritis Duodenitis Jejunitis Ileitis Peptic (duodenal) ulcer Curling's ulcer Malabsorption: Coeliac Tropical sprue Blind loop syndrome Small bowel bacterial overgrowth syndrome Whipple's Short bowel syndrome Steatorrhea Milroy disease bile acid malabsorption

Large intestine (Appendix/Colon)	Appendicitis Colitis Pseudomembranous Ulcerative Ischemic Microscopic Collagenous Lymphocytic Functional colonic disease IBS Intestinal pseudoobstruction / Ogilvie syndrome Megacolon / Toxic megacolon Diverticulitis/Diverticulosis

Large and/or small	Enterocolitis Necrotizing Gastroenterocolitis IBD Crohn's disease Vascular: Abdominal angina Mesenteric ischemia Angiodysplasia Bowel obstruction: Ileus Intussusception Volvulus Fecal impaction Constipation Diarrhea Infectious Intestinal adhesions

Rectum	Proctitis Radiation proctitis Proctalgia fugax Rectal prolapse Anismus

Anal canal	Anal fissure/Anal fistula Anal abscess Anal dysplasia Pruritus ani

GI bleeding/BIS

Accessory

Liver	Hepatitis Viral hepatitis Autoimmune hepatitis Alcoholic hepatitis Cirrhosis PBC Fatty liver NASH Vascular Budd-Chiari syndrome Hepatic veno-occlusive disease Portal hypertension Nutmeg liver Alcoholic liver disease Liver failure Hepatic encephalopathy Acute liver failure Liver abscess Pyogenic Amoebic Hepatorenal syndrome Peliosis hepatis Metabolic disorders Wilson's Disease Hemochromatosis

Gallbladder	Cholecystitis Gallstones/Cholecystolithiasis Cholesterolosis Rokitansky-Aschoff sinuses Postcholecystectomy syndrome Porcelain gallbladder

Bile duct/ Other biliary tree	Cholangitis Primary sclerosing cholangitis Secondary sclerosing cholangitis Ascending Cholestasis/Mirizzi's syndrome Biliary fistula Haemobilia Gallstones/Cholelithiasis Common bile duct Choledocholithiasis Biliary dyskinesia Sphincter of Oddi dysfunction

Pancreatic	Pancreatitis Acute Chronic Hereditary Pancreatic abscess Pancreatic pseudocyst Exocrine pancreatic insufficiency Pancreatic fistula

Abdominopelvic

Hernia	Diaphragmatic Congenital Hiatus Inguinal Indirect Direct Umbilical Femoral Obturator Spigelian Lumbar Petit's Grynfeltt-Lesshaft Undefined location Incisional Internal hernia

Peritoneal	Peritonitis Spontaneous bacterial peritonitis Hemoperitoneum Pneumoperitoneum

This article is issued from Wikipedia - version of the Friday, November 13, 2015. The text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for the media files.