Gastritis pathophysiology: Difference between revisions

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*[[Lymphocytes]] and [[plasma cell]] infiltration
*[[Lymphocytes]] and [[plasma cell]] infiltration
*[[Lymphoid follicles]] (typical feature of chronic gastritis)
*[[Lymphoid follicles]] (typical feature of chronic gastritis)
*Around one-fifth of cases with an inflamed cardia may undergo intestinal metaplasia. <ref name="pmid10566710">{{cite journal| author=Voutilainen M, Färkkilä M, Mecklin JP, Juhola M, Sipponen P| title=Chronic inflammation at the gastroesophageal junction (carditis) appears to be a specific finding related to Helicobacter pylori infection and gastroesophageal reflux disease. The Central Finland Endoscopy Study Group. | journal=Am J Gastroenterol | year= 1999 | volume= 94 | issue= 11 | pages= 3175-80 | pmid=10566710 | doi=10.1111/j.1572-0241.1999.01513.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10566710  }} </ref>


<gallery widths="150px">
<gallery widths="150px">
Chronic_gastritis_--_intermed_mag.jpg |thumb|250px|left| Chronic_gastritis_-_Intermedicate Magnification| By Nephron (Own work) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons <ref name="urlFile:Chronic gastritis -- intermed mag.jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File%3AChronic_gastritis_--_intermed_mag.jpg |title=File:Chronic gastritis -- intermed mag.jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>


Chronic_gastritis_--_intermed_mag.jpg | By Nephron (Own work) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons <ref name="urlFile:Chronic gastritis -- intermed mag.jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File%3AChronic_gastritis_--_intermed_mag.jpg |title=File:Chronic gastritis -- intermed mag.jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>
Chronic_gastritis_--_very_high_mag.jpg |thumb|250px|center| Chronic_gastritis_-_Very-High Magnification| By Nephron (Own work) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons <ref name="urlFile:Chronic gastritis -- very high mag.jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File%3AChronic_gastritis_--_very_high_mag.jpg |title=File:Chronic gastritis -- very high mag.jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>
Chronic_gastritis_--_very_high_mag.jpg | By Nephron (Own work) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons <ref name="urlFile:Chronic gastritis -- very high mag.jpg - Wikimedia Commons">{{cite web |url=https://commons.wikimedia.org/wiki/File%3AChronic_gastritis_--_very_high_mag.jpg |title=File:Chronic gastritis -- very high mag.jpg - Wikimedia Commons |format= |work= |accessdate=}}</ref>
 
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'''''Sydney system for grading of chronic gastritis'''''<ref name="pmid8827022">{{cite journal| author=Dixon MF, Genta RM, Yardley JH, Correa P| title=Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. | journal=Am J Surg Pathol | year= 1996 | volume= 20 | issue= 10 | pages= 1161-81 | pmid=8827022 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8827022  }} </ref>
'''''Sydney system for grading of chronic gastritis'''''<ref name="pmid8827022">{{cite journal| author=Dixon MF, Genta RM, Yardley JH, Correa P| title=Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. | journal=Am J Surg Pathol | year= 1996 | volume= 20 | issue= 10 | pages= 1161-81 | pmid=8827022 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8827022  }} </ref>

Revision as of 17:01, 14 December 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Overview

Gastritis depending on the causes may be classified into acute gastritis, chronic gastritis, atrophic gastritis, and H.pylori associated gastritis. In acute gastritis, the majority of patients, the initial acute phase of gastritis is subclinical and is of short duration (about 7 to 10 days). Acute gastritis also referred to as reactive gastritis occurs as a result of the trigger by factors such as NSAIDs, stress, bile reflux, radiation, alcohol abuse, cocaine addiction and ischemic damage. In chronic gastritis, the H. pylori infection persists leading to accumulation of large number chronic inflammatory cells leading to active chronic gastritis.

Pathophysiology

Acute gastritis

  • In the majority of patients, the initial acute phase of gastritis is subclinical and is of short duration (about 7 to 10 days).
  • Acute gastritis also referred to as reactive gastritis occurs as a result of the trigger by factors such as NSAIDs, stress, bile reflux, radiation, alcohol abuse, cocaine addiction and ischemic damage.
  • In the majority of cases of H.pylori infection, the infection is not eliminated and there will be gradual accumulation of chronic inflammatory cells over the next 3 or 4 weeks.[1]
  • In H.pylori infection, the organisms are spontaneously cleared in a small minority of people, especially in childhood.

Pathogenesis

Microscopic pathology

Histological features observed such as:

  • Hyperemia
  • Acute inflammation
  • Increased neutrophil polymorphonuclear leucocytes in the superficial lamina propria
  • Erosion of the surface epithelium
  • Sloughing
  • Mucosal necrosis to a greater extent
  • Scarring (later sequelae)

Chronic gastritis

In the majority of cases, the H. pylori infection persists leading to accumulation of large number chronic inflammatory cells leading to active chronic gastritis.

Pathogenesis

Also, these polymorphs accumulate around the pit isthmus, which is a proliferative compartment, causing lethal damage to stem cells resulting in glandular atrophy.

Microscopic pathology

Sydney system for grading of chronic gastritis[9]

Sydney system for grading of Chronic Gastritis
Feature Definition Grading guidelines
Chronic inflammation
  • Mild, moderate or severe increase in density
Activity
  • Mild: less than one-third of pits and surface infiltrated
  • Moderate: one-third to two-thirds
  • Severe: more than two-thirds
Atrophy
  • Loss of specialized glands from either antrum or corpus
  • Mild, moderate, or severe loss
Helicobacter pylori
  • Mild colonization: scattered organisms covering less than one-third of the surface
  • Moderate colonization: intermediate numbers
  • Severe colonization: large clusters or a continuous layer over two-thirds of surface
Intestinal Metaplasia
  • Mild: less than one-third of mucosa involved
  • Moderate: one-third to two-thirds
  • Severe: more than two-thirds

Atrophic Gastritis

Atrophy of stomach is defined as loss of glandular tissue due to continuous mucosal injury. This leads to thinning of gastric mucosa.

Pathogenesis

  • The continuous mucosal injury due to long-standing H. pylori infection, leads to atrophy of stomach.
  • This continuous pathological process results in erosion or ulceration of the mucosa leading to the destruction of the glandular layer and followed by fibrous replacement.
  • The destruction of the glandular basement membrane and the sheath of supporting cells prevents orderly regeneration. This uneven regeneration follows a divergent differentiation pathway producing metaplastic glands (pseudo-pyloric appearance) which are composed of cells of the 'ulcer-associated cell lineage'(UACL).[11]

Microscopic pathology

Videos

Chronic gastritis {{#ev:youtube|Wvn5TiiIB4Q}}


Atrophic gastritis {{#ev:youtube|760GB43AZqE}}

References

  1. Sobala GM, Crabtree JE, Dixon MF, Schorah CJ, Taylor JD, Rathbone BJ; et al. (1991). "Acute Helicobacter pylori infection: clinical features, local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid concentrations". Gut. 32 (11): 1415–8. PMC 1379180. PMID 1752479.
  2. Slomiany BL, Piotrowski J, Slomiany A (1998). "Induction of caspase-3 and nitric oxide synthase-2 during gastric mucosal inflammatory reaction to Helicobacter pylori lipopolysaccharide". Biochem Mol Biol Int. 46 (5): 1063–70. PMID 9861460.
  3. Crabtree JE (1996). "Gastric mucosal inflammatory responses to Helicobacter pylori". Aliment Pharmacol Ther. 10 Suppl 1: 29–37. PMID 8730257.
  4. 4.0 4.1 Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF; et al. (1993). "Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations". Gut. 34 (8): 1038–41. PMC 1374349. PMID 8174949.
  5. Genta RM, Hamner HW, Graham DY (1993). "Gastric lymphoid follicles in Helicobacter pylori infection: frequency, distribution, and response to triple therapy". Hum Pathol. 24 (6): 577–83. PMID 8505036.
  6. Voutilainen M, Färkkilä M, Mecklin JP, Juhola M, Sipponen P (1999). "Chronic inflammation at the gastroesophageal junction (carditis) appears to be a specific finding related to Helicobacter pylori infection and gastroesophageal reflux disease. The Central Finland Endoscopy Study Group". Am J Gastroenterol. 94 (11): 3175–80. doi:10.1111/j.1572-0241.1999.01513.x. PMID 10566710.
  7. "File:Chronic gastritis -- intermed mag.jpg - Wikimedia Commons".
  8. "File:Chronic gastritis -- very high mag.jpg - Wikimedia Commons".
  9. Dixon MF, Genta RM, Yardley JH, Correa P (1996). "Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994". Am J Surg Pathol. 20 (10): 1161–81. PMID 8827022.
  10. Neithercut WD, Milne A, Chittajallu RS, el Nujumi AM, McColl KE (1991). "Detection of Helicobacter pylori infection of the gastric mucosa by measurement of gastric aspirate ammonium and urea concentrations". Gut. 32 (9): 973–6. PMC 1379031. PMID 1916500.
  11. Pera M, Heppell J, Poulsom R, Teixeira FV, Williams J (2001). "Ulcer associated cell lineage glands expressing trefoil peptide genes are induced by chronic ulceration in ileal pouch mucosa". Gut. 48 (6): 792–6. PMC 1728308. PMID 11358897.

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